Biosketch / Results /
Bruce M Solitar, M.D.
Clinical Associate Professor;Department of Medicine (Rheum Div)
Clinical Addresses
333 EAST 34 STREETSUITE 1C
NEW YORK, NY 10016
Hours: Mon. 8 - 5; Tue. 8 - 5; Wed. 8 - 5; Thu. 8 - 5; Fri. 8 - 5
Phone: 212-889-7217
Fax: 212-545-0174
Medical Specialties
Rheumatology, Internal MedicineMedical Expertise
Osteoarthritis, Lupus, Immune Disorders, Gout, Osteoporosis/Metabollic Bone Disease, Arthritis, Fibromyalgia, General Rheumatology, Dermatomyosis, Joint Pain Rheumatology & RehabilitationInsurance
Cigna HMO/POS, Cigna PPO, UHC EPO, UHC HMO, UHC POS, UHC PPO, UHC TOP TIERInsurance 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.
Board Certification
2001 — Internal Medicine2004 — Rheumatology (Internal Med)
Education
1988 — New York University School of Medicine, Medical Education1988-1992 — NYU Medical Center (Internal Medicine), Residency Training
1992-1994 — NYU Medical Center (Rheumatology), Clinical Fellowships
All data from NYU Health Sciences Library Faculty Bibliography — -
Contact:
http://hsl.med.nyu.edu/faculty-bibliography-search#about
Fibromyalgia: knowns, unknowns, and current treatment
Solitar, Bruce M
2010 ;68(3):157-161, Bulletin of the NYU Hospital for Joint Diseases
Fibromyalgia is a chronic syndrome of diffuse musculoskeletal pain with tenderness at specific locations, often associated with persistent fatigue, cognitive and mood disorders, joint stiffness, and insomnia. Understanding the pathophysiology of fibromyalgia and the establishment of effective treatments have been complex endeavors that have not yielded simple answers. Nevertheless, recent studies have shed light on the roles of central pain processing, genetic abnormalities, and external factors on development of the fibromyalgia syndrome (FMS). These findings have led to the use of new therapies that have shown beneficial effects on symptoms. This review discusses ideas that have become accepted as well as novel associations under consideration in regard to the pathogenesis of fibromyalgia and the current and emerging therapeutics for its treatment
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id: 114052,
year: 2010,
vol: 68,
page: 157,
stat: Journal Article,
Update on fibromyalgia therapy
Abeles, Micha; Solitar, Bruce M; Pillinger, Michael H; Abeles, Aryeh M
2008 Jul;121(7):555-561, American journal of medicine
Primary fibromyalgia, a poorly-understood chronic pain syndrome, is characterized by widespread musculoskeletal pain, nonrestorative sleep, fatigue, psychological distress, and specific regions of localized tenderness, all in the absence of otherwise apparent organic disease. While the etiology of fibromyalgia is unclear, accumulating data suggest that disordered central pain processing likely plays a role in the pathogenesis of symptoms. Although various pharmacological treatments have been studied and espoused for treating fibromyalgia, no single drug or group of drugs has proved to be particularly useful in treating fibromyalgia patients as a whole, and only one drug to date has earned U.S. Food and Drug Administration approval for treating the syndrome in the United States. This review critically and systematically evaluates clinical investigations of medicinal and nonmedicinal treatments for fibromyalgia dating from 1970 to 2007
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id: 94805,
year: 2008,
vol: 121,
page: 555,
stat: Journal Article,
Narrative review: the pathophysiology of fibromyalgia
Abeles, Aryeh M; Pillinger, Michael H; Solitar, Bruce M; Abeles, Micha
2007 May 15;146(10):726-734, Annals of internal medicine
Primary fibromyalgia is a common yet poorly understood syndrome characterized by diffuse chronic pain accompanied by other somatic symptoms, including poor sleep, fatigue, and stiffness, in the absence of disease. Fibromyalgia does not have a distinct cause or pathology. Nevertheless, in the past decade, the study of chronic pain has yielded new insights into the pathophysiology of fibromyalgia and related chronic pain disorders. Accruing evidence shows that patients with fibromyalgia experience pain differently from the general population because of dysfunctional pain processing in the central nervous system. Aberrant pain processing, which can result in chronic pain and associated symptoms, may be the result of several interplaying mechanisms, including central sensitization, blunting of inhibitory pain pathways, alterations in neurotransmitters, and psychiatric comorbid conditions. This review provides an overview of the mechanisms currently thought to be partly responsible for the chronic diffuse pain typical of fibromyalgia.
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id: 72876,
year: 2007,
vol: 146,
page: 726,
stat: Journal Article,
Lyme disease presenting as ruptured synovial cysts
Kishimoto, Mitsumasa; Nguyen, Michael; Solitar, Bruce; Mitnick, Hal J
2007 Dec;13(6):365-366, Journal of clinical rheumatology. JCR
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id: 95475,
year: 2007,
vol: 13,
page: 365,
stat: Journal Article,
Rheumatic manifestations of current pharmacopeia
Brenner J; Solitar BM; Golden BD
2000 Apr;2(2):151-155, Current rheumatology reports
Patient complaints arising as manifestations of medication side effects are commonly encountered in clinical practice. A rheumatologist must routinely consider side effects of drugs in the differential diagnosis of many symptoms. This review will remind the reader of certain well-described and some newly reported side effects commonly encountered in an internal medicine practice. Focal points incude arthralgias/arthritis, myopathy/myositis, ANA/drug-induced lupus, bone loss/osteoporosis, and tendon rupture
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id: 39499,
year: 2000,
vol: 2,
page: 151,
stat: Journal Article,
Reiter's syndrome among Asian shipboard immigrants: the case of The Golden Venture
Solitar BM; Lozada CJ; Tseng CE; Lowe AM; Krajewski WM; Blanchard K; Pillinger M; Weissman G
1998 Apr;27(5):293-300, Seminars in arthritis & rheumatism
OBJECTIVE: To assess the incidence of Reiter's syndrome aboard The Golden Venture, a ship carrying illegal immigrants from China to the United States. METHODS: After identification of an index case, we conducted telephone interviews with medical staff at immigrant detention centers in Pennsylvania, New York, and Virginia. When a potential case was identified at one facility, we performed a site inspection, reviewing the medical records of all detainees and performing histories and physicals on all those with joint and/or ocular complaints. RESULTS: We identified two patients, both HLA B27 positive, with Reiter's syndrome. The observed incidence (0.87%) approximated the predicted incidence but may have underestimated the actual incidence. We review the history of shipboard Reiter's syndrome, and discuss the pathogenic roles of HLA B27 and particular infectious agents. CONCLUSION: Continued transportation of illegal immigrants from China and other parts of the world is likely to result in occasional clusters of Reiter's syndrome. Physicians treating immigrant populations should remain aware of the possibility of reactive arthritis
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id: 7801,
year: 1998,
vol: 27,
page: 293,
stat: Journal Article,
Mitogen-activated protein kinase in neutrophils and enucleate neutrophil cytoplasts: evidence for regulation of cell-cell adhesion
Pillinger MH; Feoktistov AS; Capodici C; Solitar B; Levy J; Oei TT; Philips MR
1996 May 17;271(20):12049-12056, Journal of biological chemistry
We employed neutrophils and enucleate neutrophil cytoplasts to study the activation of the mitogen-activated protein kinases (MAPKs) p44erk1 and p42erk2 in neutrophils by inflammatory agonists that engage G protein-linked receptors. Formyl-methionyl-leucyl-phenylalanine (FMLP) rapidly and transiently activated MAPK in neutrophils and cytoplasts, consistent with a role in signaling for neutrophil functions. FMLP stimulated p2lras activation in neutrophils and Raf-1 translocation from cytosol to plasma membrane in cytoplasts, with kinetics consistent with events upstream of MAPK activation. Insulin, a protein tyrosine kinase receptor (PTKR) agonist, stimulated neutrophil MAPK activation, demonstrating an intact system of PTKR signaling in these post-mitotic cells. FMLP- and insulin-stimulated MAPK activation in cytoplasts were inhibited by Bt2cAMP, consistent with signaling through Raf-1 and suggesting a mechanism for cAMP inhibition of neutrophil function. However, Bt2cAMP had no effect on FMLP-stimulated MAPK activation in neutrophils. The extent of MAPK activation by various chemoattractants correlated with their capacity to stimulate neutrophil and cytoplast homotypic aggregation. Consistent with its effects on MAPK, Bt2cAMP inhibited FMLP-stimulated aggregation in cytoplasts but not neutrophils. Insulin had no independent effect but primed neutrophils for aggregation in response to FMLP. Our studies support a p2lras-, Raf-1-dependent pathway for MAPK activation in neutrophils and suggest that neutrophil adhesion may be regulated, in part, by MAPK
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id: 8311,
year: 1996,
vol: 271,
page: 12049,
stat: Journal Article,
FMLP-INDUCED ACTIVATION OF MITOGEN-ACTIVATED PROTEIN-KINASES (MAPK) IN HUMAN NEUTROPHILS IS INDEPENDENT OF CARBOXYL METHYLATION OF RAS-RELATED PROTEINS
PILLINGER, M; FEOKTISTOV, A; SOLITAR, B; WEISSMANN, G; PHILIPS, M
1994 APR ;42(2):A204-A204, Clinical research
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id: 52494,
year: 1994,
vol: 42,
page: A204,
stat: Journal Article,


