Nicholas A Soter

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Nicholas A Soter, M.D.

Professor; Med Dir Harris Skin & Cancer
Department of Dermatology
NYU Dermatologic Associates

Clinical Addresses

530 FIRST AVENUE, SUITE 7R
NEW YORK, NY 10016
Hours: Tue. 1 - 6:30; Wed. 9:30 - 11:30; Thu. 1 - 6:30
Handicap Access: yes
Phone: 212-263-5889
Fax: 212-263-7680

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Medical Specialties

Dermatology

Medical Expertise

General Dermatology, Phototherapy, Vitiligo, Urticaria/Hives, Cutaneous T-Cell Lymphoma, Psoriasis, Vasculitis, Immunological Dermatology

Vice President, American Dermatological Association

Insurance

Medicare

Insurance Disclaimer: Insurance listed above may not be accepted at all office locations. Please confirm prior to each visit. The information presented here may not be complete or may have changed.

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Board Certification

1970 — Dermatology
1985 — Clinical & Lab Dermatol Immunology (Derm)

Education

1961-1965 — University of Texas, Medical Education
1965-1966 — Boston City Hospital (Medical), Internship
1966-1968 — Baylor University Medical Center (Dermatolgy), Residency Training
1968-1969 — Massachusetts General Hospital (Dermatology), Residency Training
1971-1973 — Harvard Medical School (Immunology), Clinical Fellowships

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Research Interests

Mast cell biology, Inflammatory mediators in dermatologic diseases, Pathophysiology of urticaria and angioedema, cutaneous necrotizing vasculitides, mastocytosis, and photosensitivity.<br>

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All data from NYU Health Sciences Library Faculty Bibliography — -

Contact:
http://hsl.med.nyu.edu/faculty-bibliography-search#about

Positive patch- and photopatch-test reactions to methylene bis-benzotriazolyl tetramethylbutylphenol in patients with both atopic dermatitis and chronic actinic dermatitis
Gonzalez, Mercedes E; Soter, Nicholas A; Cohen, David E
2011 Apr;22(2):106-111, Dermatitis
Ultraviolet filters are the most common topical photoallergens. Although currently not available on the US market, methylene bis-benzotriazolyl tetramethylbutylphenol (referred to as bisoctrizole on product labels) represents a new class of UV filters that have both organic and inorganic properties and are widely available in different preparations in Europe, South America, and Asia. We report two patients with atopic dermatitis and chronic actinic dermatitis who had positive patch- and photopatch-test reactions, which suggested both an allergic contact and a photoallergic contact dermatitis from bisoctrizole. Neither patient could identify previous or current contact with the chemical; nonetheless, it is possible that either the allergic contact or photoallergic contact dermatitis from bisoctrizole led to their chronic actinic dermatitis
— id: 132871, year: 2011, vol: 22, page: 106, stat: Journal Article,

Chronic actinic dermatitis: an analysis at a single institution over 25 years
Que, Syril K; Brauer, Jeremy A; Soter, Nicholas A; Cohen, David E
2011 Jun;22(3):147-154, Dermatitis
BACKGROUND: Chronic actinic dermatitis (CAD) is a rare photosensitivity disorder with scant epidemiologic data. OBJECTIVE: To evaluate demographic data and results of photopatch and patch tests over a 25-year period. METHODS: Retrospective chart review of patients with CAD from 1993 to 2009. RESULTS: Forty patients had a mean age of 57.8 years, and 27 (67.5%) were men. Twelve patients (30%) were skin types I and II, and 17 (42.5%) were skin types V and VI. Nine patients (22.5%) were younger than 50 years, and 4 of these (44.4%) were men. One of the nine patients (11.1%) was skin type I, and 4 (44.4%) were skin types V and VI. Carba mix and para-phenylenediamine were the two most commonly positive agents in patch tests. Sunscreens and plants and plant derivatives were the most commonly positive agents in photopatch tests. CONCLUSIONS: Our findings suggest a trend of two new classes of North American patients at our institution being diagnosed with CAD-younger women with skin types IV to VI and older men with skin types I to III. We observed a greater-than-expected number of positive patch-test reactions to para-phenylenediamine. We suggest that patch testing and photopatch testing of individuals may be useful adjuncts in the assessment of CAD
— id: 134911, year: 2011, vol: 22, page: 147, stat: Journal Article,

An unusual bullous eruption in a patient with psoriasis: Calcipotriene phototoxicity
Anolik, Robert; Brauer, Jeremy A; Soter, Nicholas A
2010 Jun;62(6):1081-1082, Journal of the American Academy of Dermatology
— id: 115876, year: 2010, vol: 62, page: 1081, stat: Journal Article,

A 20-year analysis of previous and emerging allergens that elicit photoallergic contact dermatitis
Victor, Frank C; Cohen, David E; Soter, Nicholas A
2010 Apr;62(4):605-610, Journal of the American Academy of Dermatology
BACKGROUND: Retrospective chart reviews are periodically needed to update allergen series to detect changes in photoallergic contact dermatitis (PACD) over time. OBJECTIVE: We sought to evaluate photopatch test results during a 13-year period and extend the observations to 20 years. METHODS: A retrospective chart review was conducted in patients who were photopatch tested. RESULTS: In all, 76 patients were evaluated. A total of 69 positive photopatch and 45 positive patch test reactions were detected in 30 and 23 patients, respectively. The frequencies of the positive photopatch test reactions were sunscreens 23.2%, antimicrobial agents 23.2%, medications 20.3%, fragrances 13%, plants and plant derivatives 11.6%, and pesticides 8.7%. Of the positive photopatch reactions to antimicrobial agents, 60% were caused by Fentichlor. LIMITATIONS: This study was a retrospective chart analysis, and the number of patients was small. CONCLUSIONS: Sunscreens and antimicrobial agents were the most frequent allergens eliciting PACD, and there was a decrease in PACD caused by fragrances. The number of reactions to medications increased. This study also demonstrated that pesticides can be a cause of PACD. The detection of reactions to Fentichlor was unexpected and, although they have been attributed in some studies to cross-reactions to sulfanilamides and bithionol, such a robust association was not observed in this study. This study extends our experience of the changes in the allergens that elicit PACD to 20 years
— id: 108792, year: 2010, vol: 62, page: 605, stat: Journal Article,

Lichenoid drug eruption
Brauer, Jeremy; Votava, Henry J; Meehan, Shane; Soter, Nicholas A
2009 ;15(8):13-13, Dermatology online journal
A 78-year-old man presented with an eight-month history of folliculocentric, pink, hyperkeratotic papules and plaques with thick white scale that involved the entire body, with confluence on the buttocks and genitalia. A biopsy specimen demonstrated superficial and focal, mild perivascular and perifollicular, band-like lymphocytic infiltrate and eosinophils. There were lymphocytes extending to the dermo-epidermal junction with vacuolar changes. A diagnosis of lichenoid drug eruption secondary to a proton-pump inhibitor was made. To the best of our knowledge, only one other case of lichenoid drug eruption secondary to a proton-pump inhibitor has been reported
— id: 115875, year: 2009, vol: 15, page: 13, stat: Journal Article,

Interstitial granulomatous dermatitis with arthritis
Jabbari, Ali; Cheung, Wang; Kamino, Hideko; Soter, Nicholas A
2009 ;15(8):22-22, Dermatology online journal
A 54-year-old woman with a history of arthritis presented for a long-standing history of symmetric, indurated plaques on her thighs and lateral aspects of the trunk. Histopathologic examination of skin biopsy specimens was consistent with interstitial granulomatous dermatitis, and a diagnosis of interstitial granulomatous dermatitis with arthritis was made. Administration of topical potent glucocorticoids, intralesional glucocorticoids, and narrow-band ultraviolet B phototherapy, in addition to continuation of systemic glucocorticoids and methotrexate, resulted in improvement of her cutaneous and musculoskeletal disease
— id: 108279, year: 2009, vol: 15, page: 22, stat: Journal Article,

Chronic actinic dermatitis
Booth, Alexandria V; Mengden, Stephanie; Soter, Nicholas A; Cohen, David
2008 ;14(5):25-25, Dermatology online journal
A 71-year-old man presented with a six-year history of a pruritic, erythematous, blistering eruption of the face, chest, and arms. Clinical findings, histopathologic features, and phototests were consistent with a diagnosis of chronic actinic dermatitis. The patient also had contact allergy and photocontact allergy to multiple allergens. A discussion of chronic actinic dermatitis is presented
— id: 94816, year: 2008, vol: 14, page: 25, stat: Journal Article,

Hereditary papulotranslucent acrokeratoderma
Rizzo, Carina; Bragg, Jennifer; Soldano, Anthony C; Cohen, David; Soter, Nicholas A
2008 ;14(5):3-3, Dermatology online journal
A 79-year-old woman presented with a history of peeling of the palms and soles that began in young adulthood, with exacerbation after exposure to water. Her mother, 2 sisters, and a female maternal cousin have similar symptoms. Physical examination showed scale and hyperlinearity of the palms. Brief exposure to water initiated the development of 1-to 2-mm, translucent, white papules that were distributed diffusely on the palmar surface, with a concentration at the palmar margins and pressure points. Histopathologic examination showed an acanthotic epidermis with a central depression that was filled with compact orthokeratosis. The physical examination and histopathologic findings are consistent with a diagnosis of hereditary papulotranslucent acrokeratoderma
— id: 94817, year: 2008, vol: 14, page: 3, stat: Journal Article,

Familial linear scleroderma (en coup de sabre) responsive to antimalarials and narrowband ultraviolet B therapy
Brownell, Isaac; Soter, Nicholas A; Franks, Andrew G Jr
2007 ;13(1):11-11, Dermatology online journal
A 32-year-old woman and her 35-year-old sister presented with plaques of scleroderma en coup de sabre. The younger sister's disease was more severe and preceded the older sister's by 10 years. This is the second reported case of familial en coup de sabre, and the first case of horizontal transmission. Treatment of the younger sister with antimalarials and narrow-band ultraviolet B (NB-UVB) phototherapy slowed disease progression and reversed hair loss. The observation that NB-UVB was effective in this case of linear scleroderma suggests that it may be indicated as a therapy for cutaneous scleroderma
— id: 76843, year: 2007, vol: 13, page: 11, stat: Journal Article,

Performance of a rapid dermatology referral system during the anthrax outbreak
Redd, John T; Van Beneden, Chris; Soter, Nicholas A; Hatzimemos, Eric; Cohen, David E
2005 Jun;52(6):1077-1081, Journal of the American Academy of Dermatology
The bioterrorism-related anthrax outbreak generated unanticipated demand for dermatologic services. In this study we sought to perform rapid, efficient, cost-effective evaluation of patients suspected of having cutaneous anthrax. During the outbreak, we developed an anthrax evaluation system featuring clinical field examination by nondermatologist physicians, followed by rapid referral of selected high-risk patients to a centralized dermatology center. We excluded anthrax in 29 previously screened high-risk patients. All were examined within 24 hours, costing $272.07 per patient. Diagnoses were established quickly (median, same day; range, 0-15 days). Among 2259 at-risk postal workers, 144 (6.4%) self-identified new (< or =14 days) skin lesions and were examined in the field; 8 (5.6%) were referred to our system. Our system was not the only local dermatologic resource available during the outbreak. A system featuring initial nondermatologist examination with minimal laboratory evaluation, followed by rapid centralized referral of high-risk patients, functioned efficiently in this outbreak
— id: 67942, year: 2005, vol: 52, page: 1077, stat: Journal Article,

Tumid lupus erythematosus: criteria for classification with immunohistochemical analysis
Alexiades-Armenakas, Macrene R; Baldassano, Marisa; Bince, Benji; Werth, Victoria; Bystryn, Jean-Claude; Kamino, Hideko; Soter, Nicholas A; Franks, Andrew G Jr
2003 Aug 15;49(4):494-500, Arthritis & rheumatism
OBJECTIVE: To define comprehensive criteria for the classification and differential diagnosis of tumid lupus erythematosus (LE). METHODS: A prospective study of patients fulfilling the classical description of tumid LE was performed. Clinical evaluation, histopathologic and direct immunofluorescence analyses of skin specimens, and serologic evaluation were conducted. The inflammatory cell infiltrate was quantitatively investigated by immunohistochemical analysis of fresh frozen skin specimens using multiple lymphocytic markers. RESULTS: Fifteen patients were followed for a mean of 7 years. Smooth, indurated, nonscarring, pink to violaceous papules, plaques, or nodules, devoid of surface changes were distributed on sun exposed sites. The mean lesion duration was 2 years, female:male ratio was 8:7, and racial distribution was 11 white, 2 Hispanic, and 2 African American patients. Histopathologic findings included a superficial and deep, perivascular, and frequently periadnexal infiltrate of lymphocytes, mucin deposition throughout the dermis, and absent to focal dermal-epidermal junctional involvement. Direct immunofluorescence immunoreactants and low titer antinuclear antibodies were variably present. Immunohistochemical findings included a predominance of pan-T cell marker CD3-expressing (78.0% +/- 6.3%) T lymphocytes. Most were CD4 expressing (82.7% +/- 8.0%) helper T cells; a minority were CD8 expressing (31.3% +/- 14.0%) cytotoxic T cells. The CD4:CD8 ratio was 3.1 (+/-1.3):1. One patient developed systemic LE and one a discoid LE lesion. CONCLUSION: Comprehensive clinical, histopathologic, and immunohistochemical criteria for the classification of tumid LE are proposed that differentiate tumid LE from other cutaneous disorders that may be clinically and histologically indistinguishable. The chronic, benign course indicates that tumid LE be classified as a form of chronic cutaneous LE, although it may be a cutaneous feature of systemic LE
— id: 39112, year: 2003, vol: 49, page: 494, stat: Journal Article,

Photodermatitis
Beck S; Soter NA
Current dermatologic diagnosis & treatment Philadelphia : Lippincott Williams & Wilkins, 2001,
— id: 3741, year: 2001, vol: , page: 156, stat: Chapter,

Urticaria and angioedema
Joe E; Soter N
Current dermatologic diagnosis & treatment Philadelphia : Lippincott Williams & Wilkins, 2001,
— id: 3661, year: 2001, vol: , page: 210, stat: Chapter,

Flushing
Joe E; Soter NA
Current dermatologic diagnosis & treatment Philadelphia : Lippincott Williams & Wilkins, 2001,
— id: 3658, year: 2001, vol: , page: 66, stat: Chapter,

Mastocytosis
Joe E; Soter NA
Current dermatologic diagnosis & treatment Philadelphia : Lippincott Williams & Wilkins, 2001,
— id: 3659, year: 2001, vol: , page: 112, stat: Chapter,

Cellular and immunologic mechanisms in atopic dermatitis
Leung DY; Soter NA
2001 Jan;44(1 Suppl):S1-S12, Journal of the American Academy of Dermatology
Atopic dermatitis is a chronic inflammatory skin disease that is frequently associated with respiratory allergies. Atopic dermatitis develops as a result of a complex interrelationship of environmental, immunologic, genetic, and pharmacologic factors. Efforts to understand the relative contributions of these factors have led to research seeking to identify the relevant effector cells and mediators involved in the pathogenesis of atopic dermatitis. These factors include the pattern of local cytokine release, the differentiation of helper T cells, multiple roles of IgE, skin-directed cell responses, infectious agents, and superantigens. This article reviews these cellular and immunologic mechanisms underlying atopic dermatitis and discusses how an understanding of their role in the inflammatory process may lead to improved treatments for atopic dermatitis
— id: 16945, year: 2001, vol: 44, page: S1, stat: Journal Article,

The skin
Soter N; Franks A Jr
Kelley's textbook of rheumatology Philadelphia PA : WB Saunders, 2001,
— id: 5283, year: 2001, vol: , page: 408, stat: Chapter,

Tacrolimus ointment for the treatment of atopic dermatitis in adult patients: part II, safety
Soter NA; Fleischer AB; Webster GF; Monroe E; Lawrence I
2001 Jan;44(1 Suppl):S39-S46, Journal of the American Academy of Dermatology
In two randomized, double-blind, multicenter studies, a total of 631 adult patients with moderate to severe atopic dermatitis applied tacrolimus ointment (0.03% or 0.1%) or vehicle twice daily for up to 12 weeks. The mean percent body surface area (%BSA) affected at baseline was 45%, and 56% of patients had severe atopic dermatitis. As previously reported, these studies showed that tacrolimus ointment was superior to vehicle for all efficacy parameters measured. This report focuses on the safety of tacrolimus ointment in these studies. The most common adverse events were the sensation of skin burning, pruritus, flu-like symptoms, skin erythema, and headache. Skin burning and pruritus were more common among patients with severe or extensive disease; these events were usually brief and were resolved during the first few days of treatment. Common adverse events with a significantly higher incidence in one or both of the tacrolimus ointment groups than in the vehicle group included skin burning, flu-like symptoms, and headache. More patients in the vehicle group discontinued the study because of an adverse event than in either of the tacrolimus ointment groups. There were no notable or consistent changes in any laboratory variables. Tacrolimus was not detected in 80% of blood samples collected. Measurable concentrations of tacrolimus were transitory and were not associated with adverse events. Tacrolimus ointment is a safe therapy for the treatment of adult patients with atopic dermatitis on the face, neck, or other body regions
— id: 16944, year: 2001, vol: 44, page: S39, stat: Journal Article,

Porphyrias
White KL; Soter NA
Current dermatologic diagnosis & treatment Philadelphia : Lippincott Williams & Wilkins, 2001,
— id: 3747, year: 2001, vol: , page: 168, stat: Chapter,

Plant and pesticide allergens in a phtopatch testing series
Beck S; Cohen DE; Soter NA
2000 ;11(2):129-129 abstract #14, American journal of contact dermatitis
— id: 25646, year: 2000, vol: 11, page: 129, stat: Journal Article,

Diagnostic tests for type IV or delayed hypersensitivity reactions
Cohen DE; Brancaccio RR; Soter NA
2000 ;15:287-305, Clinical allergy & immunology
— id: 11548, year: 2000, vol: 15, page: 287, stat: Journal Article,

Mastocytosis and the skin [In Process Citation]
Soter NA
2000 Jun;14(3):537-55, vi, Hematology-oncology clinics of North America
The most frequent site of organ involvement in individuals with any form of mastocytosis is the skin. Cutaneous lesions include urticaria pigmentosa, mastocytoma, diffuse and erythematous cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans. The major histologic feature is an increase in the number of mast cells in the dermis. Treatment depends on the type of skin lesions
— id: 11584, year: 2000, vol: 14, page: 537, stat: Journal Article,

Allergic contact and photoallergic contact dermatitis to plant and pesticide allergens
Mark KA; Brancaccio RR; Soter NA; Cohen DE
1999 Jan;135(1):67-70, Archives of dermatology
BACKGROUND: The panel of patch test allergens used for the evaluation of patients with suspected photoallergy typically does not include plant and pesticide allergens. The prevalence of allergic contact dermatitis and photoallergic contact dermatitis to plant and pesticide allergens was determined for this subgroup of patients. OBSERVATION: Positive reactions were detected in 12 of 26 patients who were tested with our photoallergen series: 5 with allergic contact dermatitis, 5 with photoallergic contact dermatitis, and 2 with both. Four of the 12 patients had positive patch and photo-patch test reactions to plant allergens, pesticide allergens, or both. The positive patch test reactions were to the plants Taraxacum officinale (dandelion) and Tanacetum vulgare (tansy) and to the pesticides folpet and captafol. Positive photo-patch test reactions were to the pesticides folpet and captan. The histories of the patients suggested that 2 or 3 of the 4 patients had clinically relevant reactions. In the other 8 patients, positive reactions to the patch and photo-patch tests included fragrances, sunscreens, and antibacterial agents. CONCLUSION: Plant and pesticide allergens should be included in the patch and photo-patch test series used for the evaluation of patients with suspected photoallergy
— id: 7401, year: 1999, vol: 135, page: 67, stat: Journal Article,

Hypopigmented mycosis fungoides associated with human T cell lymphotropic virus type I tax in a pediatric patient
Zucker-Franklin D; Kosann MK; Pancake BA; Ramsay DL; Soter NA
1999 May;103(5 Pt 1):1039-1045, Pediatrics
— id: 6106, year: 1999, vol: 103, page: 1039, stat: Journal Article,

Chronic actinic dermatitis: results of patch and photopatch tests with Compositae, fragrances, and pesticides
Lim HW; Cohen D; Soter NA
1998 Jan;38(1):108-111, Journal of the American Academy of Dermatology
— id: 16946, year: 1998, vol: 38, page: 108, stat: Journal Article,

Allergic and immunologic skin disorders
Leung DY; Diaz LA; DeLeo V; Soter NA
1997 Dec 10;278(22):1914-1923, JAMA
The skin represents a unique immunologic organ poised to protect the host from invading organisms and environmental antigens. The skin is also an important target for a variety of allergic and autoimmune responses. Mast cells are key to the pathogenesis of urticaria, angioedema, and mastocytosis. Atopic dermatitis is the consequence of an immunoregulatory abnormality resulting in a skin-directed T helper type 2 response. Allergic contact dermatitis is an example of classic delayed type hypersensitivity. Circulating autoantibodies against the epidermis are a key mechanism by which bullous skin diseases occur
— id: 16947, year: 1997, vol: 278, page: 1914, stat: Journal Article,

UVB phototherapy is an effective treatment for pruritus in patients infected with HIV
Lim HW; Vallurupalli S; Meola T; Soter NA
1997 Sep;37(3 Pt 1):414-417, Journal of the American Academy of Dermatology
BACKGROUND: Pruritus in patients positive for HIV may be debilitating. OBJECTIVE: Our purpose was to evaluate the efficacy of UVB therapy in the treatment of pruritus in patients positive for HIV. METHODS: Twenty-one male HIV-positive patients with intractable pruritus (14 with eosinophilic folliculitis and 7 with primary pruritus) were treated three times weekly with UVB phototherapy. Pruritus was quantified with use of a subjective score of 0 (none) to 10 (severe). RESULTS: Mean CD4 counts at the initiation of therapy were 91.0 +/- 31.9 cells/microliter. Pruritus scores before and after treatment were 8.6 +/- 0.4 and 2.2 +/- 0.5, respectively (p < 0.001). The mean number of treatments to achieve maximal improvement was 20.7 +/- 2.3, with a cumulative UVB dose of 3399.1 +/- 597.4 mJ/cm2. No significant difference was found between the group with eosinophilic folliculitis and the group with primary pruritus. CONCLUSION: UVB phototherapy can produce significant relief of pruritus and improvement in the quality of life in patients positive for HIV
— id: 16623, year: 1997, vol: 37, page: 414, stat: Journal Article,

Chronic actinic dermatitis associated with human immunodeficiency virus infection
Meola T; Sanchez M; Lim HW; Buchness MR; Soter NA
1997 Sep;137(3):431-436, British journal of dermatology
Chronic actinic dermatitis is a photodistributed, eczematous dermatitis that preferentially affects elderly men and persists for months to years. Its occurrence in individuals infected with human immunodeficiency virus (HIV) has been described in five patients. We report four additional cases of this uncommon, chronic photodermatosis associated with HIV infection. In two of the patients, photosensitivity was a presenting disorder leading to the diagnosis of HIV infection. All patients were men of skin type VI with a mean age of 50 years, all had decreased minimal erythema doses to ultraviolet B, three of the four patients had decreased minimal erythema doses to ultraviolet A and all had CD4 cell counts of < 200 x 10(6)/L
— id: 12167, year: 1997, vol: 137, page: 431, stat: Journal Article,

Skin response to ultraviolet B light in patients infected with human immunodeficiency virus
Kaporis A; Lim HW; Moy J; Soter NA; Sanchez M
1996 Oct-Dec;11(5-6):188-191, Photodermatology, photoimmunology, & photomedicine
Photosensitivity disorders have been reported in human immunodeficiency virus (HIV)-infected patients, often as the initial manifestation of the disease. The objective of this study was to evaluate whether the HIV-infected population demonstrates increased sensitivity to ultraviolet B (UVB) radiation. Minimal erythema dose values to UVB (MED-B) of 57 consecutive HIV-infected patients were compared to those of a control group of 57 consecutive patients with skin diseases, who were otherwise healthy and had no risk factors for HIV infection. MED-B determinations were performed in all individuals prior to the initiation of phototherapy for treatment of skin disease. None of the patients had a history of photosensitivity. Furthermore, the mean levels of the highest UVB doses received by each group during the treatment courses were compared. The mean age of the HIV-infected cohort was 43 years (range 26-61 years). The mean MED-B for this group was 82.8 +/- 3.8 (SEM) mJ/cm2. The mean age of the control group was 45 years (range 24-77 years), and their mean MED-B was 81.0 +/- 3.8 (SEM) mJ/cm2. After 12 weeks of treatment, one HIV-infected patient developed photosensitivity associated with a decreased MED-B value. The mean level of the highest UVB doses received by the HIV-infected group [427.5 +/- 67.2 (SEM) mJ/cm2] was lower than that received by the control group [640.8 +/- 65.9 (SEM) mJ/cm2], since HIV-infected patients received fewer treatments (mean: 34.7 treatments per patient) than the patients in the control group (mean: 65.6 treatments per patient). These data indicate that the HIV-infected patient population, without history of photosensitivity, does not show increased sensitivity to UVB light as determined by MED-B values
— id: 12537, year: 1996, vol: 11, page: 188, stat: Journal Article,

Allergic reactions to tattoo pigment after laser treatment
Ashinoff R; Levine VJ; Soter NA
1995 Apr;21(4):291-294, Dermatologic surgery
BACKGROUND. Cutaneous allergic reactions to pigments found in tattoos are not infrequent. Cinnabar (mercuric sulfide) is the most common cause of allergic reactions in tattoos and is probably related to a cell-mediated (delayed) hypersensitivity reaction. OBJECTIVE. The purpose of these case presentations is to describe a previously unreported complication of tattoo removal with two Q-switched lasers. RESULTS. Two patients without prior histories of skin disease experienced localized as well as widespread allergic reactions after treatment of their tattoos with two Q-switched lasers. CONCLUSION. The Q-switched ruby and neodymium:yttrium-aluminum-garnet lasers target intracellular tattoo pigment, causing rapid thermal expansion that fragments pigment-containing cells and causes the pigment to become extracellular. This extracellular pigment is then recognized by the immune system as foreign
— id: 12788, year: 1995, vol: 21, page: 291, stat: Journal Article,

CETIRIZINE AND ASTEMIZOLE THERAPY FOR CHRONIC IDIOPATHIC URTICARIA - A DOUBLE-BLIND, PLACEBO-CONTROLLED, COMPARATIVE TRIAL
BRENEMAN, D; BRONSKY, EA; BRUCE, S; KALIVAS, JT; KLEIN, GL; ROTH, HL; THARP, MD; TREGER, C; SOTER, N
1995 AUG ;33(2):192-198, Journal of the American Academy of Dermatology
Background: Cetirizine and astemizole have been shown to be safe and effective in the treatment of patients with chronic idiopathic urticaria. Cetirizine brings about clinical benefit more rapidly. Objective: The purpose of this study was to compare the efficacy of single daily doses of cetirizine and astemizole in relieving the symptoms of chronic idiopathic urticaria, with particular emphasis on the commencement of action. Methods: Patients with chronic idiopathic urticaria were randomly assigned to relieve either 10 mg of cetirizine, 10 mg of astemizole, or placebo for 4 weeks in a multicenter double-blind trial. Patients rated symptom severity each night, and investigators rated symptoms weekly. Results: One hundred eighty-seven patients were enrolled in the trial; 180 were included in the safety analysis and 177 were included in at least one efficacy analysis. Both cetirizine and astemizole were significantly superior to placebo in relieving symptoms of chronic idiopathic urticaria. Both patients' and investigators' ratings indicated that cetirizine acted more rapidly. Both active treatments were well tolerated, and the incidence of somnolence did not differ statistically between cetirizine (14.5%) and astemizole (10.3%). Conclusion: Both cetirizine and astemizole provide effective relief of the symptoms of chronic idiopathic urticaria with similar side-effect profiles. However, clinical benefit occurs significantly more rapidly with cetirizine
— id: 87247, year: 1995, vol: 33, page: 192, stat: Journal Article,

Efficacy of ultraviolet B phototherapy for psoriasis in patients infected with human immunodeficiency virus
Fotiades J; Lim HW; Jiang SB; Soter NA; Sanchez M; Moy J
1995 Jun;11(3):107-111, Photodermatology, photoimmunology, & photomedicine
To evaluate the efficacy of ultraviolet B (UVB) phototherapy for the treatment of psoriasis in patients infected with human immunodeficiency virus (HIV), the response of 14 patients was compared to that of matched seronegative control individuals. All patients were evaluated prior to treatment (baseline) and after 21 treatments for the extent of total body surface area (TBSA) involvement and the quantification of scale, erythema, and thickness of plaques using a scale of 0 (absent) to 4 (severe). The only concomitant medication allowed was salicylic acid in petrolatum. The cumulative score for scale, erythema, and thickness improved 1.9 +/- 0.5 [mean +/- standard error of mean (SEM)] in the HIV group and 2.4 +/- 0.3 in controls. There was 40.9 +/- 7.3% reduction of TBSA involvement in the former and 38.4 +/- 7.6% reduction in the latter group. None of the differences was statistically significant. There was no statistically significant difference in the response to therapy among various stages of immunosuppression in the HIV group. There was also no deterioration of immune status in this group. UVB phototherapy is an effective treatment for psoriasis in patients infected with HIV. The response is identical to that of matched control individuals
— id: 12765, year: 1995, vol: 11, page: 107, stat: Journal Article,

Results of evaluation of 203 patients for photosensitivity in a 7.3-year period
Fotiades J; Soter NA; Lim HW
1995 Oct;33(4):597-602, Journal of the American Academy of Dermatology
BACKGROUND: Although photosensitivity disorders have been well described, their incidence in a referral institution had not been studied. OBJECTIVE: The purpose of this study was to evaluate the incidence of photosensitivity disorders, including photocontact dermatitis, in an academic medical center. METHODS: The results of the assessment of 203 consecutive patients, all of whom had phototests, referred for the evaluation of photosensitivity disorders during a 7.3-year period were reviewed. RESULTS: The mean age was 50 years, and 63% of the patients were women. The most frequent diagnoses were polymorphous light eruption (26% of the total patient population), chronic actinic dermatitis (17%), photoallergic contact dermatitis (8%), systemic phototoxicity to therapeutic agents (7%), and solar urticaria (4%). Positive photopatch reactions, patch test reactions, or both were observed in 40 (29%) of the 138 tested patients. The frequencies of the positive photopatch test reactions were sunscreens (57%), fragrances (18%), and antimicrobial agents (13%). Of the positive patch test responses, fragrances elicited 47% of the total positive reactions, followed by sunscreens (39%) and antimicrobial agents (7%). CONCLUSION: Polymorphous light eruption, chronic actinic dermatitis, and photoallergic contact dermatitis were the most frequently made diagnoses. Sunscreens, fragrances, and antimicrobial agents were the most common clinically relevant photoallergens and allergens
— id: 12725, year: 1995, vol: 33, page: 597, stat: Journal Article,

A 3-YEAR FOLLOW-UP EVALUATION ON 28 HIV-POSITIVE PATIENTS TREATED WITH ULTRAVIOLET-B (UVB) PHOTOTHERAPY
FOTIADES, J; SOTER, NA; SANCHEZ, MR; MOY, JA
1995 APR ;104(4):660-660, Journal of investigative dermatology
— id: 87385, year: 1995, vol: 104, page: 660, stat: Journal Article,

Chronic actinic dermatitis. An immunohistochemical study of its T-cell antigenic profile, with comparison to cutaneous T-cell lymphoma
Heller P; Wieczorek R; Waldo E; Meola T; Buchness MR; Soter NA; Lim HW
1994 Oct;16(5):510-516, American journal of dermatopathology
Chronic actinic dermatitis (CAD) describes a persistent photosensitivity disorder in the absence of continued exposure to photosensitizers; it is characterized by a T-cell infiltrate within the epidermis and dermis. The purpose of this study was to characterize the T-cell infiltrate better immunohistochemically. Serial cryostat sections of fresh-frozen punch biopsy specimens of skin were analyzed in 11 patients with CAD and 3 patients with erythrodermic cutaneous T-cell lymphoma (CTCL). Monoclonal antibodies against the pan T-cell, pan B-cell, and T-cell subsets and the T cell-receptor (TCR) antigens were used. CD8-positive (T-suppressor-cytotoxic) cells were predominant in the epidermis of CAD, while CD4-positive (T-helper) cells were predominant in the epidermis and dermis of CTCL. CDw29-positive (T-memory) cells were predominant in all cases. The number of BF1 (beta-chain constant region of the TCR)-positive cells approximated the number of CD3-positive cells in all CAD cases but was significantly lower than the number of CD3-positive cells in two of three cases of CTCL. There was no clustering or preferential staining with any of the beta-chain variable-region antibodies in any of the specimens. These results indicate that CAD has a characteristic immunophenotype distinct from that of most cases of CTCL and that discordance between BF1 and CD3 expressions did not occur in the CAD cases
— id: 8258, year: 1994, vol: 16, page: 510, stat: Journal Article,

Chronic actinic dermatitis. An analysis of 51 patients evaluated in the United States and Japan
Lim HW; Morison WL; Kamide R; Buchness MR; Harris R; Soter NA
1994 Oct;130(10):1284-1289, Archives of dermatology
BACKGROUND AND DESIGN: We studied the clinical and photobiologic features of 51 patients with chronic actinic dermatitis who were evaluated at three institutions. The following criteria for patient selection were used: (1) a persistent eczematous eruption in the sun-exposed areas of greater than 3 months' duration; (2) decreased phototest results; and (3) when available, histologic changes of a dermal infiltrate of lymphocytes and macrophages, with or without epidermal spongiosis and atypical mononuclear cells in the dermis and epidermis. RESULTS: The 51 patients had a mean age of 62.7 years, a male-to-female ratio of 2.6:1, and a mean duration of eruption of 5.8 years. The most common abnormal results of the phototests were decreased minimal erythema doses to both UV-A and UV-B, followed by decreased minimal erythema doses to UV-A alone. Patients with abnormally low responses to UV-A or visible light and normal minimal erythema doses to UV-B had the same clinical profile as the overall patient population. Aside from protection from sunlight, treatment modalities that have been used include PUVA (8-methoxypsoralen and UV-A) photochemotherapy, azathioprine, hydroxychloroquine sulfate, and, for recalcitrant cases, cyclosporine. CONCLUSIONS: Chronic actinic dermatitis is a persistent photodermatosis associated with abnormal phototest responses to UV-A, and/or UV-B, and/or increased sensitivity to visible light; histopathologic changes are consistent with photodermatitis. Treatment consists of combinations of topical and oral medications
— id: 8257, year: 1994, vol: 130, page: 1284, stat: Journal Article,

A double-blind, placebo-controlled clinical trial to evaluate the safety and efficacy of thymopentin as an adjunctive treatment in atopic dermatitis
Stiller MJ; Shupack JL; Kenny C; Jondreau L; Cohen DE; Soter NA
1994 Apr;30(4):597-602, Journal of the American Academy of Dermatology
BACKGROUND: Multiple immunologic abnormalities such as impaired T-cell function, elevated serum IgE level, and increased interleukin 4 production have been demonstrated in patients with atopic dermatitis. OBJECTIVE: As part of a 12-week, multicenter, double-blind, placebo-controlled clinical trial, we evaluated the safety and efficacy of thymopentin (Timunox) as an adjunctive treatment in patients with severe atopic dermatitis. METHODS: Thirty-nine patients at least 2 years old with severe atopic dermatitis on a minimum of 20% of their cutaneous surface area were randomly selected to receive either thrice-weekly subcutaneous injections of thymopentin, 50 mg, or placebo. Use of triamcinolone 0.1% or hydrocortisone 1.0% cream and oral antihistamines were permitted during this trial. RESULTS: After 12 weeks, thymopentin-treated patients had significantly greater improvement than those receiving placebo. No thymopentin-related adverse events occurred. CONCLUSION: Thymopentin may be a safe effective adjunct to therapy in patients with severe atopic dermatitis
— id: 12978, year: 1994, vol: 30, page: 597, stat: Journal Article,

Solitary mastocytoma in an adult. Treatment by excision
Ashinoff R; Soter NA; Freedberg IM
1993 May;19(5):487-488, Journal of dermatologic surgery & oncology
BACKGROUND. In approximately 65% of patients, mastocytosis presents between birth and 15 years of age. Although solitary mastocytomas usually appear within the first 3 months of life, in unusual circumstances they may appear in adulthood. OBJECTIVE. The rare entity of solitary mastocytoma in adulthood and the simple treatment method of excision are discussed. METHODS. Simple surgical excision without manipulation of the lesion was performed. RESULTS. The lesion was surgically excised without recurrence. CONCLUSION. Solitary mastocytoma is a rare lesion in adulthood. The differential diagnosis includes a melanocytic nevus, xanthogranuloma and leukemia cutis. Surgical excision offers a rapid, relatively simple and effective mode of treatment
— id: 13164, year: 1993, vol: 19, page: 487, stat: Journal Article,

Clinical photomedicine
Lim, Henry W.; Soter, Nicholas A
New York : M. Dekker, c1993,
— id: 473, year: 1993, vol: , page: , stat: ,

The safety of UVB phototherapy in patients with HIV infection
Meola T; Soter NA; Ostreicher R; Sanchez M; Moy JA
1993 Aug;29(2 Pt 1):216-220, Journal of the American Academy of Dermatology
BACKGROUND: In patients with psoriasis and human immunodeficiency virus type 1 (HIV-1) infection, therapeutic options may be limited by their potential immunosuppressive effects. UVB radiation can activate HIV-1 gene expression in transgenic mice and in vitro. It is not known whether this viral activation leads to a clinically significant effect or if these findings can be extrapolated to humans. OBJECTIVE: This study was performed to evaluate the safety of UVB light treatment in HIV-infected persons. METHODS: We prospectively studied the effect of UVB phototherapy on five HIV-infected patients with psoriasis and one with pruritus. A complete blood cell count with differential count, CD4+ and CD8+ T-lymphocyte counts, serum beta 2-microglobulin and HIV-1 p24 antigen were obtained before UVB phototherapy and after 21 and 42 treatments. After every five treatments patients were evaluated for opportunistic infections, and psoriatic involvement was quantified with the Psoriasis Area and Severity Index (PASI). RESULTS: Cumulative UVB doses ranged from 3326 to 43,364 mJ/cm2. There were no statistically significant changes in laboratory findings after 21 and 42 treatments. Of three patients without detectable serum levels of HIV-1 p24 antigen before phototherapy, only one became positive after 42 treatments. None of the six subjects had an opportunistic infection or malignancy during phototherapy. The PASI improved in all five patients with psoriasis, and the other patient noticed decreased pruritus. CONCLUSION: Our results suggest that UVB phototherapy is efficacious in HIV-1-infected patients with UVB-responsive dermatoses and is not associated with short-term changes in immune function
— id: 6456, year: 1993, vol: 29, page: 216, stat: Journal Article,

The skin and rheumatic diseases
Soter N; Franks A Jr
Textbook of rheumatology Philadelphia PA : WB Saunders, 1993,
— id: 5284, year: 1993, vol: , page: 529, stat: Chapter,

Photosensitivity, abnormal porphyrin profile, and sideroblastic anemia
Lim HW; Cooper D; Sassa S; Dosik H; Buchness MR; Soter NA
1992 Aug;27(2 Pt 2):287-292, Journal of the American Academy of Dermatology
Cutaneous photosensitivity in a 43-year-old man with idiopathic sideroblastic anemia associated with an abnormal porphyrin profile is reported. This condition was associated with elevated free erythrocyte porphyrin, plasma protoporphyrin, urine porphyrins (predominantly coproporphyrin), stool porphyrins (predominantly protoporphyrin), decreased ferrochelatase activity, and deletion of portions of the long arms of chromosomes 18 and 20. Five other patients with sideroblastic anemia and abnormal porphyrin profiles have been described; all but one of these patients had photosensitivity. The porphyrin profile of this patient is similar to that of three other previously described patients
— id: 13488, year: 1992, vol: 27, page: 287, stat: Journal Article,

Ultraviolet-B phototherapy for early-stage cutaneous T-cell lymphoma
Ramsay DL; Lish KM; Yalowitz CB; Soter NA
1992 Jul;128(7):931-933, Archives of dermatology
BACKGROUND AND DESIGN--Cutaneous T-cell lymphoma (CTCL) is a slowly advancing disease that initially presents in the skin and may later progress to involve the lymph nodes and viscera. Since CTCL most often presents on non-sunlight-exposed regions of the body, a possible protective role for UVB irradiation has been suggested. Recent observations have also found that UVB irradiation serves an immunoregulatory role. Given that limited data are available regarding the use of UVB phototherapy in treating CTCL, a retrospective nonrandomized study of 37 nonconsecutive patients with early CTCL was performed to assess the efficacy of UVB phototherapy in the treatment of CTCL. RESULTS--Twenty-five (71%) of the 35 patients treated with UVB phototherapy (two were unavailable for follow-up) achieved a total clinical remission. Median time to remission was 5 months, and median duration of the remission was 22 months. Twenty-five (83%) of 30 patients with disease limited to patches achieved remission, whereas none of the patients with plaque-level disease achieved a remission. Of the 25 patients who achieved complete remission, five (20%) had a recurrence of CTCL. CONCLUSIONS--Phototherapy with UVB appears to be effective in patients with early patch-stage CTCL
— id: 13523, year: 1992, vol: 128, page: 931, stat: Journal Article,

Pathophysiology of dermatologic diseases
Baden, Howard P.; Soter, Nicholas A
New York : McGraw-Hill, Inc., Health Professions Division, c1991,
— id: 270, year: 1991, vol: , page: , stat: ,

AIDS-related eosinophilic pustular folliculitis
Buchness MR; Lim HW; Soter NA
1991 Nov;25(5 Pt 1):866-866, Journal of the American Academy of Dermatology
— id: 16948, year: 1991, vol: 25, page: 866, stat: Journal Article,

C5a, cutaneous mast cells, and inflammation: in vitro and in vivo studies in a murine model
Lim HW; He D; Esquenazi-Behar S; Yancey KB; Soter NA
1991 Aug;97(2):305-311, Journal of investigative dermatology
To evaluate further the interactions of C5a and mast cells in cutaneous inflammation, the ability of human native C5a (nC5a) (10 to 500 ng/ml) and human recombinant C5a (rC5a) (10 ng/ml to 100 ng/ml) to induce histamine release from purified BALB/c cutaneous mast cells (CMC) and peritoneal mast cells (PMC) was analyzed. It was found that nC5a induced histamine release from CMC but not from PMC, with a maximal net release at 250 ng/ml nC5a (22.8 +/- 2.6%). Kinetic experiments demonstrated that nC5a-induced maximal net histamine release occurred 5 min after the presentation of this stimulus (25.8 +/- 6.0%). Using rC5a and CMC, dose-response studies indicated a maximal net release of 7.0 +/- 1.7% at rC5a of 10 ng/ml, and kinetic studies showed a maximal net release at 5 min of incubation (12.9 +/- 1.6%). Release induced by rC5a was calcium-dependent, and peaked at 30 degrees C. These results indicate that functional heterogeneity exists between the CMC and the PMC of BALB/c mice, that C5a is a relevant stimulus for characterization of this heterogeneity, and that CMC from these animals can serve as a convenient in vitro model for the study of human C5a-mast cell interactions. In vivo, injections of nC5a (25-100 ng) and rC5a (25-100 ng) into the skin of BALB/c mice induced an increase in cutaneous vasopermeability, as assessed by the extravasation of intravenously injected 125I-bovine serum albumin. nC5a induced a dose-dependent increase in vasopermeability, whereas alterations induced by rC5a plateaued at 50 ng. The C5a-induced vasopermeability was markedly enhanced in animals that had been previously treated with an inhibitor of serum carboxypeptidase, which converts C5a to the less potent derivative, C5a des Arg. These findings suggest that carboxypeptidase plays an important role in vivo in the modulation of C5a-induced cutaneous inflammation in murine skin
— id: 16949, year: 1991, vol: 97, page: 305, stat: Journal Article,

Are topical corticosteroids useful adjunctive therapy for the treatment of psoriasis with ultraviolet radiation? A review of the literature
Meola T Jr; Soter NA; Lim HW
1991 Nov;127(11):1708-1713, Archives of dermatology
Adjunctive topical corticosteroids are often administered with UV-B phototherapy or oral psoralen plus UV-A (PUVA) photochemotherapy for the treatment of psoriasis. Five studies comparing PUVA alone with PUVA and topical corticosteroid preparations showed more rapid rates of clearing and a smaller total UV-A exposure with the latter regimen. However, one study demonstrated a higher relapse rate in association with corticosteroid use. Further studies to better define these risks are recommended. Six of seven reports evaluating the use of topical corticosteroid preparations with UV-B phototherapy failed to demonstrate an advantage to this regimen when compared with UV-B phototherapy alone. Therefore, the use of a topical corticosteroid preparation with UV-B phototherapy for the treatment of psoriasis is not recommended
— id: 13840, year: 1991, vol: 127, page: 1708, stat: Journal Article,

Acute and chronic urticaria and angioedema
Soter NA
1991 Jul;25(1 Pt 2):146-154, Journal of the American Academy of Dermatology
Urticaria and angioedema are clinical manifestations of various immunologic and inflammatory mechanisms, or they may be idiopathic. The respiratory and gastrointestinal tracts as well as the cardiovascular system may be involved in any combination. Patients with urticaria and/or angioedema can be classified based on pathophysiologic mechanisms into those with IgE-dependent or complement-mediated immunologic disorders, those with nonimmunologic disorders in which there is a direct effect on the mast cell or on arachidonic acid metabolism, and those whose condition is idiopathic. Evaluation of patients should focus on a thorough history. Laboratory tests provide minimal additional information. About one half of patients with urticaria alone and 25% with urticaria and angioedema or angioedema alone are free of lesions within 1 year. With urticaria, angioedema, or both, 20% of patients experience episodes for more than 20 years
— id: 13983, year: 1991, vol: 25, page: 146, stat: Journal Article,

Treatment of urticaria and angioedema: low-sedating H1-type antihistamines
Soter NA
1991 Jun;24(6 Pt 2):1084-1087, Journal of the American Academy of Dermatology
H1-type antihistamines are considered the therapeutic agents of choice for treating urticaria and angioedema. The use of traditional H1 antihistamines is limited by their side effects. In recent years low-sedating H1 antihistamines with reduced sedative and anticholinergic side effects have become popular choices for the treatment of urticaria and angioedema. Terfenadine and astemizole are currently available in the United States, and cetirizine and loratadine, currently under review at the Food and Drug Administration, are available in other countries. Terfenadine, cetirizine, and loratadine achieve rapid peak plasma concentrations in 1 to 2 hours, whereas astemizole has a slow onset of action. In double-blind, placebo-controlled studies of chronic idiopathic urticaria, low-sedating H1 antihistamines were more effective than placebo. The choice of a particular low-sedating H1 antihistamine depends on pharmacokinetic considerations and frequency of administration
— id: 14016, year: 1991, vol: 24, page: 1084, stat: Journal Article,

The skin in mastocytosis
Soter, N A
1991 Mar;96(3 Suppl):32S-39S, Journal of investigative dermatology
The most frequent site of organ involvement in patients with any form of mastocytosis is the skin. Cutaneous expressions include urticaria pigmentosa, mastocytoma, diffuse and erythrodermic cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans. The cutaneous lesions tend to appear early in life. Although urticaria pigmentosa has been reported in 12 pairs of twins and one set of triplets, the majority of affected individuals have no familial association. Most patients with systemic mastocytosis have skin lesions; however, an occasional patient will have systemic disease with no other skin features than flushing. In lesional cutaneous sites and in non-lesional skin, there is an increase in the number of mast cells. Electron microscopy shows quantitative differences between lesional skin mast cells from patients with and without systemic disease. The mast cells from adult patients with systemic disease have a larger mean cytoplasmic area, nuclear size, and granule diameter. The granules contain predominantly grating/lattice structures. The cutaneous mast cells contain tryptase and chymase. They retain their functional reactivities to relevant secretory stimuli, such as C3a, morphine sulfate, and calcium ionophore A23187. Lesional skin contains histamine, leukotriene B4, prostaglandin D2, 5-hydroxyeicosatetraenoic acid, platelet-activating factor, and heparin. Treatment of the cutaneous manifestations includes the use of H1 and H2 antihistamines, oral disodium cromoglycate, psoralens plus ultraviolet A photochemotherapy, and potent topical corticosteroid preparations.Journal of Investigative Dermatology (1991) 96, 32S-39S; doi:10.1111/1523-1747.ep12468973
— id: 67943, year: 1991, vol: 96, page: 32S, stat: Journal Article,

The skin in mastocytosis
Soter, N A
1991 Mar;96(3):32S-38S, Journal of investigative dermatology
The most frequent site of organ involvement in patients with any form of mastocytosis is the skin. Cutaneous expressions include urticaria pigmentosa, mastocytoma, diffuse and erythrodermic cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans. The cutaneous lesions tend to appear early in life. Although urticaria pigmentosa has been reported in 12 pairs of twins and one set of triplets, the majority of affected individuals have no familial association. Most patients with systemic mastocytosis have skin lesions; however, an occasional patient will have systemic disease with no other skin features than flushing. In lesional cutaneous sites and in non-lesional skin, there is an increase in the number of mast cells. Electron microscopy shows quantitative differences between lesional skin mast cells from patients with and without systemic disease. The mast cells from adult patients with systemic disease have a larger mean cytoplasmic area, nuclear size, and granule diameter. The granules contain predominantly grating/lattice structures. The cutaneous mast cells contain tryptase and chymase. They retain their functional reactivities to relevant secretory stimuli, such as C3a, morphine sulfate, and calcium ionophore A23187. Lesional skin contains histamine, leukotriene B4, prostaglandin D2, 5-hydroxyeicosatetraenoic acid, platelet-activating factor, and heparin. Treatment of the cutaneous manifestations includes the use of H1 and H2 antihistamines, oral disodium cromoglycate, psoralens plus ultraviolet A photochemotherapy, and potent topical corticosteroid preparations
— id: 115870, year: 1991, vol: 96, page: 32S, stat: Journal Article,

Cimetidine-induced augmentation of allergic contact hypersensitivity reactions in mice
Belsito DV; Kerdel FA; Potozkin J; Soter NA
1990 Apr;94(4):441-445, Journal of investigative dermatology
BALB/c mice were treated with cimetidine (100 mg/kg) or saline, intraperitoneally, twice daily, from days 0-2 or days 7-9 after sensitization with 0.1%, 2,4,6-trinitro-1-chlorobenzene (TNCB) on day 0. On day 7, the mice were challenged with 1% TNCB to one ear. Ear swelling responses (as an index of sensitization), serum histamine levels, and biopsy specimens of challenged ears were evaluated in groups of cimetidine- or saline-treated mice at 0, 0.5, 1, 1.5, 2, 4, 6, 8, 12, 24, and 48 h after challenge. Additional controls included mice injected with saline or cimetidine and challenged with, but not sensitized to, TNCB (irritant controls). Treatment with cimetidine during the induction but not the elicitation of allergic contact hypersensitivity (ACH) produced a significant enhancement of the response throughout the first 48 h. There was no effect of cimetidine on antigen-presenting cells within the epidermis which might account for this enhancement. Similarly, no difference in mast cell morphology or serum histamine levels between cimetidine- and saline-treated groups was observed. Histologically, the cimetidine-treated animals showed a more intense cellular infiltrate, which was most noticeable at 24 to 48 h, at which time numerous subcorneal and perifollicular neutrophilic abscesses were observed. To further investigate the mechanism of action of cimetidine, mice were injected with cyclophosphamide (150 mg/kg) 2 d prior to sensitization. Mice treated with cyclophosphamide alone or in combination with cimetidine showed no additive or synergistic effect upon the ear swelling response. We conclude that enhancement of ACH by cimetidine is independent of any effect on mast cells or antigen-presenting cells, but may relate to a cimetidine-induced inhibition of the induction of T-suppressor cells at the time of sensitization
— id: 16951, year: 1990, vol: 94, page: 441, stat: Journal Article,

Elevated plasma histamine levels in systemic sclerosis (scleroderma)
Falanga V; Soter NA; Altman RD; Kerdel FA
1990 Mar;126(3):336-338, Archives of dermatology
Systemic sclerosis is characterized by excessive deposition of collagen and other matrix proteins in the skin and internal organs. One hypothesis supports fibroblast stimulation for production of excess amounts of collagen by factors present in the blood or released by cells composing inflammatory tissue infiltrates. Increased numbers of mast cells are present in the involved skin of patients with systemic sclerosis, and histamine has been thought to be a possible mediator of fibrosis in this and other fibrotic conditions. We therefore measured plasma histamine levels in 32 patients with systemic sclerosis and found elevated levels in 18 patients (56%). Elevated plasma histamine levels were more common in patients with diffuse disease (74%), in contrast to limited disease (31%). The degree of clinical activity and the duration of disease could not be correlated with histamine levels
— id: 16952, year: 1990, vol: 126, page: 336, stat: Journal Article,

Mast-cell heterogeneity: functional comparison of purified mouse cutaneous and peritoneal mast cells
He D; Esquenazi-Behar S; Soter NA; Lim HW
1990 Aug;95(2):178-185, Journal of investigative dermatology
To investigate the functional heterogeneity of mouse mast cells, we extracted and purified cutaneous and peritoneal mast cells from 10- to 18-week-old BALB/c mice and compared their responses to secretagogues. Cutaneous mast cells (CMC) were extracted from mouse ears after digestion with hyaluronidase and collagenase in MEM containing 25% fetal calf serum and purified on a discontinuous Percoll gradient. The histamine content of cells obtained from the 30/40% interface was 1.0 +/- 0.1 pg/cell (mean +/- SE), with a mast-cell purity of 68.6 +/- 4.4% and a viability of greater than 93%. Peritoneal mast cells (PMC) were obtained by lavage with modified Tyrode's buffer followed by purification on 22.5% and 3-9% metrizamide gradients. The histamine content of cells was 12.2 +/- 0.8 pg/cell, with a mast-cell purity of 95.9 +/- 0.6% and a viability of greater than 95%. Histamine release induced by A23187 from CMC peaked at 3.0 microM A23187 (19.1 +/- 4.2%), at 3.0 min (22.3 +/- 2.3%), and at 30 degrees C (17.6 +/- 2.6%). In contrast, histamine release from PMC peaked at 8.0 microM of A23187 (49.4 +/- 12.1%) and at 15.0 min (48.5 +/- 12.2%). Release of histamine from PMC was observed at all the temperatures tested from 22 to 45 degrees C. Histamine release from CMC and PMC induced by A23187 was calcium dependent. Histamine release induced by compound 48/80 from CMC peaked at 0.5 micrograms/ml of compound 48/80 (23.0 +/- 7.4%) and at 5.0 min incubation (16.3 +/- 2.0%), whereas release from PMC peaked at 10.0 micrograms/ml (31.9 +/- 2.6%); release from PMC was similar at all the time points examined (1-15 min). Histamine release induced by substance P (SP) from both CMC and PMC peaked at 5.0 microM (18.8 +/- 6.6% and 12.6 +/- 3.7%, respectively); however, the maximal release from CMC occurred at 3.0 min (18.2 +/- 3.2%) and from PMC at 30.0 min (11.4 +/- 2.0%). SP-induced histamine release from CMC was calcium dependent, whereas release from PMC was only partially inhibited by EDTA. This study demonstrated that functional heterogeneity exists between these two populations of mast cells
— id: 16950, year: 1990, vol: 95, page: 178, stat: Journal Article,

Chronic actinic dermatitis. Study of the spectrum of chronic photosensitivity in 12 patients
Lim HW; Buchness MR; Ashinoff R; Soter NA
1990 Mar;126(3):317-323, Archives of dermatology
Twelve patients with photodermatitis for longer than 3 months' duration were identified: 1 patient with chronic photocontact dermatitis, 1 with persistent photosensitivity following exposure to a systemic medication, 6 with persistent light reactivity, and 4 with actinic reticuloid. There were 10 men and 2 women, ranging in age from 27 to 81 years, with a mean age of 62 years. The duration of the eruption ranged from 6 months to 20 years. Persistence of photosensitivity to quinidine, which is analogous to persistent light reactivity, was documented in 1 patient, and evolution from photocontact dermatitis to actinic reticuloid was observed in 2 others. These data, along with those reported in the literature, indicate that chronic photocontact dermatitis, persistent photosensitivity to systemic agents, persistent light reactivity, photosensitive eczema, and actinic reticuloid should be considered as entities occurring along a continuum, and the term 'chronic actinic dermatitis' is suggested to refer to these entities. Eight (67%) of the 12 patients had skin type VI and 2 others (17%) had skin type V, percentages markedly higher than those of the general patient population, demonstrating that chronic actinic dermatitis is not uncommon among individuals with dark skin
— id: 16102, year: 1990, vol: 126, page: 317, stat: Journal Article,

AGE-RELATED-CHANGES IN CONTACT HYPERSENSITIVITY
Potozkin, J; Soter, NA; Belsito, DV
1990 Apr;38(2):A620-A620, Clinical research
— id: 31982, year: 1990, vol: 38, page: A620, stat: Journal Article,

AGE-RELATED-CHANGES IN CONTACT HYPERSENSITIVITY
Potozkin, J; Soter, NA; Belsito, DV
1990 Apr;94(4):567-567, Journal of investigative dermatology
— id: 32001, year: 1990, vol: 94, page: 567, stat: Journal Article,

Acute effects of ultraviolet radiation on the skin
Soter NA
1990 Mar;9(1):11-15, Seminars in dermatology
The responses of normal skin to ultraviolet (UV) irradiation are an example of inflammation. The chromophores initiating the reaction are unknown. Characteristic clinical findings are erythema, heat, swelling, and pain. Histopathologic changes include epidermal keratinocyte damage with Langerhans cell depletion and dermal edema, endothelial swelling, mast cell degranulation, and cellular infiltration with neutrophils and monocytes. Biochemical changes include release of histamine, cyclo-oxygenase, and lipoxygenase-derived products of arachidonic acid, kinins, and cytokines, probably from a range of epidermal and dermal cell types. These substances very likely assist in mediation of the reaction. The response is more pronounced in young subjects. UVB (280 to 315 nm) and UVA (315 to 400 nm) radiation both produce inflammation, but with marked qualitative and quantitative differences. UVB having more effect on the epidermis, UVA more on the dermis
— id: 16953, year: 1990, vol: 9, page: 11, stat: Journal Article,

Urticaria: current therapy
Soter NA
1990 Dec;86(6 Pt 2):1009-1014, Journal of allergy & clinical immunology
Although the ideal treatment for urticaria is identification and removal of its cause, no underlying cause can be discerned in the majority of instances. The chief clinical problem is the treatment of chronic idiopathic urticaria. H1-receptor antagonists are the major class of therapeutic agents used in the management of chronic idiopathic urticaria. The H1 antagonists have been divided into subgroups based on their chemical structure. The second-generation H1 antagonists now available are particularly advantageous for individuals who must remain alert while working. Terbutaline, a beta-adrenergic agonist, is of occasional benefit as an adjunct therapy in combination with an H1 antagonist. The oral administration of disodium cromoglycate is ineffective in patients with chronic idiopathic urticaria, although a few individuals with urticaria caused by food allergy may respond to this drug. It is best to avoid repeated injections of epinephrine and the systemic administration of corticosteroids. Urticaria has a capricious course: it may respond to the administration of placebos or it may resolve spontaneously. About 50% of the patients with urticaria are free of lesions within 1 year, but 20% continue to have episodes for more than 20 years
— id: 14272, year: 1990, vol: 86, page: 1009, stat: Journal Article,

THE ROLE OF MAST-CELLS AND EOSINOPHILS IN EOSINOPHILIC PUSTULAR FOLLICULITIS OF THE ACQUIRED IMMUNODEFICIENCY SYNDROME
Buchness, MR; Gregory, N; Lim, HW; Soter, NA
1989 Apr;37(2):A665-A665, Clinical research
— id: 31722, year: 1989, vol: 37, page: A665, stat: Journal Article,

THE ROLE OF MAST-CELLS AND EOSINOPHILS IN EOSINOPHILIC PUSTULAR FOLLICULITIS OF THE ACQUIRED IMMUNODEFICIENCY SYNDROME
Buchness, MR; Gregory, N; Lim, HW; Soter, NA
1989 Mar;92(3):408-408, Journal of investigative dermatology
— id: 31813, year: 1989, vol: 92, page: 408, stat: Journal Article,

Cutaneous late-phase response to allergen. Mediator release and inflammatory cell infiltration
Charlesworth EN; Hood AF; Soter NA; Kagey-Sobotka A; Norman PS; Lichtenstein LM
1989 May;83(5):1519-1526, Journal of clinical investigation
To better define the inflammatory infiltrates and kinetics of mediator release during the cutaneous late-phase reaction (LPR), we examined skin biopsies at 8 h, and skin chamber cell counts and mediator release for 12 h after antigen challenge. Compared with the control sites, the antigen-stimulated biopsy sites contained 14 times as many basophils (P less than 0.01) and six times as many eosinophils (P less than 0.001) with one to two fold more mononuclear cells (P less than 0.03) and neutrophils (P less than or equal to 0.01). Similar changes were found in the skin chambers. Although there were neutrophils in the control chamber, they were only twice as numerous in the antigen challenged site (P less than 0.01). Eosinophils were 35-fold (P less than or equal to 0.03) more prevalent in the antigen chamber than the control chamber for hours 8-12 and basophils were noted starting in the eighth hour and were 20-fold (P less than or equal to 0.03) more concentrated in the antigen chamber during the next 4 h. The mononuclear cells were not significantly different between antigen and control blisters. With respect to inflammatory mediators, there was an initial peak of histamine (13.2 +/- 2.9 ng/ml) in the blister fluid at 1 h. The level then fell to approximately 2 ng/ml, followed by a secondary rise starting at the eighth hour and increasing to 9.8 +/- 2.8 ng/ml by the twelfth hour. This secondary increase in histamine correlated significantly (r = 0.81, P less than 0.05) with the observed influx of basophils.(ABSTRACT TRUNCATED AT 250 WORDS)
— id: 16956, year: 1989, vol: 83, page: 1519, stat: Journal Article,

Increased plasma histamine level in eosinophilic fasciitis
Falanga V; Soter NA; Kerdel FA
1989 Jun;125(6):805-808, Archives of dermatology
In a patient with eosinophilic fasciitis, a biopsy specimen obtained within 4 weeks of the onset of symptoms showed infiltration of the subcutis and fascia with mast cells, and there was up to a 19-fold increase in plasma histamine levels. The patient improved and experienced softening of the skin when treated with systemic corticosteroids and a histamine2-receptor antagonist, and her plasma histamine level returned to normal. Tissue mast cell infiltration and excessive plasma histamine levels were not present in two otherwise similar patients with eosinophilic fasciitis who were studied 7 months after disease onset. It is possible that mast cells play a pathogenic role in some patients with eosinophilic fasciitis
— id: 16955, year: 1989, vol: 125, page: 805, stat: Journal Article,

The late phase of hematoporphyrin derivative-induced phototoxicity in mice: release of histamine and histologic changes
He D; Soter NA; Lim HW
1989 Jul;50(1):91-95, Photochemistry & photobiology
This study was designed to directly examine the role of mast cells and the histologic changes in the late phase (4-48 h) of hematoporphyrin derivative-induced phototoxicity. BALB/c mice were rendered phototoxic by intraperitoneal injection of HpD, followed by exposure to 1.59 kJ/m2 of 396-406 nm radiation. Immediately before radiation, and at 4, 8, 12, 18, 24 and 48 h after radiation, the ear thickness, serum histamine levels and histologic changes of ears were examined. A maximal net increase in ear thickness of 33.5 +/- 0.3 X 10(-2) mm (mean +/- SE) was noted at 12 h, associated with a maximal net increase of serum histamine (43.3 +/- 11.6 ng/ml, mean +/- SE), and a maximal mast cell degranulation. Other histologic changes consisted of mild epidermal spongiosis at 18-24 h, and a predominant neutrophilic infiltrate, which peaked at 24 h (211.6 +/- 0.4 cells/mm2). No significant alteration was observed in control mice. These data indicated that mast cells participate in the late phase of HpD-induced phototoxicity in mice
— id: 16954, year: 1989, vol: 50, page: 91, stat: Journal Article,

SELECTIVE STIMULATION OF CUTANEOUS MAST-CELLS BY C5A - INVITRO AND INVIVO STUDIES
He, D; Soter, NA; Yancey, KB; Lim, HW
1989 Apr;37(2):A351-A351, Clinical research
— id: 31796, year: 1989, vol: 37, page: A351, stat: Journal Article,

The mast cell in mastocytosis and pediatric dermatologic disease
Kerdel FA; Soter NA
1989 ;4(5):159-180, Advances in dermatology
— id: 16957, year: 1989, vol: 4, page: 159, stat: Journal Article,

Morphology of atopic eczema
Soter NA
1989 ;44 Suppl 9:16-19, Allergy
The routine examination of skin biopsy specimens embedded in paraffin and strained with hematoxylin-eosin has failed to allow differentiation of atopic eczema from other types of eczematous dermatitis. The use of 1-micron plastic-embedded sections permits the recognition of infiltrating cell types and blood vessel alterations, thus allowing a refined method to examine cutaneous lesions and permit better definition of cutaneous structures than can be achieved in routinely-processed specimens. Acute vesicular lesions exhibited marked epidermal intercellular edema (spongiosis) and a dermal inflammatory infiltrate of lymphocytes, and activated lymphocytes with normal numbers of mast cells that exhibited various degrees of hypogranulation. Only rare eosinophils, neutrophils, and basophils were noted. Venular alterations included endothelial cell hypertrophy without necrosis. In lichenified plaques there was epidermal hyperplasia with a dermal inflammatory infiltrate that included increased numbers of fully granulated mast cells and increased numbers of lymphocytes and monocyte-macrophages. Alterations of venules included marked endothelial cell hypertrophy and basement membrane thickening. Cutaneous nerves exhibited demyelination and fibrosis. Also, increased numbers of Langerhans' cells have been noted in the epidermis of chronic lesions. Despite the absence of eosinophils, major basic protein has been demonstrated in the dermis by direct immunofluorescence techniques. Studies of lymphocyte subsets have shown increased numbers of CD4+ T lymphocytes
— id: 10783, year: 1989, vol: 44 Suppl 9, page: 16, stat: Journal Article,

EFFECT OF CYTOKINES ON PURIFIED MURINE MAST-CELLS
Soter, NA; Kopelson, P; Karas, E; Lim, HW
1989 Apr;37(2):A702-A702, Clinical research
— id: 31804, year: 1989, vol: 37, page: A702, stat: Journal Article,

EFFECT OF CYTOKINES ON PURIFIED MURINE MAST-CELLS
Soter, NA; Kopelson, P; Karas, E; Lim, HW
1989 Mar;92(3):521-521, Journal of investigative dermatology
— id: 31819, year: 1989, vol: 92, page: 521, stat: Journal Article,

Cutaneous inflammation: effects of hydroxy acids and eicosanoid pathway inhibitors on vascular permeability
Waldman JS; Marcus AJ; Soter NA; Lim HW
1989 Jan;92(1):112-116, Journal of investigative dermatology
Four metabolic products of arachidonic acid lipoxygenation, 5-hydroxyeicosatetraenoate (5-HETE), 12-HETE, 15-HETE, 5(S),12(S)-DiHETE, were injected intradermally into depilated dorsae of albino guinea pigs. The presence of intravenously injected 125I-bovine serum albumin (10uCi/kg) in 13-mm punch biopsy specimens served as a marker for altered vascular response; histologic changes were evaluated at 6 and 24 h after the injection in 1-micron-thick sections. Thirty minutes after the injections of 15 nanomoles and 60 nanomoles of 5-HETE, the ratios of radioactivity in HETE-injected to that in buffer-injected sites were 1.35 +/- 0.06 (mean +/- SE) and 2.80 +/- 0.27, respectively. Corresponding effects of 15-HETE were 1.39 +/- 0.17 and 1.63 +/- 0.21, respectively. Values for 60 nanomoles of 12-HETE and 5,12-DiHETE were intermediate in comparison with the above eicosanoids. The most notable histologic changes were a neutrophilic infiltrate induced by 12-HETE at 6 and 24 h, and neutrophilic and eosinophilic infiltrates in response to 5,12-DiHETE injection at 6 and 24 h. Effects of topically applied eicosanoid pathway inhibitors were also evaluated, using intradermally injected sodium arachidonate (AA) as agonist. Three mixed cyclooxygenase/lipoxygenase inhibitors, BW755C, phenidone, and nordihydroguaiaretic acid, suppressed vascular response by 9%, 9%, and 6% for 150 nmol of AA, and by 9%, 13%, and 12% for 300 nmol of AA, respectively. The cyclooxygenase inhibitor, indomethacin, induced suppressions of 39% for 150 nmol AA and 22% for 300 nmol AA, respectively. These data demonstrate that metabolites of both cyclooxygenase and lipoxygenase eicosanoid pathways are involved in alteration in vascular response accompanying cutaneous inflammation
— id: 16958, year: 1989, vol: 92, page: 112, stat: Journal Article,

AGE-RELATED DEFECTS IN MURINE ALLERGIC CONTACT HYPERSENSITIVITY
BELSITO D V; KERDEL F A; DERSARKISSIAN R M; SOTER N A
1988 ;1(2):139-147, Aging immunology & infectious disease
Allergic contract hypersensitivity (ACH)1 in young (3-5 mos.) and aged (16.18 mos.) BALB/c mice was evaluated by sensitizing the nape of the neck and subsequently challenging one ear with 1-chloro-2,4,6-trinitrobenzene (TNCB). Prior to sensitization, biopsy specimens of the contralateral unchallenged ears were obtained to determine the numbers of Ia+ Langerhans cells (LC) and mast cells (MC). Ear swelling responses, serum histamine levels, and histologic alterations of the challenged ears were evaluated in each age group at 0, 1.5, 4, 12 and 24 hrs. after challenge with TNCB. ACH was similar in young and aged mice during the first 12 hrs.; however, a significant difference in ear swelling was noted at 24 hrs. (38.0 .+-. 4.6 .times. 10-2 mm in young; 21.2 .+-. 2.0 in aged, p = 0.01.) There were no differences in MC number, degree of MC granulation, or serum histamine levels between young and aged mice at any time point. By 12 hrs., the inflammatory infiltrate in the ears of aged mice was slightly less intense and this difference became more marked at 24 hrs. At this time, the infiltrate consisted of neutrophils in young mice but continued to consist of mononuclear cells in the aged mice. Since the early ACH response in young and aged mice is similar, it is unlikely that decreased numbers of Ia+ LC in aged (449 .+-. 19 cells/mm2) as compared to young mice (720 .+-. 40) accounted for the decreased response at 24 hrs. We speculate that alterations in functional I cells in the age mice result in a diminished recruitment of neutrophils
— id: 98830, year: 1988, vol: 1, page: 139, stat: Journal Article,

Eosinophilic pustular folliculitis in the acquired immunodeficiency syndrome. Treatment with ultraviolet B phototherapy
Buchness MR; Lim HW; Hatcher VA; Sanchez M; Soter NA
1988 May 5;318(18):1183-1186, New England journal of medicine
— id: 11094, year: 1988, vol: 318, page: 1183, stat: Journal Article,

INVIVO RELEASE OF HISTAMINE IN THE LATE PHASE OF HEMATOPORPHYRIN DERIVATIVE-INDUCED PHOTOTOXICITY IN MICE
HE, D; SOTER, NA; LIM, HW
1988 APR ;36(3):A654-A654, Clinical research
— id: 41795, year: 1988, vol: 36, page: A654, stat: Journal Article,

INVIVO RELEASE OF HISTAMINE IN THE LATE PHASE OF HEMATOPORPHYRIN DERIVATIVE-INDUCED PHTOTOXICITY IN MICE
HE, D; SOTER, NA; LIM, HW
1988 APR ;90(4):568-568, Journal of investigative dermatology
— id: 41803, year: 1988, vol: 90, page: 568, stat: Journal Article,

FUNCTIONAL COMPARISON OF PURIFIED MOUSE CUTANEOUS AND PERITONEAL MAST-CELLS
LIM, HW; HE, D; SCOTTOCHINNICI, R; SOTER, NA
1988 APR ;90(4):582-582, Journal of investigative dermatology
— id: 41805, year: 1988, vol: 90, page: 582, stat: Journal Article,

FUNCTIONAL COMPARISON OF PURIFIED MOUSE CUTANEOUS AND PERITONIAL MAST-CELLS
LIM, HW; HE, D; SCOTTOCHINNICI, R; SOTER, NA
1988 APR ;36(3):A668-A668, Clinical research
— id: 41797, year: 1988, vol: 36, page: A668, stat: Journal Article,

AGE-RELATED DEFECTS IN ALLERGIC CONTACT HYPERSENSITIVITY (ACH)
Belsito, DV; Kerdel, FA; Dersarkissian, RM; Soter, NA
1987 Apr;88(4):477-477, Journal of investigative dermatology
— id: 31232, year: 1987, vol: 88, page: 477, stat: Journal Article,

EFFECT OF CIMETIDINE ON MURINE ALLERGIC CONTACT HYPERSENSITIVITY (ACH)
Belsito, DV; Kerdel, FA; Zhang, D; Soter, NA
1987 Apr;35(3):A386-A386, Clinical research
— id: 31189, year: 1987, vol: 35, page: A386, stat: Journal Article,

Evidence for histamine in the urticating hairs of Hylesia moths
Dinehart SM; Jorizzo JL; Soter NA; Noppakun N; Voss WR; Hokanson JA; Smith EB
1987 Jun;88(6):691-693, Journal of investigative dermatology
An urticarial dermatosis after contact with the urticating hairs of the adult female Hylesia moth may occur by several mechanisms including the intradermal injection of inflammatory mediators through the urticating hairs. Extracts were prepared from whole moths, urticating hairs, and other moth parts. Each of these extracts was subjected to a radioenzyme assay for histamine. Histamine was present in extracts made from whole moths and from urticating hairs. Extracts made from other moth parts contained no histamine. Cutaneous wheals occurred after intradermal injections of histamine and various concentrations of Hylesia extract (HE) into the backs of cynomolgus monkeys. This whealing response was suppressed by pretreatment of the animals with diphenhydramine hydrochloride, but not by pretreatment with indomethacin. Histologic examinations showed a perivascular lymphocytic infiltrate around dilated capillaries without evidence of mast cell degranulation in HE-injected sites but not in controls. These findings provide evidence that histamine may be the mediator responsible for the urticarial lesions seen after contact with Hylesia moths
— id: 16961, year: 1987, vol: 88, page: 691, stat: Journal Article,

INVIVO RELEASE OF HISTAMINE IN THE LATE PHASE OF HEMATOPORPHYRIN DERIVATIVE-INDUCED PHOTOTOXICITY IN MICE
He, D; Soter, NA; Lim, HW
1987 Sep;35(5):A811-A811, Clinical research
— id: 31354, year: 1987, vol: 35, page: A811, stat: Journal Article,

Mast cell participation during the elicitation of murine allergic contact hypersensitivity
Kerdel FA; Belsito DV; Scotto-Chinnici R; Soter NA
1987 Jun;88(6):686-690, Journal of investigative dermatology
In order to evaluate mast cell participation in allergic contact hypersensitivity (ACH), BALB/c mice were sensitized with 0.1% trinitrochlorobenzene (TNCB). Immediately before challenge and at 1, 1.5, 2, 4, 6, 8, 12, 24, and 48 h after challenge with 1% TNCB, groups of animals had ear thickness measured, had blood collected for histamine determinations, and had both ears removed for histologic evaluation of mast cells. The increase in ear swelling was triphasic with peak increases at 1.5 h (14.3 +/- 1.6 X 10(-2) mm; mean +/- SEM), 8 h (19.9 +/- 1.8 X 10(-2) mm), and 24 h (30.2 +/- 2.9 X 10(-2) mm). A triphasic pattern of increased serum histamine was noted at 1-4 h (117% over control levels), at 12 h (131%), and at 48 h (133%). Examination of the tissue specimens from challenged animals showed modest (1+) degranulation of mast cells between 1 and 6 h with extensive (2+) degranulation at 12 h. In addition, hypogranulated mast cells were evident between 1 and 6 h, at 24 h, and at 48 h. There were no statistically significant differences in mast cell numbers at any time. Neither platelets nor other formed elements of the blood contributed to the increased blood histamine levels. These data show that mast cells are activated in a triphasic pattern during ACH, and thus suggest both early and late roles for the mast cell and its products in the evolution of ACH
— id: 16962, year: 1987, vol: 88, page: 686, stat: Journal Article,

In vivo mediator release and degranulation of mast cells in hematoporphyrin derivative-induced phototoxicity in mice
Kerdel FA; Soter NA; Lim HW
1987 Mar;88(3):277-280, Journal of investigative dermatology
This study was designed to assess the role of the mast cell in the early phase of hematoporphyrin derivative (HPD)-induced phototoxicity. BALB/c mice were rendered phototoxic by i.p. injection of hematoporphyrin derivative, followed by exposure to 13.6 kJ/m2 of 400-410 nm radiation. The phototoxic response was quantified by measurement of ear thickness immediately before the irradiation, and at 0, 0.5, 1, 1.5, and 2 h after. At these time-points, determinations of serum histamine and plasma leukotriene C4 levels and histologic examination of the ears were undertaken. Mice injected i.p. with buffered saline and subsequently irradiated served as controls. In mice exposed to HPD and radiation, a maximal peak increased ear-thickness of 125.7 +/- 14.4% (mean +/- SEM) was noted at 2 h; this was associated with a net increased serum histamine of over 120% and histologic evidence of mast cell degranulation. In addition, moderate increases in plasma levels of leukotriene C4 were observed at 0 h and 1.5 h in the HPD- and irradiation-treated animals. These data provide direct evidence for the participation of mast cells in the early phase of HPD-induced phototoxicity
— id: 16963, year: 1987, vol: 88, page: 277, stat: Journal Article,

ALLERGIC CONTACT HYPERSENSITIVITY IN MAST-CELL DEFICIENT (W/WV) MICE
Kerdel, FA; Scottochinnici, R; Spencer, C; Belsito, DV; Soter, NA
1987 Apr;35(3):A694-A694, Clinical research
— id: 31378, year: 1987, vol: 35, page: A694, stat: Journal Article,

ALLERGIC CONTACT HYPERSENSITIVITY IN MAST-CELL DEFICIENT (W/WV) MICE
Kerdel, FA; Scottochinnici, R; Spencer, C; Belsito, DV; Soter, NA
1987 Apr;88(4):498-498, Journal of investigative dermatology
— id: 31389, year: 1987, vol: 88, page: 498, stat: Journal Article,

IDENTIFICATION AND QUANTITATION OF PAF FROM PSORIATIC SCALES
Ramesha, CS; Soter, N; Pickett, WC
1987 Aug;21(3-4):382-383, Agents & actions
— id: 31313, year: 1987, vol: 21, page: 382, stat: Journal Article,

Comparative aspects of canine and human atopic dermatitis
Rhodes KH; Kerdel F; Soter NA
1987 Aug;2(3):166-172, Seminars in veterinary medicine & surgery (small animal)
— id: 16960, year: 1987, vol: 2, page: 166, stat: Journal Article,

Investigation into the immunopathogenesis of canine atopy
Rhodes KH; Kerdel F; Soter NA; Chinnici R
1987 Aug;2(3):199-201, Seminars in veterinary medicine & surgery (small animal)
— id: 16959, year: 1987, vol: 2, page: 199, stat: Journal Article,

PHYSICAL URTICARIA ANGIOEDEMA
SOTER, NA
1987 DEC ;6(4):302-312, Seminars in dermatology
— id: 41771, year: 1987, vol: 6, page: 302, stat: Journal Article,

INDIRECT AND DIRECT EVIDENCE FOR HISTAMINE IN THE URTICATING HAIRS OF HYLESIA MOTHS
Dinehart, SM; Jorizzo, JL; Soter, NA; Noppakun, N; Voss, WR; Hokanson, JA; Smith, EB
1986 Jan;34(1):A263-A263, Clinical research
— id: 31027, year: 1986, vol: 34, page: A263, stat: Journal Article,

INDIRECT AND DIRECT EVIDENCE FOR HISTAMINE IN THE URTICATING HAIRS OF HYLESIA MOTHS
Dinehart, SM; Jorizzo, JL; Soter, NA; Noppakun, N; Voss, WR; Hokanson, JA; Smith, EB
1986 Apr;34(2):A746-A746, Clinical research
— id: 31048, year: 1986, vol: 34, page: A746, stat: Journal Article,

INDIRECT AND DIRECT EVIDENCE FOR HISTAMINE IN THE URTICATING HAIRS OF HYLESIA MOTHS
Dinehart, SM; Jorizzo, JL; Soter, NA; Noppakun, N; Voss, WR; Hokanson, JA; Smith, EB
1986 Apr;86(4):472-472, Journal of investigative dermatology
— id: 31072, year: 1986, vol: 86, page: 472, stat: Journal Article,

PARTICIPATION OF MAST-CELLS DURING THE ELICITATION OF ALLERGIC CONTACT HYPERSENSITIVITY REACTIONS
Kerdel, FA; Belsito, DV; Scottochinnici, R; Dersarkissian, R; Soter, NA
1986 Apr;34(2):A758-A758, Clinical research
— id: 31049, year: 1986, vol: 34, page: A758, stat: Journal Article,

PARTICIPATION OF MAST-CELLS DURING THE ELICITATION OF ALLERGIC CONTACT HYPERSENSITIVITY REACTIONS
Kerdel, FA; Belsito, DV; Scottochinnici, R; Dersarkissian, R; Soter, NA
1986 Apr;86(4):484-484, Journal of investigative dermatology
— id: 31073, year: 1986, vol: 86, page: 484, stat: Journal Article,

INVIVO RELEASE OF HISTAMINE AND DEGRANULATION OF MAST-CELLS IN HEMATOPORPHYRIN DERIVATIVE-INDUCED PHOTOTOXICITY IN MICE
Kerdel, FA; Parker, D; Soter, NA; Lim, HW
1986 Apr;34(2):A417-A417, Clinical research
— id: 31032, year: 1986, vol: 34, page: A417, stat: Journal Article,

Erythema nodosum leprosum: nature and extent of the cutaneous microvascular alterations
Murphy GF; Sanchez NP; Flynn TC; Sanchez JL; Mihm MC; Soter NA
1986 Jan;14(1):59-69, Journal of the American Academy of Dermatology
Skin biopsy specimens from four patients with erythema nodosum leprosum, when examined as Epon-embedded, 1-micron sections, exhibited a necrotizing vasculitis involving capillaries, venules, and small-to-medium arteries and veins. In the superficial dermis, affected venules and capillaries showed endothelial cell enlargement and focal necrosis associated with perivascular infiltrates of lymphocytes. In the deep dermis and subcutaneous tissue, affected venules, arterioles, and arteries exhibited endothelial cell necrosis and matted fibrin in the vessel walls associated with perivascular infiltrates of neutrophils. Throughout the dermis, mononuclear phagocytes with vacuoles containing numerous fragmented organisms were observed. By electron microscopy, electron-dense material resembling immune complexes was observed in the walls of these vessels. These observations support the concept that erythema nodosum leprosum is an immune complex-mediated necrotizing vasculitis involving capillaries, arterioles, arteries, venules, and veins
— id: 16965, year: 1986, vol: 14, page: 59, stat: Journal Article,

Mixed organic brain syndrome as a manifestation of systemic mastocytosis
Rogers MP; Bloomingdale K; Murawski BJ; Soter NA; Reich P; Austen KF
1986 Jul-Aug;48(6):437-447, Psychosomatic medicine
Systemic mastocytosis is a disease characterized by an excessive accumulation of mast cells, and associated with skin lesions, flushing, diarrhea, tachycardia, and psychiatric manifestations. In order to define more clearly the psychiatric manifestations, ten patients with this disorder underwent unstructured psychiatric interviews and a battery of psychologic testing. Both revealed a pattern of cognitive and affective changes in the majority of these patients, best categorized as an atypical or mixed organic brain syndrome. The cognitive changes consisted of diminished attention and memory, and the affective changes of anger, irritability, and, to a lesser extent, depression. These manifestations fluctuated with the level of disease activity, and appeared in some cases to respond to histamine antagonists and disodium cromoglycate, medications used to control the excessive mast cell activity. It is important for psychiatrists to be aware that mental status changes can represent psychiatric manifestations of mastocytosis, a readily treatable medical disorder
— id: 16964, year: 1986, vol: 48, page: 437, stat: Journal Article,

Effects of trimethaphan on arterial blood histamine and systemic hemodynamics in humans
Fahmy NR; Soter NA
1985 May;62(5):562-566, Anesthesiology
Because of lack of direct evidence of histamine release by trimethaphan, the authors determined serum histamine levels and hemodynamic responses to trimethaphan administration in 19 consecutive patients. Group 1 patients (n = 7) received a single intravenous injection of trimethaphan, 0.5 mg X kg-1, while awake and again during stable halothane-nitrous oxide anesthesia. Group 2 patients (n = 6) were pretreated with intravenous H1 (chlorpheniramine, 0.1 mg X kg-1) and H2 (cimetidine, 4 mg X kg-1) receptor antagonists administered 15 min before trimethaphan, 0.5 mg X kg-1, in the awake and anesthetized states. In Group 3 (n = 6), the effects of infusion of trimethaphan, 3 mg X min-1 for 15 min, were studied during halothane-nitrous oxide anesthesia. In Group 1, bolus doses of trimethaphan were associated with maximal increases in serum histamine from 0.56 +/- 0.14 to 2.56 +/- 0.35 ng X ml-1 (P less than 0.01) and from 0.60 +/- 0.11 to 2.58 +/- 0.33 ng X ml-1 (P less than 0.01) 2 min after drug administration in the awake and anesthetized states, respectively; there were also clinical manifestations of histamine release. Mean arterial pressure decreased maximally after 5 min in the awake (from 92.0 +/- 3.4 to 69.9 +/- 2.2 mmHg; P less than 0.01) and anesthetized (from 82.6 +/- 3.7 to 57.3 +/- 2.5 mmHg; P less than 0.01) states, and was associated with increases in cardiac output and heart rate; stroke volume increased in the awake state only.(ABSTRACT TRUNCATED AT 250 WORDS)
— id: 16967, year: 1985, vol: 62, page: 562, stat: Journal Article,

Localization of tryptase to human cutaneous mast cells and keratinocytes by immunofluorescence and immunoperoxidase cytochemistry with monoclonal antitryptase antibody
Schwartz LB; Foley JV; Austen KF; Soter NA; Shepard R; Murphy GF
1985 Aug;76(2 Pt 1):182-188, Journal of allergy & clinical immunology
A monoclonal antibody (H4) against tryptase purified from human pulmonary mast cells was prepared and used as an immunoreactive marker for the cellular localization of tryptase in normal human skin and in lesional skin from subjects with systemic mastocytosis. Mast cells had characteristic metachromatic staining of cytoplasmic granules with Giemsa reagent and were detected in small numbers about superficial vessels in the papillary dermis of nonlesional skin and in large numbers about deep as well as superficial vessels of lesional skin. By both direct immunofluorescence with fluorescein isothiocyanate-H4 and indirect immunoperoxidase cytochemistry with H4, all mast cells were selectively stained. The reactivity was confined to the cytoplasm and was granular in character. In addition, keratinocytes in epidermal tissue and in cell suspensions stained diffusely with H4 antibody. A tryptase-like activity that cleaved tosyl-L-arginine methyl ester (0.003 U/10(6) cells) and was not inhibited by soy bean and lima bean trypsin inhibitors was detected in sonicated suspensions of purified epidermal keratinocytes. Monoclonal antitryptase antibody represents an immunologic probe for the presence of tryptase, a preformed mediator of human mast cells, in tissues and cells
— id: 16966, year: 1985, vol: 76, page: 182, stat: Journal Article,

Pathophysiology of dermatologic diseases
Baden, H.; Soter, Nicholas A
New York : McGraw-Hill, c1984,
— id: 234, year: 1984, vol: , page: , stat: ,

Dermatologic needs in drugs and instrumentation
Bickers DR; Elias PM; Marks R; Soter NA; Voorhees JJ; Ziboh VA
1984 Nov;11(5 Pt 2):983-990, Journal of the American Academy of Dermatology
— id: 16968, year: 1984, vol: 11, page: 983, stat: Journal Article,

Eczematous and immunologic diseases
Gigli I; Hanifin JM; Katz SI; Provost TT; Soter NA
1984 Nov;11(5 Pt 2):948-956, Journal of the American Academy of Dermatology
— id: 16969, year: 1984, vol: 11, page: 948, stat: Journal Article,

Localization of histaminase to the specific granule of the human neutrophil
Ringel EW; Soter NA; Austen KF
1984 Aug;52(4):649-658, Immunology
The release of histaminase, a diamine oxidase of the human neutrophil, is initiated by soluble secretagogues. Histaminase is simultaneously inactivated by the reactive oxygen intermediates generated by the respiratory burst. Thus, quantitative assessment of histaminase release relative to other granule markers is best achieved in the presence of superoxide dismutase and catalase. Human neutrophils activated with secretagogues preferential for the specific granule, such as calcium ionophore A23187 in a limited concentration, phorbol myristate acetate (PMA), formyl-methionyl-leucylphenylalanine (fMLP), and concanavalin A, release vitamin B12-binding protein, lysozyme, and histaminase but not beta glucuronidase. PMA activation in the presence of cytochalasin B augments the release of lysozyme and initiates the release of beta glucuronidase through recruitment of the azurophilic granule but has no incremental effect on the release of vitamin B12-binding protein and histaminase observed with PMA alone. Subcellular fractionation of resting neutrophils by sucrose density gradient centrifugation to separate specific granules from two classes of azurophilic granules selectively distributes vitamin B12-binding protein and histaminase to the specific granule fractions
— id: 16970, year: 1984, vol: 52, page: 649, stat: Journal Article,

Role of histamine in the hemodynamic and plasma catecholamine responses to morphine
Fahmy NR; Sunder N; Soter NA
1983 May;33(5):615-620, Clinical pharmacology & therapeutics
The role of histamine in the hemodynamic and plasma catecholamine responses to intravenous morphine in subjects without cardiovascular disease and not receiving prior medication has not been reported. Systemic hemodynamics and serum histamine and plasma catecholamine concentrations were measured in 10 subjects before and 2, 5, 10, and 20 min after, 0.3 mg kg-1 IV morphine. Serum histamine concentration increased 2, 5, and 10 min after the morphine. Systolic and mean arterial pressures and systemic vascular resistance decreased and cardiac output increased because of increases in heart rate and stroke volume. The most important changes in hemodynamic function occurred after 2 min in association with a 400% increase in serum histamine concentration; these variables, together with serum histamine concentration, returned toward baseline values after 20 min. There was a negative correlation between peak increase in serum histamine concentration and maximum decrease in systemic vascular resistance. Plasma epinephrine concentrations were elevated 5, 10, and 20 min after morphine injection, suggesting activation of the adrenal medulla by histamine. Our data suggest that histamine plays an important role in the acute hemodynamic and plasma epinephrine response to morphine
— id: 16977, year: 1983, vol: 33, page: 615, stat: Journal Article,

Histologic changes associated with ultraviolet A--induced erythema in normal human skin
Gilchrest BA; Soter NA; Hawk JL; Barr RM; Black AK; Hensby CN; Mallet AI; Greaves MW; Parrish JA
1983 Aug;9(2):213-219, Journal of the American Academy of Dermatology
We have examined the effects of a standardized, moderately erythemogenic dose of long-wave ultraviolet (UVA) radiation on normal human skin, with the use of an appropriately filtered solar simulator and sequential biopsy specimens processed as 1-micron Epon-embedded sections. Histologic changes were present immediately after irradiation and evolved slowly during the 48-hour study. The epidermis manifested slight intracellular and intercellular edema and progressive loss of Langerhans cells to approximately one-fifth control values. A dermal infiltrate of neutrophilic polymorphonuclear leukocytes was present in all postirradiation specimens and peaked at 3 hours. A perivascular lymphocytic infiltrate, moderate endothelial cell enlargement, mast cell hypogranulation, occasional massive venular dilation, and sparse red blood cell extravasation were also noted. Overall, our findings expand and quantify earlier impressions that, compared to UVB, UVA has a relatively greater histologic effect on the dermis than on the epidermis, depletes epidermal Langerhans cells, and recruits neutrophils into irradiated human skin
— id: 16973, year: 1983, vol: 9, page: 213, stat: Journal Article,

Necrotizing vasculitis within cutaneous lesions of mycosis fungoides
Granstein RD; Soter NA; Haynes HA
1983 Jul;9(1):128-133, Journal of the American Academy of Dermatology
Mycosis fungoides is a T cell lymphoma with a predilection for cutaneous involvement. This paper describes the clinical manifestations and histopathologic features of a case of mycosis fungoides with necrotizing vasculitis localized to the lesions of cutaneous lymphoma. Elevated levels of circulating immune complexes were found in this patient. The large numbers of perivascular malignant helper T lymphocytes may have induced immunoglobulin synthesis, resulting in the formation of these complexes followed by deposition in vessel walls and subsequent necrotizing vasculitis. Possible alternative mechanisms include the presence of anti-T cell antibodies, or cytotoxic effector cells
— id: 16974, year: 1983, vol: 9, page: 128, stat: Journal Article,

Increased concentrations of arachidonic acid, prostaglandins E2, D2, and 6-oxo-F1 alpha, and histamine in human skin following UVA irradiation
Hawk JL; Black AK; Jaenicke KF; Barr RM; Soter NA; Mallett AI; Gilchrest BA; Hensby CN; Parrish JA; Greaves MW
1983 Jun;80(6):496-499, Journal of investigative dermatology
The buttock skin of clinically normal human subjects was subjected to approximately 2.5 minimal erythema doses of ultraviolet A irradiation. Deep red erythema developed during irradiation, faded slightly within the next few hours, increased to maximum intensity between 9-15 h, and decreased gradually thereafter although still persisting strongly at 48 h. Suction blister exudates were obtained at 0, 5, 9, 15, 24, and 48 h after irradiation as well as suction blister exudates from a contralateral control site and assayed for arachidonic acid, prostaglandins D2 and E2, and the prostacyclin breakdown product 6-oxo-prostaglandin F1 alpha by gas chromatography-mass spectrometry, and for histamine by radioenzyme assay. Increased concentrations of arachidonic acid and prostaglandins D2, E2, and 6-oxo-prostaglandin F1 alpha were found maximally between 5-9 h after irradiation, preceding the phase of maximal erythema. Elevations of histamine concentration occurred 9-15 h after irradiation, preceding and coinciding with the phase of maximal erythema. At 24 h, still at the height of the erythemal response, all values had returned to near control levels. Hence increased concentrations of arachidonic acid and its products from the cyclooxygenase pathway, and of histamine, accompany the early stages up to 24 h. A causal role in production of the erythema seems likely for these substances although other mediators are almost certainly involved
— id: 16976, year: 1983, vol: 80, page: 496, stat: Journal Article,

Lymphocyte subsets and Langerhans cells/indeterminate cells in erythema multiforme
Margolis RJ; Tonnesen MG; Harrist TJ; Bhan AK; Wintroub BU; Mihm MC; Soter NA
1983 Nov;81(5):403-406, Journal of investigative dermatology
A peroxidase-antiperoxidase study using monoclonal antibodies directed against T and B lymphocytes and Langerhans cells/indeterminate cells (LC/IC) was undertaken in order to understand more clearly the changes observed in erythema multiforme. At the various stages of development, from normal skin to target lesions, the quantity of inflammatory cells differed, but in each case the number of T8+ (cytotoxic/suppressor) cells was greater than the number of T4+ (helper/inducer) cells in the epidermis, whereas the latter exceeded the former in the dermis. Concomitant with the initial epidermis changes, there was an increase in the number of T6+ (LC/IC) cells in the upper and lower epidermis. With slight to moderate basal unit destruction, the number of LC/IC in the upper epidermis exceeded those in the lower epidermis. With severe basal unit destruction, there was a loss of LC/IC in the lower epidermis as detected by T6 reactivity. In fully formed blisters, the LC/IC in the upper half of the epidermis were decreased in parallel with the degree of epidermal necrosis. The character of the lymphocytic inflammatory infiltrate and redistribution in LC/IC are similar to those findings described in allergic contact dermatitis. The clinical, histologic, and immunopathologic changes in erythema multiforme appear to be due in part to cellular immune mechanisms with the lymphocyte as the predominant effector cell, and our data suggest a possible role for LC/IC in this disorder
— id: 16971, year: 1983, vol: 81, page: 403, stat: Journal Article,

Inhibition of rat mast cell arachidonic acid cyclooxygenase by dapsone
Ruzicka T; Wasserman SI; Soter NA; Printz MP
1983 Oct;72(4):365-370, Journal of allergy & clinical immunology
Dapsone (diaminodiphenylsulfone) has been used therapeutically for a variety of disorders in which mast cell participation has been demonstrated, including bullous pemphigoid and some form of necrotizing vasculitis. The mechanism of action of dapsone in these disorders is unknown but potentially relates to inhibition of mast cell activation and prevention of generation and/or release of mast cell mediators. Evidence for this possibility has been obtained in rat mast cells in which dapsone in a concentration-dependent manner prevented generation of prostaglandin D2 PGD2 from exogenous or endogenous arachidonic acid with 50% inhibition achieved at 1 and 0.2 to 0.4 mM, respectively. Dapsone inhibited cyclooxygenase conversion of arachidonic acid to PGD2 but not the GSH-dependent conversion of 14C-PGH2 to PGD2 by PGH-D isomerase in broken cell preparations. Dapsone prevented the immunologic generation of PGD2 from antigen-challenged rat mast cells but did not affect the release of histamine. Thus dapsone may exert some of its therapeutic effects by prevention of mast cell PGD2 generation
— id: 16972, year: 1983, vol: 72, page: 365, stat: Journal Article,

Exercise-induced anaphylaxis: a distinct form of physical allergy
Sheffer AL; Soter NA; McFadden ER; Austen KF
1983 Mar;71(3):311-316, Journal of allergy & clinical immunology
Seven individuals with exercise-induced anaphylaxis under natural circumstances, characterized by the appearance of pruritic cutaneous erythema and urticaria and associated vascular collapse and/or upper respiratory tract symptoms and signs of angioedema, were subjected to a controlled period of exercise in a laboratory. Experimental challenge consisted of running in an occlusive suit on a treadmill of moving grade with maintenance or acceleration of speed for 5 to 17 min. Cutaneous pruritus and erythema without urticaria developed in four of the subjects and progressed to angioedema in two of them; the other three subjects were unaffected. Repeat challenge of three of the abnormal responders elicited a clinical response similar to that of the previous exercise challenge. In those subjects with a clinical response to exercise challenge, mean change from baseline levels of histamine to peak levels was 7.0 +/- 3.0 ng/ml (mean +/- SEM), whereas in the group without clinical symptoms the mean change from baseline was an increase of 0.6 +/- 1.6 ng/ml (mean +/- SEM). The abnormal elevations in serum histamine during the seven exercise-induced symptomatic episodes returned to normal in about 20 min while clinical signs were also subsiding. There were no changes in pulmonary function. Exercise-induced anaphylaxis is clinically separable from cholinergic urticaria and represents a distinct form of physical allergy
— id: 16979, year: 1983, vol: 71, page: 311, stat: Journal Article,

Exercise-induced anaphylaxis: a distinct form of physical allergy
Sheffer AL; Soter NA; McFadden ER; Austen KF
1983 ;18(2):138-138, Monographs in allergy
— id: 16981, year: 1983, vol: 18, page: 138, stat: Journal Article,

Mast cells in cutaneous inflammatory disorders
Soter NA
1983 Jun;80 Suppl(1):22s-25s, Journal of investigative dermatology
Mast cells in skin are distributed around dermal and subcutaneous blood vessels. Activation of tissue mast cells produces secretion and/or generation and secretion of a variety of biologically active molecules. Mast-cell-dependent mediators may be classified as smooth-muscle-contracting and vasoactive activities, chemotactic factors, enzymes, and proteoglycans. These mediators alter the microenvironment to produce a biphasic response. The initial or humoral phase of the response is mediated by materials that alter vascular permeability; peripheral blood leukocytes attracted by chemotactic factors establish the cellular phase. Failure to limit the humoral phase creates a pharmacologic state that may be recognized in skin as urticaria/angioedema. The inability to control the cellular phase permits progression to a local inflammatory state with subacute and chronic tissue injury recognized in skin, for example, as necrotizing vasculitis. As an example of the former, certain forms of physical urticaria have provided experimental models in humans to allow observation of the clinical manifestations, study of tissue alterations by histologic analysis, measurement of mediators released into the circulation, and assessment of motility of peripheral blood leukocytes. An example of the role of the mast cell in the production of subacute and chronic inflammatory cutaneous disease is suggested by studies in a patient in whom exposure to the physical stimuli of cold and trauma was followed by initial mast cell degranulation, subsequent tissue deposition of circulating immune complexes, and the development of a necrotizing vasculitis
— id: 16975, year: 1983, vol: 80 Suppl, page: 22s, stat: Journal Article,

Local effects of synthetic leukotrienes (LTC4, LTD4, LTE4, and LTB4) in human skin
Soter NA; Lewis RA; Corey EJ; Austen KF
1983 Feb;80(2):115-119, Journal of investigative dermatology
The local effects of intracutaneous injections into humans of 1-3 nmol of five products of arachidonic acid metabolism, leukotrienes (LT) C4, D4, E4, and B4 from the 5-lipoxygenase pathways and prostaglandin (PG) D2 from the cyclooxygenase pathway, were assessed clinically and histologically. In equimolar concentrations, LTC4, LTD4, and LTE4, elicited erythema and wheal formation, in which a wheal with central pallor was present up to 2 hr, and the erythema persisted as long as 6 hr. PGD2 elicited a wheal that lasted up to 1 hr and erythema that lasted up to 2 hr. The dermal vascular sites affected by LTD4 and PGD2 included capillaries, superficial and deep venules, and arterioles. LTB4 elicited a transient wheal and flare, followed in 3-4 hr by induration that was characterized by a dermal infiltrate comprised predominantly of neutrophils. The combination of LTB4 and PGD2 elicited tenderness and increased induration associated with a more intense neutrophil infiltration. Thus, the products of the 5-lipoxygenase pathway of arachidonic acid metabolism in nanomole amounts can induce cutaneous vasodilation with edema formation and a neutrophil infiltrate, and these responses are enhanced by a cyclooxygenase pathway product, PGD2
— id: 16980, year: 1983, vol: 80, page: 115, stat: Journal Article,

Erythema multiforme: microvascular damage and infiltration of lymphocytes and basophils
Tonnesen MG; Harrist TJ; Wintroub BU; Mihm MC; Soter NA
1983 Apr;80(4):282-286, Journal of investigative dermatology
The sequence of alterations occurring in recurrent erythema multiforme was studied with clinical observations, 1-micrometer tissue sections, and immunofluorescence techniques. Lesions evolved through 3 stages: an initial red papule, a vesicle surmounting a red papule, and a target (iris) lesion. Focal endothelial cell swelling was present in clinically normal skin. In the red papule, endothelial cytoplasmic swelling, vacuolization, and nuclear hypertrophy with luminal obliteration of superficial venules developed. These venular alterations were more marked with endothelial cell necrosis, and involved deeper venules as well in vesicular and target lesions. Lymphocytes surrounded the venules and infiltrated the lower epidermis in the red papule and the vesicular lesions. Venular damage was correlated with the degree of infiltration by lymphocytes, apparently the primary effector cell, suggesting the venule as a primary target of injury. Hypogranulated basophils were noted around venules in vesicular and target lesions. Fibrin deposits were identified within and interstitially beneath the vesicles. The presence of lymphocytes, basophils, and interstitial fibrin deposition is similar to the changes of cutaneous delayed-type hypersensitivity and suggests a role for cell-mediated immunity in the pathogenesis of erythema multiforme
— id: 16978, year: 1983, vol: 80, page: 282, stat: Journal Article,

Abnormal histamine-induced suppressor-cell function in atopic subjects
Beer DJ; Osband ME; McCaffrey RP; Soter NA; Rocklin RE
1982 Feb 25;306(8):454-458, New England journal of medicine
To detect a potential defect in immunoregulatory function in atopic subjects, we studied histamine-induced suppressor-T-cell activity and histamine Type 1 and Type 2 receptors on T cells. Peripheral-blood mononuclear cells from 16 atopic subjects generated less histamine-induced suppressor activity than did those from 20 nonatopic normal controls (P less than 0.005). The percentage of T lymphocytes bearing histamine Type 2 receptors was lower in the atopic group than in the control group (P less than 0.001), but the percentage of cells with Type 1 receptors was the same in both groups. In the atopic subjects, the functional suppressor-cell abnormality positively correlated with the decreased phenotypic expression of histamine Type 2 receptors. No abnormality in concanavalin A-induced suppressor activity was detected in these subjects. Nonatopic control subjects with systemic mastocytosis had normal functional and phenotypic data, suggesting that chronic activation of atopic T cells in vivo by circulating histamine does not explain the abnormal histamine-induced suppressor response
— id: 16988, year: 1982, vol: 306, page: 454, stat: Journal Article,

Effect of chronologic aging and ultraviolet irradiation on Langerhans cells in human epidermis
Gilchrest BA; Murphy GF; Soter NA
1982 Aug;79(2):85-88, Journal of investigative dermatology
The effect of aging on epidermal Langerhans cells (LC) and on their response to a single ultraviolet (UV) exposure was studied in skin biopsy specimens of healthy adults, 4 aged 22-26 yr and 7 aged 62-86 yr. In unirradiated skin, old adults had fewer LC than young adults, 5.8 +/- 1.1 versus 10.0 +/- 0.8 (mean +/- SEM) per 3 mm wide cross-section (p = .015). Following irradiation with 3 times the minimal erythema dose, recognizable LC were absent in all but 2 subjects within 24 hr. However, LC number fell less rapidly in old adults and was almost unchanged at 4 hours (5.8 +/- 1.1 versus 5.0 +/- 1.2), while in young adults LC number decreased from 10.0 +/- 0.8 to 3.3 +/- 1.3 during the same period (p less than .05). Other changes noted in both young and old subjects following irradiation included cytoplasmic vacuolization, frequent apposition of LC to severely damaged keratinocytes, and the finding of LC in the basal layer of the epidermis rather than exclusively suprabasilarly as in control sections. These data demonstrate an age-associated loss of epidermal LC and slowing of LC response to UV irradiation. UV-induced LC changes appear qualitatively similar in young and old adults and include histological evidence of cellular damage, transient association of LC with damaged keratinocytes, and possible migration of LC from the irradiated epidermis within 24 hr
— id: 16984, year: 1982, vol: 79, page: 85, stat: Journal Article,

Chronologic aging alters the response to ultraviolet-induced inflammation in human skin
Gilchrest BA; Stoff JS; Soter NA
1982 Jul;79(1):11-15, Journal of investigative dermatology
In order to determine the effect of age on the capacity of human skin to mount an inflammatory response, the sunburn reaction was studied quantitatively in 4 subjects aged 22-26 yr and 7 subjects aged 62-86 yr. Buttock skin of each subject was exposed to 3 time his minimal erythema dose, using the Hanovia mercury vapor lamp; 1 micrometer histologic sections and determinations of histamine and prostaglandin E2 (PGE2) from suction blister aspirates were used to monitor the reaction. Clinically, erythema and edema were less (p less than .05) in irradiated skin of the old subjects during the first 24 hr. Nonirradiated skin contained less histamine and PGE2 in old adults (p less than .05), approximately 50% of young adult levels. Histamine levels rose early in the reaction and returned to baseline by 24 hr; 4 hr peak values averaged 9.2 ng/ml in old vs. 18.3 ng/ml in young adults. PGE2 rose more slowly in blister aspirates from old adults (P less than .05), but reached comparable peaks, 6-9 pg/T.V., in both groups at 24 hr. Biopsies of control skin from old adult specimens contained fewer mast cells and venules (P less than .01). At 4 and 24 hr, old specimens revealed fewer sunburn cells and less striking alterations of perivenular mast cells and endothelial cells, but at 72 hr these changes were more prominent than in young adult specimens. The data suggest that with advancing age the sunburn reaction is quantitatively reduced and evolves more slowly following a standardize ultraviolet exposure
— id: 16985, year: 1982, vol: 79, page: 11, stat: Journal Article,

Structure, function, and metabolism of leukotriene constituents of SRS-A
Lewis RA; Austen KF; Drazen JM; Soter NA; Figueiredo JC; Corey EJ
1982 ;9(8):137-151, Advances in prostaglandin thromboxane & leukotriene research
— id: 16989, year: 1982, vol: 9, page: 137, stat: Journal Article,

Prostaglandin D2 generation after activation of rat and human mast cells with anti-IgE
Lewis RA; Soter NA; Diamond PT; Austen KF; Oates JA; Roberts LJ
1982 Oct;129(4):1627-1631, Journal of immunology
Anti-IgE-dependent activation of rat and human mast cells resulted in the preferential generation of the cyclooxygenase products prostaglandin D2 (PGD2) and prostaglandin I2 (PGI2) in the rat and PGD2 in the human. The average net generation of PGD2, determined by gas chromatography-mass spectrometry, was 13.1 ng/10(6) purified rat mast cells and 39.5 ng/10(6) dispersed, enriched human mast cells. After IgE-dependent activation, there was a linear relationship between the net quantities of PGD2 generated and of histamine secreted from dispersed human pulmonary cells when the number of mast cells was varied but the total number of cells was held constant, indicating that it is the number of mast cells participating in IgE-dependent activation, rather than total mast cell number, that determines PGD2 generation. A linear relationship was also shown between PGD2 generation, determined by radioimmunoassay, and the release of the granule marker beta-hexosaminidase from purified rat mast cells on the dose-response portion of the plot of their response to anti-IgE challenge. With higher concentrations of anti-IgE, PGD2 generation from rat mast cells plateaued, whereas net percent beta-hexosaminidase release increased further. In kinetic studies of rat mast cells activated with anti-IgE, the onset (1 to 2 min) and time of maximum generation (5 to 10 min) for PGD2 were delayed relative to the onset (15 to 30 sec) and completion (1 to 2 min) of beta-hexosaminidase release. Thus, the extracellular appearance of PGD2 during IgE-dependent mast cell activation represents a response additional to the secretion of granule-associated mediators
— id: 16983, year: 1982, vol: 129, page: 1627, stat: Journal Article,

Gypsy-moth-caterpillar dermatitis
Shama SK; Etkind PH; Odell TM; Canada AT; Finn AM; Soter NA
1982 May 27;306(21):1300-1301, New England journal of medicine
— id: 16986, year: 1982, vol: 306, page: 1300, stat: Journal Article,

Lymphocytes and necrosis of the cutaneous microvasculature in malignant atrophic papulosis: a refined light microscope study
Soter NA; Murphy GF; Mihm MC
1982 Nov;7(5):620-630, Journal of the American Academy of Dermatology
Malignant atrophic papulosis is a disease characterized by multiple distinctive cutaneous and often lethal visceral infarctions. In some individuals, the diagnosis is not made until the skin manifestations are noted in a seriously ill patient with gastrointestinal and/or central nervous system disease. In other individuals, the disorder may pursue a benign course with only skin manifestations for many years. Using refined light microscopy to examine the skin lesions, the extensive nature of the necrotic microvascular alterations, a predominant lymphocytic infiltrate, and neural changes are documented. These findings suggest that the cutaneous lesions of malignant atrophic papulosis may result from a lymphocyte-mediated necrotizing vasculitis that affects the entire cutaneous microvasculature
— id: 16982, year: 1982, vol: 7, page: 620, stat: Journal Article,

The functional and physicochemical characterization of three eosinophilotactic activities released into the circulation by cold challenge of patients with cold urticaria
Wasserman SI; Austen KF; Soter NA
1982 Mar;47(3):570-578, Clinical & experimental immunology
The eosinophilic activity appearing in the venous effluent of the cold-induced angioedematous extremity of patients with cold urticaria has been resolved into three fractions by gel filtration and Dowex-1 chromatography. The low molecular weight activity, 300-700 mw, is highly acidic while the activity of 1000-3000 mw is composed of highly acidic and less acidic moieties. Each of the three activities has a different retention time on high pressure liquid chromatography, indicating that they represent distinct fractions which differ in size, charge, and hydrophobicity. Each fraction requires a gradient to attract eosinophils in a dose-response fashion and each deactivates eosinophils at subchemotactic concentrations. The more acidic 1000-3000 mw fractions also attract human monocytes in a chemotactic gradient at concentrations identical to those which attract human eosinophils. These three classes of eosinophil chemotactic activities and the activity for monocytes appear and disappear from the venous effluent with essentially the same time course as a distinct neutrophil chemotactic factor and histamine with cold induction of angioedema in patients with cold urticaria. The elaboration of these diverse chemoattractants in experimentally induced physical allergy provides potential pathways for mast cell-mediated infiltrative reactions
— id: 16987, year: 1982, vol: 47, page: 570, stat: Journal Article,

The human sunburn reaction: histologic and biochemical studies
Gilchrest BA; Soter NA; Stoff JS; Mihm MC
1981 Oct;5(4):411-422, Journal of the American Academy of Dermatology
The ultraviolet-induced erythema reaction was investigated histologically and biochemically in four subjects, utilizing suction blister aspirates, analyzed for histamine and prostaglandin E2 (PGE2), and Epon-embedded 1-mu skin biopsy sections from control skin and from irradiated skin at intervals for 72 hours after exposure to a Hanovia lamp. Major histologic alterations in the epidermis included dyskeratotic and vacuolated keratinocytes (sunburn cells), and disappearance of Langerhans cells. In the dermis the major changes were vascular, involving both the superficial and deep venular plexuses. Endothelial cell enlargement was first apparent within 30 minutes of irradiation, peaked at 24 hours, and persisted throughout the 72-hour study period. Mast cell degranulation and associated perivenular edema were first apparent at 1 hour and striking at the onset of erythema, 3 to 4 hours postirradiation; edema was absent and mast cells were again normal in number and granule content at 24 hours. Histamine levels rose approximately fourfold above control values immediately after the onset of erythema and returned to baseline within 24 hours. PGE2 levels were statistically elevated even before the onset of erythema and reached approximately 150% of the control value at 24 hours. These data provide the first evidence that histamine may mediate the early phase of the human sunburn reaction and increase our understanding of its complex histologic and biochemical sequelae
— id: 16990, year: 1981, vol: 5, page: 411, stat: Journal Article,

Functional characterization of synthetic leukotriene B and its stereochemical isomers
Lewis RA; Goetzl EJ; Drazen JM; Soter NA; Austen KF; Corey EJ
1981 Oct 1;154(4):1243-1248, Journal of experimental medicine
Leukotriene B (LTB), a potent lipid chemotactic factor for neutrophils, is 5S,12R-dihydroxy-6,14-cis,8,10-trans-eicosatetraenoic acid (Fig 1), based upon direct comparison of natural LTB with synthetic 5S,12R-dihydroxy-6,8,10,14-eicosatetraenoic acid (5,12-di-HETE) stereoisomers in three biological assays. Of the six synthetic stereoisomers evaluated, only the 5S,12R,6,14-cis,8,10-trans compound had chemotactic potency for human neutrophils in vitro that was comparable to that of natural LTB, with a concentration of 3 X 10(9-9) M eliciting a one-half maximum response. In contrast, the racemic mixture of 5R,12R- and 5S,12S-6,10-trans,8,14-cis, the racemic mixture of 5S,12R- and 5R,12S-6,10-trans,8,14-cis, the 5S,12R-6,8-trans,10,14-cis, the 5S,12R-6,8,10-trans,14-cis, and the 5S,12S-6,8,10-trans,14-cis stereoisomers required concentrations of 3 X 10(-7) to 1 X 10(-6) M to elicit comparable responses. Only natural LTB and its synthetic counterpart elicited a local neutrophil infiltration when injected into the skin of the rhesus monkey at 10 ng and 100 ng per site. Natural and synthetic LTB at a concentration of 3 X 10(-8) M each provoked an EC25 contractile response of guinea pig pulmonary parenchymal strips in vitro, whereas the other four tested stereoisomers of 5,12-di-HETE were inactive at this concentration. Structure-function analyses suggest that the neutrophil chemotactic activity depends critically upon the C-1 to C-12 domain, including the stereochemistry of the 6-,8-,and 10-olefinic bonds and the presence of both hydroxyl groups
— id: 16991, year: 1981, vol: 154, page: 1243, stat: Journal Article,

Physical urticaria/angioedema as an experimental model of acute and chronic inflammation in human skin
Soter NA
1981 Jun;4(1):73-81, Springer seminars in immunopathology
— id: 16992, year: 1981, vol: 4, page: 73, stat: Journal Article,

Biology of the mast cell and its role in cutaneous inflammation
Wintroub BU; Soter NA
1981 Jun;4(1):55-63, Springer seminars in immunopathology
— id: 16993, year: 1981, vol: 4, page: 55, stat: Journal Article,

Evaluation of role played by mediators of immediate hypersensitivity in exercise-induced asthma
Deal EC; Wasserman SI; Soter NA; Ingram RH; McFadden ER
1980 Mar;65(3):659-665, Journal of clinical investigation
— id: 17003, year: 1980, vol: 65, page: 659, stat: Journal Article,

Erythropoietic protoporphyria. Photoactivation of the complement system
Gigli I; Schothorst AA; Soter NA; Pathak MA
1980 Sep;66(3):517-522, Journal of clinical investigation
The complement system was analysed in 14 asymptomatic patients with erythropoietic protoporphyria. In the majority of the sera studied the levels of complement components C1, C4, C2, and C3 were within the normal range. Upon ultraviolet light (330--460 nm) irradiation of the serum samples in vitro, a marked decrease in total hemolytic activity accompanied by reduction of C1, C4, C2, and C3 levels was observed. The loss of total hemolytic activity can be directly correlated with the levels of protoporphyrin (PP) and similar changes can be obtained in normal serum upon addition of PP followedf by ultraviolet light irradiation. It is postulated that after irradiation the excited PP develops the capacity to activate the complement sequence with the production of cleavage products, which may contribute to the skin changes observed in these patients upon sun exposure
— id: 16996, year: 1980, vol: 66, page: 517, stat: Journal Article,

Circulating immune complexes in patients with necrotizing vasculitis
Kammer GM; Soter NA; Schur PH
1980 Apr;15(4):658-672, Clinical immunology & immunopathology
— id: 17000, year: 1980, vol: 15, page: 658, stat: Journal Article,

Magnitude and site of airway response to exercise in asthmatics in relation to arterial histamine levels
McFadden ER; Soter NA; Ingram RH
1980 Dec;66(6):472-477, Journal of allergy & clinical immunology
In order to determine if there is a relationship among arterial histamine levels, state of disease activity, and the magnitude and site of obstruction in exercise-induced asthma, we recorded airway resistance, lung volumes, spirometry, and density dependence of maximum expiratory flow before and after an exercise challenge in 17 asymptomatic individuals. These observations were then related to the concentration of histamine in systemic arterial blood. This study demonstrates that those individuals whose disease process was the most active at the time of investigation had more depressed lung function and higher baseline histamine levels, and responded to the challenge with severe obstruction that involved the airways in the periphery of the lung. In contrast, those subjects whose underlying disease was more quiescent had lower histamine values and the response to provocation was less severe and predominated in the larger airways. In neither group did the postchallenge values for histamine increase. It is suggested that the factor that determines these patterns of response is the state of inflammation of the airways, for which histamine may serve as a marker
— id: 16994, year: 1980, vol: 66, page: 472, stat: Journal Article,

Identification of sulfated mucopolysaccharides including heparin in the lesional skin of a patient with mastocytosis
Metcalfe DD; Soter NA; Wasserman SI; Austen KF
1980 Apr;74(4):210-215, Journal of investigative dermatology
Comparison of the [35S]mucopolysaccharides extracted after in vitro incubation of skin biopsy specimens from nonlesional and lesional sites of a patient with mastocytosis showed that lesional sites incorporated sulfate into heparin. After in vitro incorporation of the [35S]sulfate, the tissues were extracted sequentially by a 3-step procedure which utilized high salt concentrations, enzymatic digestion and base hydrolysis to liberate essentially all the counts. The extracted [35S]mucopolysaccharides were separated from free [35S]sulfate, histamine, protein, and hyaluronic acid by ion-exchange chromatography utilizing Dowex 1. The [35S]mucopolysaccharide extracts of the nonlesional skin were completely degraded by treatment with chondroitinase ABC, as they age predominantly dermatan sulfate with small amounts of chondroitin sulfates. The absolute quantity of sulfated mucopolysaccharides after Dowex 1 chromatography in micrograms of uronic acid per mg wet weight of starting tissue was higher in the lesional than the nonlesional specimen, while the specific incorporation of [35S]sulfate per microgram of uronic acid was the same. Approximately one-half of the [35S]mucopolysaccharides obtained in the 3 sequential extracts of lesional tissue was resistant to degradation by chondroitinase ABC as determined by gel filtration before and after enzyme treatment, indicating the presence of sulfated mucopolysaccharides in addition to chondroitin and dermatan sulfates. Heparinase treatment of the chondroitinase ABC-resistant [35S]mucopolysaccharides followed by gel filtration revealed an equal distribution of label between heparin and heparinase-resistant material presumed to be heparan sulfate. Heparin was also directly demonstrated in extracts of lesional mastocytosis skin by chemical and functional criteria
— id: 17001, year: 1980, vol: 74, page: 210, stat: Journal Article,

Possible naproxen-associated vasculitis
Mordes JP; Johnson MW; Soter NA
1980 Jul;140(7):985-985, Archives of internal medicine
— id: 16997, year: 1980, vol: 140, page: 985, stat: Journal Article,

High molecular weight neutrophil chemotactic factor: recognition, characterization, and role in the deactivation of neutrophillic leukocytes
Soter NA
1980 May;74(5):354-356, Journal of investigative dermatology
Idiopathic acquired cold-induced urticaria has provided a model to study release of mast cell-derived chemical mediators into the blood and alterations of neutrophilic leukocyte motility. A factor chemotactic for neutrophilic leukocytes appeared in the circulation after local experimental challenge with ice. After partial purification by Sephadex G-200 gel filtration and by anion and cation exchange chromatography the neutrophil chemotactic activity was excluded on Sepharose 4B gel filtration, indicating a molecular weight in excess of 750,000. On isoelectric focusing it exhibited a neutral isoelectric point. This chemotactic factor showed preferential chemotactic activity for neutrophils and deactivated these cells in vitro and in vivo. HMW-NCF may prove to be a useful marker of mast cell activation and its release may modulate the capacity for motility of neutrophilic leukocytes in humans
— id: 16998, year: 1980, vol: 74, page: 354, stat: Journal Article,

The skin in individuals with lupus erythematosus
Soter NA
1980 May-Jun;7(3):392-395, Journal of rheumatology
— id: 16999, year: 1980, vol: 7, page: 392, stat: Journal Article,

Physical urticaria/angioedema: an experimental model of mast cell activation in humans
Soter NA; Wasserman SI
1980 Nov;66(5):358-365, Journal of allergy & clinical immunology
Urticaria and angioedema may occur in skin and mucus membranes when mast cells are activated by various physical stimuli, including trauma, pressure, vibration, light, cold, heat, and (in rare cases) water. Experimental challenge of patients with cold-induced and cholinergic urticaria/angioedema in particular provides an in vivo model of mast cell activation in humans. This model synthesizes observations of the evolution of clinical manifestations, histologic analysis of tissue alterations, measurement of mediators released into the circulation, and assessment of leukocyte motility. The model in turn allows a characterization of mediators that exist preformed in mast cell granules or that are generated through interactions with other cell types. Release of these mediators produces a variety of biologic effects, including elaboration of certain enzymes and alterations in venular permeability, smooth muscle contraction, leukocyte motility, and the release of substances from other cell types
— id: 16995, year: 1980, vol: 66, page: 358, stat: Journal Article,

Release of mast-cell mediators and alterations in lung function in patients with cholinergic urticaria
Soter NA; Wasserman SI; Austen KF; McFadden ER
1980 Mar 13;302(11):604-608, New England journal of medicine
Cholinergic urticaria was elicited in seven subjects by experimental challenge that consisted of running on a treadmill in a plastic occlusive suit. A sensation of generalized warmth of the skin was followed by pruritus, erythema, urticaria, and transient respiratory-tract symptoms consisting of shortness of breath or wheezing or both. Statistically significant falls in one-second forced-expiratory volumes (FEV1), maximal midexpiratory flow rates (MMF), and specific conductance (SGaw) and a rise in residual volume were detected. The serum histamine concentration rose, with an augmentation of eosinophil and neutrophil chemotactic activities. Gel-filtration chromatography showed that the eosinophil chemotactic activity consisted of at least two principles. The chemotactic activities are similar in magnitude to those recognized in other skin disorders dependent on mast cells. These observations extend to the lungs the manifestations of a condition previously thought to be restricted to the skin
— id: 17002, year: 1980, vol: 302, page: 604, stat: Journal Article,

Inhibition of neutrophil chemotaxis in association with experimental angioedema in patients with cold urticaria: a model of chemotactic deactivation in vivo
Center DM; Soter NA; Wasserman SI; Austen KF
1979 Jan;35(1):112-118, Clinical & experimental immunology
Deactivation is a phenomenon in which leucocytes exposed in vitro to a chemotactic factor in the absence of a concentration gradient are rendered relatively unresponsive to stimulation by a subsequent chemotactic gradient. In patients with idiopathic cold-induced urticaria, the elicitation of a local experimental angioedematous lesion causes the release of two chemotactic principles previously shown to deactivate leucocytes in vitro, high molecular weight neutrophil chemotactic factor (HMW-NCF) and eosinophil chemotactic factor of anaphylaxis (ECF-A), into the venous circulation draining the challenged extremity. However, biopsy specimens of lesional skin sites obtained for up to 24 hr show no infiltration of cells. For this reason, the in vitro chemotactic responsiveness of neutrophils to the chemotactic factor HMW-NCF and C5 fragments were assessed in three patients at various times after experimental challenge. Leucocytes from venous effluent draining an experimentally-induced angioedematous lesion were markedly impaired in their chemotactic responsiveness to both chemotactic factors 5 min after challenge, while cells taken from an unchallenged extremity at the same time responded normally. Cells from both arms were equally impaired in their responsiveness 1 hr later, thereby demonstrating that the chemotactic defect becomes systemic. The acquired defect was dissipated 4 hr after challenge. These data suggest that deactivation may occur in vivo and may alter host responsiveness in states where chemotactic factors are released into the circulation
— id: 17010, year: 1979, vol: 35, page: 112, stat: Journal Article,

Psoriatic arthritis: a clinical, immunologic and HLA study of 100 patients
Kammer GM; Soter NA; Gibson DJ; Schur PH
1979 Nov;9(2):75-97, Seminars in arthritis & rheumatism
— id: 17004, year: 1979, vol: 9, page: 75, stat: Journal Article,

Cutaneous necrotizing venulitis
Melski JW; Soter NA
1979 Apr;23(4):434-439, Cutis
The term vasculitis describes a variety of inflammatory changes in vessels. The most common type to affect the skin is a necrotizing venulitis associated with a neutrophilic polymorphonuclear leukocyte infiltrate. The most frequent presentation is palpable purpura on the lower extremities, but the lesions may include urticaria and ulcers. A diagnosis of cutaneous necrotizing venulitis obliges the physician to search for the cause, associated diseases, and the extent of the vascular involvement. Antigens, either in circulating immune complexes or as haptens bound to vessel proteins, are presumed to trigger immmune responses. The differentiation of large from small vessel disease and the prediction of systemic involvement may be difficult in a specific patient. Treatment, other than removal of the antigen, is theoretic or anecdotal
— id: 17009, year: 1979, vol: 23, page: 434, stat: Journal Article,

Oral disodium cromoglycate in the treatment of systemic mastocytosis
Soter NA; Austen KF; Wasserman SI
1979 Aug 30;301(9):465-469, New England journal of medicine
A double-blind crossover study of the efficacy of disodium cromoglycate given by mouth to control the cutaneous, gastrointestinal and central-nervous-system manifestations of systemic mastocytosis was carried out in five patients for periods of eight to 32 months. In 15 of 18 trials, disodium cromoglycate produced marked amelioration of the clinical manifestations of pruritus, whealing, flushing, diarrhea, abdominal pain and disorders of cognitive function. By contrast, in all 19 trials with placebo, there was no improvement in these symptoms and signs. Histaminuria and peripheral-blood eosinophilia were unrelated to disease activity and were unaffected by drug therapy. Although it is poorly absorbed after administration by mouth, disodium cromoglycate is of clinical benefit to patients with systemic mastocytosis
— id: 17007, year: 1979, vol: 301, page: 465, stat: Journal Article,

Cutaneous necrotizing venulitis in patients with cystic fibrosis
Soter NA; Mihm MC; Colten HR
1979 Aug;95(2):197-201, Journal of pediatrics
Palpable purpura was noted to occur late in the course of some patients with cystic fibrosis. Skin biopsy specimens showed necrotizing venulitis characterized by a perivenular infiltrate composed of neutrophilic leukocytes, fibrin, hypogranulated mast cells, and endothelial cell necrosis. Circulating immune complexes were detected. Recurrent pulmonary infections and the chronic administration of therapeutic agents provide sources of potential antigens
— id: 17008, year: 1979, vol: 95, page: 197, stat: Journal Article,

Urticaria/angioedema: a consideration of pathogenesis and clinical manifestations
Soter NA; Wasserman SI
1979 Sep;18(7):517-532, International journal of dermatology
— id: 17006, year: 1979, vol: 18, page: 517, stat: Journal Article,

Erythema multiforme
Tonnesen MG; Soter NA
1979 Oct;1(4):357-364, Journal of the American Academy of Dermatology
Erythema multiforme (EM) is an episodic, variable, self-limited, and often recurrent inflammatory disorder of the skin and mucous membranes. In this article a definition of EM is proposed, its known clinical and histopathologic spectrum is reviewed, an approach to diagnosis and treatment is suggested, and documented evidence regarding its etiology and pathogenesis is presented. EM would appear to be a hypersensitivity reaction to a variety of precipitating agents. It has been directly linked to Mycoplasma pneumoniae and herpes simplex virus infections and possibly is triggered by a number of other infectious agents and by certain drugs. Accumulating observations of diverse immunologic phenomena suggest an underlying immune mechanism of as yet unclear type. Future investigation should be directed toward defining diagnostic criteria, evaluating reported etiologic associations, and clarifying the immunologic basis of this complex and enigmatic disorder
— id: 17005, year: 1979, vol: 1, page: 357, stat: Journal Article,

H2 receptor mediated inhibition of immediate type hypersensitivity reactions in vivo
Drazen JM; Venugopalan CS; Soter NA
1978 Mar;117(3):479-484, American review of respiratory disease
The effects of H2-blocking agents and the H2 receptor agonist, 4-methylhistamine, on the severity of anaphylactic reactions were studied in the guinea pig in vivo. The increase in gas volume of the lungs 90 sec after intravenous infusion of ovalbumin in animals immunized previously by intraperitoneal ovalbumin injection was used as an index of the severity of the reaction in vivo. The H2 receptor antagonists burimamide (1.0 and 3.0 mg per kg) and metiamide (3 mg per kg) significantly increased the severity of the reaction but did not significantly alter the effects of subcutaneous histamine. Neither 3 nor 30 mg of cimetidine per kg increased the severity of the reaction, and the higher dose significantly blunted the response to subcutaneous histamine. The H2 receptor agonist, 4-methylhistamine, significantly diminished the severity of the reation. These experiments demonstrate that H2 receptor stimulation may act to limit the severity of the anaphylactic reactions in vivo
— id: 17012, year: 1978, vol: 117, page: 479, stat: Journal Article,

Cutaneous necrotizing venulitis: a sequential analysis of the morphological alterations occurring after mast cell degranulation in a patient with a unique syndrome
Soter NA; Mihm MC; Dvorak HF; Austen KF
1978 Apr;32(1):46-58, Clinical & experimental immunology
An unusual patient, with dermal nodules, flexion contractures of the fingers and toes, cold-induced urticaria, dermographism and serum hypocomplementaemia, had necrotizing cutaneous venulitis underlying the spontaneous lesions. Since necrotizing cutaneous venulitis could be experimentally induced by the physical stimuli of cold or trauma, the time-course of histopathological events was documented in the skin of this patient. The histopathological alterations were studied in 1 micron thick, Epon-embedded skin biopsy specimens over an interval of 6 days. The early massive degranulation of the mast cells was followed by the sequential infiltration of neutrophilic, eosinophilic and basophilic polymorphonuclear leucocytes, by the development of venular endothelial cell necrosis and by the deposition of fibrin. The persistent serum hypocomplementaemia involved the classic activating and amplification pathways. It seems possible that the unusual combination of pathobiological processes involving the mast cells and the complement system in this patient has created a unique syndrome, in which venules are damaged and the sheaths of the extensor tendons of the hands and feet become affected in time
— id: 17011, year: 1978, vol: 32, page: 46, stat: Journal Article,

Morphologic and functional evidence for release of mast-cell products in bullous pemphigoid
Wintroub BU; Mihm MC; Goetzl EJ; Soter NA; Austen KF
1978 Feb 23;298(8):417-421, New England journal of medicine
We studied nine patients with bullous pemphigoid, a generalized cutaneous eruption- for evidence of mast-cell involvement during development of lesions. As in other reports, six of nine patients demonstrated a serum antibody directed against the epidermal basement-membrane zone. Direct immunofluorescence studies of lesions revealed depostion of immunoglobulin and complement proteins at the basement-membrane zone in six of nine and nine of nine patients, respectively. Participation of mast cells was suggested by a sequence of pathologic alterations in which there was progressive mast-cell degranulation and late eosinophil infiltration. In addition, a factor chemotactic for human eosinophils with the size and charge characteristics of the eosinophil chemotactic factor of anaphylaxis was identified in blullous fluid. The data indicate that, in addition to activation of the complement system, involvement of mast cells is an early and continuing event in the development of the cutanenous lesions of bullous pemphigoid
— id: 17013, year: 1978, vol: 298, page: 417, stat: Journal Article,

Histamine in human tears
Abelson MB; Soter NA; Simon MA; Dohlman J; Allansmith MR
1977 Mar;83(3):417-418, American journal of ophthalmology
Tear samples from 13 normal volunteers and nine patients with vernal conjunctivitis were assayed for histamine. Tears in both groups contained histamine. The normal subjects had values ranging from 2.2 to 36 ng/ml with a mean of 10.3 ng/ml. The vernal patients had histamine values ranging from 0 to 125 ng/ml with a mean of 3,.2 ng/ml. The presence of histamine in tears indicates a role for this important mediator in both the physiologic and immunologic processes of the external eye
— id: 17020, year: 1977, vol: 83, page: 417, stat: Journal Article,

Graft-versus-host reaction. Cutaneous manifestations following bone marrow transplantation
Hood AF; Soter NA; Rappeport J; Gigli I
1977 Aug;113(8):1087-1091, Archives of dermatology
The distinctive cutaneous changes that occur in both the acute and chronic forms of the graft-vs-host reaction (GVHR) are described in two living patients in whom the GVHR developed after bone marrow transplantation for aplastic anemia. In the skin, the mild form of the acute GVHR is recognized as a subtle macular erythema, and the severe form appears as erythematous papules and violaceous macules with scale. Skin biopsy specimens in both of the acute forms show vacuolar alterations of the epidermal basal-cell layer with a perivenular infiltrate of lymphocytes. The chronic GVHR evolves from generalized scaling to diffuse areas of aclerotic and atrophic skin with a curious reticulated hyperpigmentation, ulcerations, and alopecia. Histopathologic study shows collagenization of the dermis that can be correlated with the clinical sclerodermoid changes. Owing to its visibility, the skin offers a unique opportunity for the early recognition of the GVHR
— id: 17014, year: 1977, vol: 113, page: 1087, stat: Journal Article,

Lymphocytotoxic antibodies. HLA antigen associations, disease associations, and family studies
Raum D; Glass D; Soter NA; Stillman JS; Carpenter CB; Schur PH
1977 May;20(4):933-936, Arthritis & rheumatism
Lymphocytotoxic antibodies (LCTAB) were sought in sera of patients with rheumatic diseases and in family members. Patients with SLE and cutaneous necrotizing venulitis and family members of JRA patients had an increased frequency of LCTAB; JRA patients and family members of SLE patients did not. The only association between LCTAB and the HLA phenotype of persons with LCTAB was a decreased frequency of LCTAB in individuals with HLA-B27
— id: 17017, year: 1977, vol: 20, page: 933, stat: Journal Article,

Chronic urticaria as a manifestation of necrotizing venulitis
Soter NA
1977 Jun 23;296(25):1440-1442, New England journal of medicine
In a group of patients with a syndrome consisting of recurrent episodes of urticaria, arthralgia, abdominal pain, and (rarely) glomerulonephritis, examination of skin biopsy specimens showed necrotizing venulitis. An elevated erythrocyte sedimentation rate was the most common laboratory abnormality. Analyses of serum immunoglobulins revealed random abnormalities of immunoglobulin levels, and assessment of the complement system showed two groups of patients--some with hypocomplementemia and others with a normal complement system. In those with hypocomplementemia, there were low levels of C1q, C4 and, occasionally, C3, compatible with activation of the classic complement pathway. Although the cause of this syndrome is unknown, the complement profiles suggest that more than one mechanism of vascular damage may be operative
— id: 17016, year: 1977, vol: 296, page: 1440, stat: Journal Article,

Urticaria, angioedema, and mediator release in humans in response to physical environmental stimuli
Soter NA; Austen F
1977 Apr;36(5):1736-1741, Federation Proceedings (Federation of American Societies for Experimental Biology)
The activation of mast cells by immunologic or physical stimuli leads to the generation of unstored intermediates (mediators) such as slow reacting substance of anaphylaxis (SRS-A) and platelet activating factor (PAF), and to their release along with performed mediators, histamine, eosinophil chemotactic factor of anaphylaxis (ECF-A), and neutrophil chemotactic factor (NCE), and macromolecular heparin. The internal regulation of mast cell-dependent phenomenons occurs at at least four levels: 1) the intensity and nature of the activating stimulus, 2) the regulation of mediator generation and release of cellular levels of the cyclic nucleotides, 3) the capacity of target cells to bind and respond to primary mediators, and 4) the rate at which mediators undergo biodegradation. Inasmuch as the mast cell is present at cutaneous and mucosal surfaces about venules, it seems likely that the initial or humoral phase of its response achieves an influx of plasms proteins, such as immunoglobulins and complement components, whereas the subsequent cellular phase augments local host defense through the entrance of neutrophils and eosinophils that terminate the humoral phase. The activation of mast cells is considered herein in terms of defined physical stimuli that are characterized by urticaria and angioedema
— id: 17018, year: 1977, vol: 36, page: 1736, stat: Journal Article,

Delayed cold-induced urticaria: a dominantly inherited disorder
Soter NA; Joshi NP; Twarog FJ; Zeiger RS; Rothman PM; Colten HR
1977 Apr;59(4):294-297, Journal of allergy & clinical immunology
A delayed cutaneous response to cold, characterized by areas of erythematous, edematous deep swelling at 9 to 18 hr after experimental ice challenge, was recognized in a 10-yr-old boy and several members of his family. Biopsy of the cold-induced lesion showed edema and an infiltrate of mononuclear cells; mast cells were normal, and immunoglobulins, complement factors, and fibrin were not detected by immunofluorescence techniques. Local cold challenge did not release histamine or induce alterations in the complement system or the enzymes, histaminase, and histamine methyl transferase. The delayed cutaneous response to cold could not be passively transferred with serum or tissue extracts to monkey skin. Family studies suggested an autosomal-dominant mode of inheritance
— id: 17019, year: 1977, vol: 59, page: 294, stat: Journal Article,

Cold urticaria. Recognition and characterization of a neutrophil chemotactic factor which appears in serum during experimental cold challenge
Wasserman SI; Soter NA; Center DM; Austen KF
1977 Jul;60(1):189-196, Journal of clinical investigation
— id: 17015, year: 1977, vol: 60, page: 189, stat: Journal Article,

Vasculitis with urticaria, hypocomplementemia, and multiple system involvement
Feig PU; Soter NA; Yager HM; Caplan L; Rosen S
1976 Nov 1;236(18):2065-2068, JAMA
A patient with cutaneous necrotizing vasculitis had chronic urticaria associated with multiple system involvement including arthralgias, glomerulonephritis, myositis, pseudotumor cerebri, and adenopathy. Persistent hypocomplementemia is noted with classic pathway activation. The syndrome recognized in this patient and those few individuals reported previously seems to constitute a distinct category of collagen-vascular disease
— id: 17021, year: 1976, vol: 236, page: 2065, stat: Journal Article,

Association between HLA and cutaneous necrotizing venulitis
Glass D; Soter NA; Gibson D; Carpenter CB; Schur PH
1976 Sep-Oct;19(5):945-949, Arthritis & rheumatism
A group of patients has been identified with cutaneous necrotizing venulitis (vasculitis). These patients, some with concomitant connective tissue disorders, have skin lesions that separate them from the arteritis commonly described as rheumatoid vasculitis. HLA typing has been performed on 31 of these unrelated patients with cutaneous necrotizing venulitis, including 19 with associated chronic disorders. The antigen pair A11, BW35 was found in 5 of these 19 patients and in 11 of 346 controls. This difference in frequency is statistically significant. Because HLA genes appear to be linked to immune response genes, these data suggest that such genes may exist in patients with this form of cutaneous necrotizing venulitis with associated connective tissue disease
— id: 17026, year: 1976, vol: 19, page: 945, stat: Journal Article,

Rheumatoid vasculitis
Glass D; Soter NA; Schur PH
1976 Sep-Oct;19(5):950-952, Arthritis & rheumatism
— id: 17025, year: 1976, vol: 19, page: 950, stat: Journal Article,

The structure of normal skin and the morphology of atopic eczema
Mihm MC; Soter NA; Dvorak HF; Austen KF
1976 Sep;67(3):305-312, Journal of investigative dermatology
— id: 17022, year: 1976, vol: 67, page: 305, stat: Journal Article,

Clinical presentations and mechanisms of necrotizing angitis of the skin
Soter NA
1976 Sep;67(3):354-359, Journal of investigative dermatology
Cutaneous necrotizing angiitis may be present as either palpable purpura or less commonly as recurrent urticaria, and each clinical presentation may be associated with hypocomplementemia or a normal complement system. A variety of mechanisms may be operative in the production of necrotic vascular skin lesions that appear as similar, recognizable morphologic lesions. These mechanisms include immune complexes, cellular-type hypersensitivity reactions, and initiation or modulation by mast cells. Two cellular patterns have been recognized in the skin of patients with cutaneous necrotizing angiitis that can be correlated with the involvement of the complement system in serum. In patients with hypocomplementemia, there is an infiltrate of neutrophils that is consistent with a process involving immune complexes; in patients with normocomplementemia there are lymphocytes and activated lymphocytes consistent with participation in part by cellular mechanisms. In both the hypocomplementemic and normocomplementemic forms and as well as in a unique patient in whom the mast cell may initiate the venular damage, the mast cell, which its content of chemical mediators, has the capacity to initiate as well as modulate subacute and chronic vascular damage
— id: 17023, year: 1976, vol: 67, page: 354, stat: Journal Article,

The diversity of mast cell-derived mediators: implications for acute, subacute, and chronic cutaneous inflammatory disorders
Soter NA; Austen KF
1976 Sep;67(3):313-319, Journal of investigative dermatology
The mast cell in tissues represents an effector cell capable of elaboration of all the essential mediators of inflammation. The effects of uncontrolled activation may be divided into pharmacologic and inflammatory phases with attendant implications for the initiation of both acute and subacute pathologic processes. The elaboration of chemical mediators by the mast cell makes it possible to recruit blood cells and proteins essential to host defense by a controlled physiologic process that can proceed without significant local tissue damage. When uncontrolled, the same potentiality can be injurious, with the nature of the clinical problem depending upon the location of the cells, the intensity of activation, and the ratio of newly generated and preformed mediators released. The evidence that the mast cell can participate in each form of immunologic reaction--immediate, immune complex, and delayed- as a primary or secondary effector cell and the diversity of its products foretell an evolving recognition of its role in host defense and tissue injury. It is pertinent to develop further methods and criteria to define the nature and extent of mast cell participation in disease processes
— id: 17024, year: 1976, vol: 67, page: 313, stat: Journal Article,

Two distinct cellular patterns in cutaneous necrotizing angiitis
Soter NA; Mihm MC; Gigli I; Dvorak HF; Austen KF
1976 Jun;66(6):344-350, Journal of investigative dermatology
Two distinct cellular patterns of necrotizing angiitis involving venules in skin of patients with clinically identical cutaneous lesions were appreciated by the 1 -mum-thick section technique. In those individuals with serum hypocomplementemia, there was a perivenular inflitrate composed predominantly of neutrophils with fibrin deposition and nuclear debris. In patients with normal serum complement levels, in addition to an infiltrate of neutrophils and fibrin deposition, perivenular lymphocytes in various stages of activation were prominent. In both patterns the venules and not the arterioles were affected, mast cells exhibited various degrees of hypogranulation, and basophils and eosinophils were recognized only rarely. Lesions of different clinical age obtained from one hypocomplelmentemic patient and one normocomplementemic patient exhibited consistent cellular patterns, as did a single crop of lesions biopsied twice, 24 hr apart, in a patient with hypocomplementemia. No patient with hypocomplementemia became normocomplementemic or vice versa with persistence of lesions
— id: 17027, year: 1976, vol: 66, page: 344, stat: Journal Article,

Cold urticaria: release into the circulation of histamine and eosinophil chemotactic factor of anaphylaxis during cold challenge
Soter NA; Wasserman SI; Austen KF
1976 Mar 25;294(13):687-690, New England journal of medicine
Patients with idiopathic acquired cold-induced urticaria were evaluated for the release of the preformed mast-cell mediators of immediate-type hypersensitivity during a study in which one arm was immersed in ice water while the other arm remained as a control. Blood specimens were obtained from each arm serially over a one-hour interval, and serum speciments were assessed for histamine, eosinophil chemotactic factor of anaphylaxis, and complement components. Levels of histamine and eosinophil chemotactic factor rose in the arm subjected to cold immersion for three minutes, with peak values occurring between two and five minutes and returning to base line by 30 minutes. No changes occurred in the control arm or in the immersed arm of normal subjects. Assessment of the classical and alternative complement pathways showed no abnormalities. This initial observation of release of eosinophil chemotactic factor of anaphylaxis in vivo along with histamine assigns the mast cell a central role in cold urticaria
— id: 17028, year: 1976, vol: 294, page: 687, stat: Journal Article,

Acquired ichthyosis. A sign of nonlymphoproliferative malignant disorders
Flint GL; Flam M; Soter NA
1975 Nov;111(11):1446-1447, Archives of dermatology
Acquired ichthyosis was recognized in four patients, in whom the associated malignant disorders were carcinoma of the lung, breast, and cervix. This skin lesion may be a valuable clinical sign in recognizing the existence of a malignant condition. Although the emergence of an ichthyosiform dermatosis may have serious prognostic implications, it may also be useful in monitoring the course of the malignant disorder and the patient's response to therapy. The relationship to nonlymphoproliferative malignant neoplasms may be more common than has been previously recognized
— id: 17029, year: 1975, vol: 111, page: 1446, stat: Journal Article,

Inhibition by epsilon-aminocaproic acid of the activation of the first component of the complement system
Soter NA; Austen KF; Gigli I
1975 Mar;114(3):928-932, Journal of immunology
The influence of EACA on C1 in whole human serum and on C1 and C (see article) as isolated molecules was assessed hemolytically. There was selective inhibition of C1 without effect on the levels of C4, C2, C3, and C9 in whole human serum that was reversed by dialysis. EACA was found to inhibit the intrinsic activation of C1 without inhibiting the already active molecule. This was confirmed by the capacity of trypsin to uncover C1 activity in cellular intermediates formed by C1 treated with EACA that did not evolve in the absence of this extrinsic activating mechanism. Inasmuch as the trypsin-dependent recovery of C1 was incomplete, an effect on binding cannot be excluded
— id: 17030, year: 1975, vol: 114, page: 928, stat: Journal Article,

The complement system in necrotizing angiitis of the skin. Analysis of complement component activities in serum of patients with concomitant collagen-vascular diseases
Soter NA; Austen KF; Gigli I
1974 Aug;63(2):219-226, Journal of investigative dermatology
— id: 17032, year: 1974, vol: 63, page: 219, stat: Journal Article,

Urticaria and arthralgias as manifestations of necrotizing angiitis (vasculitis)
Soter NA; Austen KF; Gigli I
1974 Dec;63(6):485-490, Journal of investigative dermatology
— id: 17031, year: 1974, vol: 63, page: 485, stat: Journal Article,

Dermatitis herpetiformis
Soter NA
1973 May 10;288(19):1020-1021, New England journal of medicine
— id: 17036, year: 1973, vol: 288, page: 1020, stat: Journal Article,

Clinical dermatology (third of three parts)
Soter NA; Wilkinson DS; Fitzpatrick TB
1973 Aug 9;289(6):296-302, New England journal of medicine
— id: 17033, year: 1973, vol: 289, page: 296, stat: Journal Article,

Clinical dermatology. 1
Soter NA; Wilkinson DS; Fitzpatrick TB
1973 Jul 26;289(4):189-195, New England journal of medicine
— id: 17035, year: 1973, vol: 289, page: 189, stat: Journal Article,

Clinical dermatology. 2
Soter NA; Wilkinson DS; Fitzpatrick TB
1973 Aug 2;289(5):242-249, New England journal of medicine
— id: 17034, year: 1973, vol: 289, page: 242, stat: Journal Article,

Stucco keratosis
Willoughby C; Soter NA
1972 Jun;105(6):859-861, Archives of dermatology
— id: 17037, year: 1972, vol: 105, page: 859, stat: Journal Article,

Vasculitis
Soter NA; Gallagher WF
1970 Jul;102(1):117-119, Archives of dermatology
— id: 17038, year: 1970, vol: 102, page: 117, stat: Journal Article,

Fitzpatrick TB: Diet and the skin
Soter NA
1969 Jan;202(207):102-108, Practitioner
— id: 17040, year: 1969, vol: 202, page: 102, stat: Journal Article,

Ultrastructural pathology of erythema dyschromicum perstans
Soter NA; Wand C; Freeman RG
1969 Feb;52(2):155-162, Journal of investigative dermatology
— id: 17039, year: 1969, vol: 52, page: 155, stat: Journal Article,