Biomedical subjects
Publications and source records attributed to Sima Halevy.
Acute generalized exanthematous pustulosis (AGEP) is a rare severe cutaneous adverse reaction caused mostly by drugs. Three of 22 AGEP cases (13.6%), recruited by us as part of two prospective multinational studies, occurred 24 to 48 hours after a spider bite. We suggest that a spider bite is a possible trigger for AGEP.
INTRODUCTION: Acute generalized exanthematous pustulosis (AGEP) is an acute pustular eruption with unique clinical features, a rapid clinical course and a typical histopathology. The causative agents are mostly drugs but other triggers have also been described. CASE REPORT: A 52 year-old woman with a history of diabetes mellitus type II, dyslipidemia and osteomyelitis was treated for about a year with metformin (Glucophage) and simvastatin (Simovil) tablets. Due to the osteomyelitis, the patient was started on a regimen of intravenous vancomycin as well as furosemide tablets (Fusid) for pedal edema. About seventeen days after beginning treatment with vancomycin and a week after starting furosemide the patient was hospitalized due to an acute pruritic pustular eruption, involving most of her body surface area. Both vancomycin and furosemide treatment were discontinued, and topical treatment was provided. The clinical course was rapid with spontaneous resolution of the pustules followed by a characteristic pin-point post-pustular desquamation. The morphological, clinical and histological findings suggested a definite case of AGEP based on the EuroSCAR scoring system. The latent period between the initiation of medication intake and the appearance of AGEP, as well as a literature search, suggest that furosemide might be the incriminated drug. CONCLUSION: We have described a rare case of typical AGEP most probably induced by furosemide.
BACKGROUND: Drug-specific T cells are involved in the pathogenesis of cutaneous adverse drug reactions (CADRs). OBJECTIVE: We sought to evaluate the diagnostic role of in vitro drug-induced release of interferon gamma in CADRs. METHODS: The study group consisted of 36 patients with CADRs after intake of 106 drugs that were classified into 3 categories of drug suspicion: high, possible, and low. The control group consisted of 22 individuals taking a similar profile of 54 drugs, without CADRs. In vitro drug-induced interferon gamma release was determined by enzyme-linked immunosorbent assay in culture supernatants after incubation of peripheral blood lymphocytes with parent drug compounds. The in vitro tests were conducted after the acute phase of the CADRs. In vitro tests were compared with in vivo withdrawal and/or challenge drug tests. RESULTS: Positive interferon gamma tests were recorded in 77.8% of the patients for 49.0% of the drugs. The proportion of positive interferon gamma tests was directly associated with the degree of drug suspicion (64.4%, 36.4%, and 27.8% for high, possible, and low, respectively). There were significantly more positive tests for high- compared with low-suspicion drugs (P=.001). The degree of agreement between the results of the in vitro interferon gamma release tests and the in vivo tests was intermediate to good (kappa=0.47). CONCLUSION: In vitro drug-induced interferon gamma release may help to identify the responsible drug in CADRs.
Intake of drugs is considered a risk factor for psoriasis. The aim of this study was to investigate the association between drugs and psoriasis. A case-control study including 110 patients who were hospitalized for extensive psoriasis was performed. A control group (n = 515) was defined as patients who had undergone elective surgery. A case-crossover study included 98 patients with psoriasis. Exposure to drugs was assessed during a hazard period (3 months before hospitalization) and compared to a control period in the patient's past. Data on drug sales were extracted by data mining techniques. Multivariate analyses were performed by logistic regression and conditional logistic regression. In the case-control study, psoriasis was associated with benzodiazepines (OR 6.9), organic nitrates (OR 5.0), angiotensin-converting enzyme (ACE) inhibitors (OR 4.0) and non-steroidal anti-inflammatory drugs (NSAIDs) (OR 3.7). In the case-crossover study, psoriasis was associated with ACE inhibitors (OR 9.9), beta-blockers (OR 9.9), dipyrone (OR 4.9) and NSAIDs (OR 2.1). Extensive psoriasis may be associated with intake of ACE inhibitors, NSAIDs or beta-blockers.
BACKGROUND: More than 80% of leg ulcers are caused by venous insufficiency. The actual causes of venous ulcers, beyond the presence of venous insufficiency, are rarely referred to in the literature. This study evaluates the direct triggers for ulceration in patients with venous insufficiency. METHODS: Sixty-four patients with 110 chronic venous ulcers, treated in the Chronic Wounds Clinic of Soroka University Medical Center from 1999 through 2002, were included in the study. In each patient, the actual trigger of ulceration was determined by history taking and reviewing of the medical chart. RESULTS: The actual triggers of ulceration, based on data for 64 patients with an overall total of 110 ulcers, were identified as follows: cellulitis (or erysipelas), 17 ulcers (15.4% of 110 ulcers); penetrating injury, 13 ulcers (11.8%); contact dermatitis, 12 ulcers (10.9%); rapidly aggravating leg edema, 12 ulcers (10.9%); burn wound, seven ulcers (6.3%); dry skin with subsequent scratching, six ulcers (5.4%); blunt trauma, five ulcers (4.5%); deliberately self-inflicted trauma, five ulcers (4.5%); insect bite, two ulcers (1.8%); bleeding from a supeficial varicose vein, two ulcers (1.8%). In 29 ulcers (26.3%) no specific trigger was identified. CONCLUSIONS: The development of a cutaneous ulcer is not necessarily "spontaneous" and should not be attributed solely to the presence of venous insufficiency. In many cases, it is possible to identify a specific trigger that causes the ulceration. Clinical implementation of the above findings in routine examination and treatment of patients with venous insufficiency may prevent the development of venous ulcers.
Pemphigus vulgaris (PV) is only rarely associated with severe ocular involvement. We present a case of PV with bilateral severe swelling, induration and thickening of eyelids, and multiple conjunctival and lid margin erosions, complicated by high intraocular pressure secondary to steroid treatment. After successful systemic immunosuppressive, steroid, and antiglaucomatous treatment, clinical features were resolved, and intraocular pressure returned to normal. Severe ocular diseases without dermatological involvement may be present in PV patients.
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Trichodiscomas are hamartomas of the hair disk and appear as multiple, firm, well-circumscribed papules measuring a few millimeters. In most cases, trichodiscomas are distributed on the face and neck. Trichodiscomas may occur as isolated tumors or in association with other follicular tumors. In some cases, multiple trichodiscomas appear in association with fibrofolliculomas or acrochordons. We herein describe multiple agminated trichodiscomas in the earlobe.
A serum sickness-like reaction (SSLR) to drug administration usually consists of cutaneous rash, arthralgia/arthritis, and, often, fever. This entity rarely has been discussed in the dermatologic literature. We describe the case of a 3-year-old girl with urticaria, fever, and arthralgia that appeared 8 days after starting cefaclor therapy for otitis media.
Autoimmune progesterone dermatitis was manifested as deep-type erythema annulare centrifugum. Sensitivity to progesterone was studied in vivo by means of intradermal and patch tests, which revealed immediate-type and delayed-type hypersensitivity, respectively. Sensitivity to progesterone was further confirmed in vitro by results of an interferon-gamma release test, which imply a possible role for T(H)1-type cytokines in autoimmune progesterone dermatitis.