Bernard A. Feigenbaum

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Bernard A. Feigenbaum, M.D.

Clinical Assistant Professor;
Departments of Medicine (GIM Div Dir) and Otolaryngology (Otolaryngology)

Clinical Addresses

323 EAST 34TH STREET, SUITE 904
NEW YORK, NY 10016
Handicap Access: yes
Phone: 212-981-7260
Fax: 866-903-3908


Additional Clinical Addresses

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Medical Specialties

Pediatric Allergy & Immunology, Allergy & Immunology

Medical Expertise

Allergy And Immunology, Sinusitis, Asthma, Drug Allergy, Allergic Rhinitis (Hayfever), Food Allergy, Chronic Cough, Eosinophilic Esophagitis, Eczema/Atopic Dermatitis

Clinical Responsibilities

Bernard A. Feigenbaum, MD, FACP, FAAAAI is Director of the NYU Adverse Drug Reaction and Desensitization Program, and Clinical Assistant Professor of Medicine and Otolaryngology. He has over fifteen years of clinical and teaching experience and is Board-Certified in Allergy & Immunology.

Dr. Feigenbaum serves as a Medical Expert Consultant for an office of the NY State Board for Professional Medical Conduct, and has served as an expert witness and/or consultant in federal or state actions in five states.

Dr. Feigenbaum is passionate about improving medical care, and is known for his friendly, caring manner and for his teaching skills. He has given presentations about Professionalism in Medicine for the American Board of Internal Medicine, and recently lectured at Memorial Sloan-Kettering, Hospital for Special Surgery, Hospital for Joint Diseases, NYU Langone Medical Center, and the NYC Department of Health.

Dr. Feigenbaum is a Principal Investigator at NYULMC, and his recent translational study of mycotoxins in chronic rhinosinusitis will be published in Otolaryngology-Head and Neck Surgery. Research interests include asthma; sinus disease; drug allergy; and dermatologic allergy. He has had 15 articles, abstracts and/or letters accepted for publication and is a peer reviewer for Annals of Internal Medicine and Journal of Allergy & Clinical Immunology. National committee assignments include Vice Chair of the Asthma & Respiratory Disease Committee (American College of Allergy, Asthma & Immunology); and Asthma Diagnosis Committee; Rhinosinusitis Committee; and (Drug) Desensitization Task Force (American Academy of Allergy, Asthma & Immunology).

Dr. Feigenbaum has been featured on the air on Good Morning America, Sirius Radio, CBS News Radio, and the Rachael Ray Show, and has been quoted by NY Daily News and Los Angeles Times.

Dr. Feigenbaum is one of the few allergists in NYC to routinely perform aspirin desensitization, antibiotic desensitization, chemotherapy desensitization, and monoclonal desensitization.

Conditions treated in the office include allergic rhinitis and asthma; eczema/dermatitis; chronic cough; acute and chronic sinusitis; food allergy and eosinophilic esophagitis; aspirin exacerbated respiratory disease (AERD) and other allergic diseases. Office testing and procedures include skin testing for food and airborne allergies; patch testing for contact dermatitis; drug desensitization; and pulmonary function testing.

Insurance

AETNA HMO, AETNA INDEMNITY, AETNA MEDICARE, AETNA POS, AETNA PPO, Beech St PPO, Cigna HMO/POS, Cigna PPO, EBCBS CHLD HLTH, EBCBS EPO, EBCBS HLTHY NY, EBCBS HMO, EBCBS INDEMNITY, EBCBS MEDIBLUE, EBCBS POS, EBCBS PPO, FIDELIS FAM HLTH, FIDELIS MEDICARE, Fidelis Medicaid, GREATWEST PPO, HEALTHPLUS CHLD HLTH, HEALTHPLUS FAM HLTH, HIP ACCESS I, HIP ACCESS II, HIP CHLD HLTH, HIP EPO/PPO, HIP HMO, HIP MEDICARE, HIP POS, HealthPlus Medicaid, LOCAL 1199 PPO, MULTIPLAN/PHCS PPO, NYS EMPIRE PLAN, OXFORD FREEDOM, Oxford Liberty, Oxford Medicare, UHC EPO, UHC HMO, UHC POS, UHC PPO, UHC TOP TIER, UPN Elite

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

2003 — Allergy & Immunology

Education

1989 — Boston University Medical Center, Medical Education
1989-1990 — Mercy Hospital and Medical Center (Internal Medicine), Internship
1990-1992 — Mercy Hospital and Medical Center (Internal Medicine), Residency Training
1993-1995 — Mercy Hospital and Medical Center (Immunology & Allergy), Residency Training
1993-1995 — Scripps Memorial Hospital-La Jolla (Allergy), Clinical Fellowships

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Research Interests

Dr. Feigenbaum is a Principal Investigator at NYU Langone, in a translational study relating to the etiology of chronic sinusitis; and in a study of knowledge of pulmonary function, anaphylaxis and radiocontrast media (RCM) allergy. He has a research interest in asthma, sinus disease and drug allergy and is a peer reviewer for the Annals of Internal Medicine and the Journal of Allergy & Clinical Immunology. He has published articles, abstracts or letters on: aspirin-sensitive asthma; reflux in asthma; bee sting allergy; vocal cord dysfunction; and nitric oxide in asthma.

Research Keywords

Asthma; "Food Allergy"; Hives; Allergy

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All data from NYU Health Sciences Library Faculty Bibliography — -

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

Measurement of mycotoxins in patients with chronic rhinosinusitis
Lieberman S.M.; Jacobs J.B.; Lebowitz R.A.; Feigenbaum B.A.
2011 ;127(2 SUPPL 1):AB123-AB123, Journal of allergy & clinical immunology
RATIONALE: Rhinosinusitis is one of the most common chronic conditions in the US. The etiology of chronic rhinosinusitis (CRS) remains unknown and controversial. Mycotoxins are toxic secondary metabolites produced by fungi including aspergillus, alternaria, and penicillium species. The presence of mycotoxins in sinonasal tissue and secretions and any possible link to CRS has not been reported. METHODS: Sinonasal tissue and mucus specimens, predominantly from the ethmoid sinuses, were collected from 18 subjects undergoing endoscopic sinus surgery for CRS. The specimens were pulverized and centrifuged, then the resultant supernatant fraction was collected. The following mycotoxins were analyzed using commercial ELISA test kits: aflatoxin, deoxynivalenol, zearalenone, ochratoxin, and fumonisin. Mycotoxin concentrations were quantified from a standard curve. All standards and samples were analyzed in duplicate. We considered a sample positive when the mean value of the sample was two standard deviations above the limit of detection for the test kit. RESULTS: Four (22%) of 18 specimens were positive for ochratoxin. All specimens were negative for aflatoxin, deoxynivalenol, zearalenone, and fumonisin. CONCLUSIONS: Ochratoxin was identified in the sinonasal tissue and/or mucus of some subjects with CRS. The clinical significance of this is not known
— id: 127252, year: 2011, vol: 127, page: AB123, stat: Journal Article,

Measurement of Mycotoxins in Patients with Chronic Rhinosinusitis
Lieberman SM; Jacobs JB; Lebowitz RA; Fitzgerald MB; Crawford J; Feigenbaum BA
2011 Aug;145(2):327-329, Otolaryngology, head & neck surgery
Mycotoxins are toxic secondary metabolites produced by a variety of fungi including Aspergillus, Alternaria, and Penicillium species. The presence of mycotoxins in sinonasal tissue and secretions and any possible link to chronic rhinosinusitis (CRS) or other diseases of the head and neck have not been reported. The authors performed an exploratory study to determine the presence and levels of mycotoxins in the sinonasal tissue and secretions of 18 subjects undergoing endoscopic sinus surgery for CRS. Using commercial enzyme-linked immunosorbent assay kits, samples were analyzed for the following mycotoxins: aflatoxin, deoxynivalenol, zearalenone, ochratoxin, and fumonisin. All specimens were negative for aflatoxin, deoxynivalenol, zearalenone, and fumonisin. Four (22%) of 18 specimens were positive for ochratoxin. The clinical significance of this finding remains to be determined
— id: 137919, year: 2011, vol: 145, page: 327, stat: Journal Article,

Rapid desensitization did not prevent febrile idiosyncratic reactions to oxaliplatin
Mathew A.; Ballas M.S.; Gorsky M.; Feigenbaum B.A.
2011 ;127(2 SUPPL 1):AB195-AB195, Journal of allergy & clinical immunology
RATIONALE: Immediate hypersensitivity reactions (HSR) are commonly encountered during infusion of chemotherapy, especially with platinum agents suchas oxaliplatin. The literature contains reports of4 patients who developed reactions during, or up to 24 hours after oxaliplatin infusion, with fever being a predominant symptom. Since fever is not an expected feature of an immediate HSR, the term idiosyncratic has been used to describe these reactions. While rapid drug desensitization has been shown effective in allowing infusion of drugs despite a history of immediate HSR, there are no reports indicating whether rapid drug desensitization is helpful is the management of febrile idiosyncratic reactions to oxaliplatin. METHODS: We report two patients with a history of immediate HSR to oxaliplatin, referred for rapid drug desensitization. During or within 1 hour after rapid drug desensitization with oxaliplatin, both patients developed signs and symptoms similar to previously reported cases of febrile idiosyncratic reactions to oxaliplatin, with maximum temperatures of 101.8 and 103.0 respectively. Both patients were hospitalized for several days, during which infection was ruled out. RESULTS: Rapid drug desensitization did not prevent febrile idiosyncratic reactions to oxaliplatin. CONCLUSION: The optimal management of patients with febrile idiosyncratic reactions to oxaliplatin remains unclear
— id: 127253, year: 2011, vol: 127, page: AB195, stat: Journal Article,

Immediate hypersensitivity reaction and successful rapid desensitization to rituximab followed by serum sickness in a 4 year old
Romanos-Sirakis E.; Feigenbaum B.A.
2011 ;127(2 SUPPL 1):AB198-AB198, Journal of allergy & clinical immunology
RATIONALE: Rituximab is a monoclonal antibody shown to be effective in treating pediatric chronic idiopathic thrombocytopenic purpura (ITP). Hypersensitivity reactions (HSR), both immediate HSR and systemic delayed HSR have been reported to rituximab, but not in the same patient. METHODS: We report a pediatric patient with immediate HSR to rituximab who underwent successful rapid drug desensitization and later developed serum sickness. RESULTS: On Day 0, this 4 YO male with chronic refractory ITP, developed urticaria and bronchospasm during initial rituximab infusion and the infusion was terminated. On Day 4, rituximab was infused without immediate HSR, utilizing a published 3-bag, 12-step, rapid desensitization protocol, with a maximum infusion rate of 40 ml/hour. On Day 11, rituximab was infused again without immediate HSR, utilizing the same protocol and infusion rates. On Day 14, he developed serum sickness. CONCLUSIONS: This 3-bag, 12-step rapid desensitization protocol, previously shown effective in adult subjects, was successful in a 4 YO. The patient later developed serum sickness, which rapid desensitization would not be expected to prevent. There are published reports of patients developing both immediate and delayed HSRs to a drug, however the delayed HSRs in those cases were cutaneous due to topical drug exposure, whereas in the present case, the delayed HSR was systemic from intravenous administration. We believe this is the first report of a pediatric patient receiving rituximab by rapid desensitization and first report of a pediatric patient developing both immediate HSR and systemic delayed HSR to the same drug, in this case, rituximab
— id: 127255, year: 2011, vol: 127, page: AB198, stat: Journal Article,

Special considerations for rapid drug desensitization with natalizumab
Sutaria M.; Miro K.; Mathew A.; Kister I.; Feigenbaum B.A.
2011 ;127(2 SUPPL 1):AB196-AB196, Journal of allergy & clinical immunology
RATIONALE: Natalizumab is a monoclonal antibody (mAb) indicated for treatment of multiple sclerosis. Natalizumab has special attributes which must be addressed when planning rapid desensitization for immediate hypersensitivity reactions (HSR.) Immediate HSRs during rapid desensitization are common, with consequent need to hold the infusion, treat the HSR, and possibly maintain a slower infusion rate. Complete infusion could require more than 8 hours, however, per FDA approved instructions, each bag of natalizumab solution must be infused within 8 hours of preparation or be discarded. Natalizumab is only supplied as 300 mg singledose vials. One published 3-bag, 12-step rapid desensitization protocol wastes approximately 10% of the drug, by discarding most solution in the first 2 bags. Accordingly, one must open another vial of natalizumab, costing approximately $3,000, or the patient will only receive approximately 90% of the typical intended dose. METHODS: Report of two patients with history of immediate HSR to natalizumab, and adaptation of a 3-bag, 12-step, rapid desensitization protocol as follows: Bag #1-0.6 mg in 50ml; Bag #2-6 mg in 50ml; Bag #3 and Bag #4-each 146.7 mg in 122.25ml. Bag #4 was not prepared until Bag #2 was mostly infused. Bags #2, #3 and #4 were infused completely. RESULTS: 99.8% of the intended dose was infused, without immediate HSR. CONCLUSIONS: With adaptation of a published protocol, rapid desensitization to natalizumab 300 mg is possible, utilizing only one single-dose vial, and with minimal chance of exceeding the FDA-approved eight hour infusion window from the time of preparation of each bag
— id: 127254, year: 2011, vol: 127, page: AB196, stat: Journal Article,

Iatrogenic Hypogammaglobulinemia Resembling Common Variable Immunodeficiency
Mathew A; Feigenbaum BA; Miro K; Weinfeld JN
2010 ;105:A101-A101, Annals of allergy, asthma & immunology
— id: 134324, year: 2010, vol: 105, page: A101, stat: Journal Article,

Successful Oxaliplatin Desensitization After Unsuccessful Infusion Using A Hypersensitivity Protocol
Miro K; Feigenbaum BA; Mathew A; Weinfeld JN
2010 ;105:A27-A27, Annals of allergy, asthma & immunology
— id: 134323, year: 2010, vol: 105, page: A27, stat: Journal Article,

Fractional exhaled nitric oxide in patients with atopic asthma: correct definitions of the terms atopy and asthma
Feigenbaum, Bernard A
2008 Jul;101(1):110-110, Annals of allergy, asthma & immunology
— id: 80334, year: 2008, vol: 101, page: 110, stat: Journal Article,

Self-reported, doctor-diagnosed "asthma" is not necessarily asthma: 78.9% of these "asthma" cases were atopic
Feigenbaum, Bernard A
2008 May;121(5):1291-1291, Journal of allergy & clinical immunology
— id: 80335, year: 2008, vol: 121, page: 1291, stat: Journal Article,

Insect-sting challenges--all risk and no benefit?
Feigenbaum BA
1995 Nov;96(5 Pt 1):704-705, Journal of allergy & clinical immunology
— id: 64106, year: 1995, vol: 96, page: 704, stat: Journal Article,

A case of vocal cord dysfunction mimicking asthma
Feigenbaum BA; Simon RA
1995 ;74:92-92, Annals of allergy
— id: 64758, year: 1995, vol: 74, page: 92, stat: Journal Article,

Remission of steroid dependent asthma following fundoplication for asymptomatic reflux
Feigenbaum BA; Simon RA
1995 ;95:202-202, Journal of allergy & clinical immunology
— id: 64757, year: 1995, vol: 95, page: 202, stat: Journal Article,

Aspirin intolerance
Feigenbaum BA; Simon RA; Stevenson DD
1995 Feb;74(2):193-194, Annals of allergy, asthma & immunology
— id: 64108, year: 1995, vol: 74, page: 193, stat: Journal Article,

Hydrocortisone sodium succinate does not cross-react with aspirin in aspirin-sensitive patients with asthma
Feigenbaum BA; Stevenson DD; Simon RA
1995 Oct;96(4):545-548, Journal of allergy & clinical immunology
BACKGROUND: Bronchospasm after intravenous hydrocortisone treatment has been reported in some patients with aspirin-sensitive respiratory disease. OBJECTIVE: This study was designed to determine the prevalence of sensitivity to hydrocortisone among patients with aspirin-sensitive respiratory disease. METHODS: We performed double-blind, placebo-controlled challenges with aspirin and 100 mg of hydrocortisone sodium succinate administered intravenously in 53 subjects. RESULTS: Forty-five of the 53 subjects (85%) undergoing oral aspirin challenge experienced respiratory reactions to aspirin. Forty-four of these 45 patients had neither naso-ocular, cutaneous, nor respiratory reactions to hydrocortisone sodium succinate. One aspirin-sensitive subject had bronchospasm and a naso-ocular reaction to hydrocortisone sodium succinate and a naso-ocular reaction with minimal bronchospasm to methylprednisolone sodium succinate. After desensitization to aspirin, and while receiving maintenance aspirin therapy, this subject again reacted to hydrocortisone sodium succinate with bronchospasm and naso-ocular reaction. CONCLUSION: We conclude that aspirin-sensitive patients with asthma are not preferentially sensitive to hydrocortisone and that hydrocortisone sodium succinate does not cross-react or cross-desensitize with aspirin
— id: 64107, year: 1995, vol: 96, page: 545, stat: Journal Article,

Lack of cross-sensitivity to IV hydrocortisone in aspirin-sensitive subjects with asthma
Feigenbaum BA; Stevenson DD; Simon RA
1994 ;93:242-242, Journal of allergy & clinical immunology
— id: 64760, year: 1994, vol: 93, page: 242, stat: Journal Article,

Respiratory succinate sensitivity that does not cross-react in an aspirin sensitive asthmatic
Feigenbaum BA; Stevenson DD; Simon RA
1994 ;72:94-94, Annals of allergy
— id: 64759, year: 1994, vol: 72, page: 94, stat: Journal Article,

Aspirin intolerance
Feigenbaum BT; Simon RA; Stevenson DD
1994 Nov;73(5):455-456, Annals of allergy
— id: 64737, year: 1994, vol: 73, page: 455, stat: Journal Article,