Abstracts S227
J ALLERGY CLIN IMMUNOL VOLUME 117, NUMBER 2
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A Case Of Carbamazepine Induced Onychomadesis
K. You1, J. Jeong2, S. Nahm2, E. Kim3; 1Internal Medicine, Kun-Kuk University Hospital, Seoul, REPUBLIC OF KOREA, 2Internal Medicine, ILSAN PAIK HOSPITAL, Kyungki-do, REPUBLIC OF KOREA, 3Internal Medicine, Dong-Kuk University Hospital, Kyungki-do, REPUBLIC OF KOREA. RATIONALE: Onychomadesis describes the presence of a transverse whole-thickness line. All drugs responsible for development of onychomadesis, depending on the dosage of the drug and possibly on the patients’ conditions. Recently we experienced a case of patient with carbamazepine-induced onychomadesis. CASE REPORT: A 35-year-old male had developed finger nail abnormality 1 month ago. He had met with a car accident 8 months ago and had undergone operation for ruptured aortic arch. Also he had amputated left leg above knee. He was prescribed to receive carbamazepine 200mg/day. In that time, test for CBC and chemistry were within normal limits. After three months’ carbamazepine, transverse surface depressions dominant in finger nails. He continued taking carbamazepine. Four months later, his nail had whole-thickness sulcus that divided the nail into two parts. Also, had complaint of pain in the area of fissuration, where the nail bed is not covered by nail plates. WBC was 8,130/mm3 with 11% eeosinophil. After counseling, he did not take carbamazepine. During 3- months period, his finger nails had regenerated slowly. Blood eosinophil count were also normalized. CONCLUSIONS: We present a case of the amputated patient with onychomadesis after administration of carbamazepine. Onychomadesis represents the extreme degree of Beau’s lines and shares same pathogenesis, i.e. a temporary arrest of nail matrix mitotic activity. Onychomadesis is frequent in patients receiving cancer chemotherapeutics, or carbamazepine, lithium, cefaloridine and cloxacillin. There’s no treatment for onychomadesis, which will gradually progress distally with nail growth. So, early recognition of adverse drug reaction with administered drug is most essential.
Anaphylaxis After Epidermal Contact with Cefotiam Hydrochloride J. Jeong1, K. You2, S. Nahm1, E. Kim3; 1Internal Medicine, ILSAN PAIK HOSPITAL, Kyungki-do, REPUBLIC OF KOREA, 2Internal Medicine, Kun-Kuk University, Seoul, REPUBLIC OF KOREA, 3Internal Medicine, Dong-Kuk University, Kyungki-do, REPUBLIC OF KOREA. RATIONALE: Contact urticaria is characterized by local immediate or delayed urticarial reaction, with swelling and redness at sites of epidermal contact with certain agents. The symptoms may involve generalized immediate hypersensitivity reactions including anaphylaxis, and such cases are called contact urticaria syndrome. Cefotiam is one of popular cephem antibiotics in Korea and Japan. Recently we experienced a case of nurse with cefotiam-induced contact urticaria syndrome. CASE REPORT: A 26-year-old nurse had worked in surgical ward for 4 years and had developed hand eczema 1 year ago. She experienced whealing on her hands, facial swelling, mild abdominal pain while preparing a solution of cefotiam in March 2004. In August 2004, urticaria developed on her hands first and progressing to facial edema with nausea, vomiting, and severe abdominal cramp after eczematous hand’s contact with splashed-out cefotiam solution. Initial blood pressure was 100/70 mmHg, and pulse rate 100/min. Emergency CBC and blood chemistry were within normal limits. She made rapid recovery after systemic glucocorticoid administration. Blood pressure after management was130/80 mmHg. Allergen skin prick test were positive to house dust mites, cockroach, dog epithelium. Prick test with cefotiam (300mcg/ml) produced positive wheal response (A/H ration: 4.6). CONCLUSIONS: We present a case of the nurse with occupational contact anaphylaxis after contact with cefotiam hydrochloride solution. Considering increasing usage of cefotiam hydrochloride in Korea, we expect more cases will occurring hereafter. Also, It is advisable that occupational handler of cefotiam hydrochloride who are atopic or has hand eczema should be examined regularly by allergist to prevent lethal anaphylactic reaction.
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Drug-Induced Petechial Eruption during Aspirin Therapy in a Patient with Positive Aspirin Allergy History but Negative Oral Challenge A. P. Hope, R. A. Simon, K. M. Woessner; Allergy and Immunology, Scripps Clinic/Green Hospital, La Jolla, CA. RATIONALE: Oral aspirin challenge can provide access to therapy for patients mistakenly classified as allergic. Delayed cutaneous drug eruptions can lead to discontinuation of non-causative lifesaving medications. Recognition of a medication’s risk-benefit ratio and a rational approach to drug eruptions may allow use of critical drugs. METHODS: We present a patient with a history of aspirin allergy treated with aspirin through a drug-induced eruption found to be secondary to nitrofurantoin. RESULTS: A 75 year-old woman was admitted with unstable angina. Ten years earlier, she was labeled aspirin allergic after an urticarial-type eruption three days into aspirin use following CABG. She received coumadin until this presentation. Allergy was now consulted to determine ASA sensitivity status. The patient underwent a negative aspirin challenge, and received an intra-coronary stent; she started aspirin and clopidogrel. Two days later, she developed a rash with petechiae and confluent non-painful purpuric change over her torso and thighs, was treated in the ED with systemic corticosteroids and referred back to Allergy for recurrent ASA hypersensitivity. There were no blisters or mucosal involvement; no constitutional signs or laboratory abnormalities suggested systemic hypersensitivity. The rash progressed with new petechial lesions. A careful history determined nitrofurantoin had been taken 5-8 days prior to rash onset. Aspirin and clopidogrel were continued with careful follow up. The rash resolved over the next 7 days, allowing for continued ASA/clopidogrel therapy. CONCLUSIONS: Life-saving aspirin therapy may be continued through a suspected delayed drug rash, provided there is an alternative explanation for the reaction and no evidence of bullous disease.
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Anaphylaxis to Multiple HIV-1 Protease Inhibitors (PIs) with Successful Desensitization to Ritonavir P. Saengaram, H. Chantaphakul, K. Ruxrungtham; Division of Allergy and Clinical Immunology, Department of Medicine, Chulalongkorn University, Bangkok, THAILAND. RATIONALE: HIV protease inhibitors (PIs) are important drugs included in the preferred highly active antiretroviral treatment (HAART) regimens. We present the first reported case of anaphylaxis to multiple PIs with successful desensitization to ritonavir. METHODS: Case report. RESULTS: A 32-yr-old HIV-infected female who has been on antiretroviral treatment for 8 years has developed multiple drug resistance to nucleoside analog RT inhibitors (NRTIs) and required switching to a PIbased regimen. She developed generalized urticaria and angioedema shortly after taking a HAART regimen containing ritonavir-boosted indinavir. Either indinavir or ritonavir has been implicated as the cause. She was admitted to ICU and graded-challenged with ritonavir (RTV). Although urticaria and angioedema occurred at 80 mg of the RTV challenge, desensitization was eventually accomplished. Ethanol, it’s key solvent ingredient, had a negative graded-challenge result. She was able to take ritonavir at a recommended booster dose of 100 mg every 12 hours without reactions. Indinavir was subsequently graded-challenged which resulted in anaphylactic shock after the half-usual dose. The next gradedchallenged was saquinavir, urticaria and angioedema were also developed. The patient eventually was successfully challenged with atazanavir. She has continued taking HAART that contained ritonavir-boosted atazanavir. The risk of emerging of viral resistance associated to the single drug graded-challenge and desensitization being evaluated. CONCLUSIONS: This is the first report of anaphylactic reactions to multiple PIs: indinavir, ritonavir, and saquinavir, but not atazanavir. Ritonavir, the only PI pharmacokinetic enhancer, was successfully desensitized. The mechanisms (IgE/non-IgE)) of this life-threatening reaction against multiple PIs are warranted further investigation.
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