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B Bernstein

Publications and source records attributed to B Bernstein.

63 records · Page 4Linked to original sources
PubMedDate not supplied

Drug-induced linear immunoglobulin A bullous disease that clinically mimics toxic epidermal necrolysis.

Drug-induced linear immunoglobulin A bullous disease is a subepidermal blistering disorder that most commonly occurs after exposure to vancomycin. It can clinically mimic toxic epidermolytic necrolysis. We describe an 87-year-old white woman in whom linear immunoglobulin A bullous disease developed while she was taking vancomycin and phenytoin. A few days after the linear immunoglobulin A bullous disease developed, both medications were discontinued. No new bullae developed, and the eruption completely resolved within 2 weeks. The patient was treated with only topical therapy.

Aged↗
PubMedDate not supplied

Circulating immune complexes in Kawasaki syndrome.

Sera of 42 patients with Kawasaki syndrome were evaluated for the presence of circulating immune complexes (CICs) by Raji cell radioimmune and C1q solid phase assays. Overall 69% of sera tested were positive by one or both assays, 52% by Raji cell radioimmune and 48% by C1q solid phase assay. CICs were detected most frequently 2 to 4 weeks after the onset of illness, but their presence did not correlate with the clinical severity of the illness or incidence of coronary artery aneurysms. Antibody to mite antigen was found in only 2 of 30 patients tested, and only one of these had CICs. CICs are frequently associated with Kawasaki syndrome, but their role in its pathogenesis remains to be determined.

Aneurysm↗
PubMedDate not supplied

Scleroderma-like changes in insulin-dependent diabetes mellitus: clinical and biochemical studies.

Children with insulin-dependent diabetes mellitus (IDDM) were examined for scleroderma-like changes of digital sclerosis and joint contractures. Of the 104 patients, 19 (18%) demonstrated these features; five patients had both multiple joint involvement and skin changes; three were studied in detail. All three had restrictive pulmonary disease. Histopathology of skin in these three patients demonstrated increased accumulation of collagen in the lower dermis. In two of the patients, the extractability of collagen in 0.5 N acetic acid was decreased by about 50% as compared with normal controls, which suggests increased cross-linkage of collagen. In addition, the mean nonenzymatic glycosylation of collagen in these three patients was 13 times that of controls. The results indicate that distinct histopathologic and biochemical changes can be detected in the skin of these patients. The results further support the hypothesis that nonenzymatic glycosylation may alter the turnover of collagen, thus contributing to the development of a scleroderma-like syndrome with skin, joint, and pulmonary findings in patients with IDDM.

Adolescent↗
PubMedDate not supplied

Treatment of collagen induced arthritis in DBA/1 mice with L-asparaginase.

OBJECTIVE: To evaluate the safety and efficacy of L-asparaginase as an immunosuppressive agent in a mouse model of rheumatoid arthritis. METHODS: Male DBA/1 mice with collagen-induced arthritis (CIA) were treated at different intervals with various doses of native and pegylated L-asparaginase from E. coli. The mice were observed for 4 weeks during which time arthritis was scored. Outcome parameters included effect on severity and progression of established arthritis as well as prevention of disease. In addition, X-rays from the affected joints were obtained for comparison. RESULTS: Both native L-asparaginase at a dose of 50 IU/injection intraperitoneally three days a week and pegylated asparaginase (PEG-L-asparaginase) at a dose of 25 IU/injection twice a week, significantly reduced the mean arthritic score (MAS) in mice with established arthritis (p < 0.001 for PEG-L-asparaginase). When native L-asparaginase was administered before the onset of arthritis (days 14-post immunization) the number of mice developing arthritis as well as the number of arthritic paws and the severity of arthritis in the treatment group were significantly decreased (p < 0.0001). Significant differences were found in the X-ray evaluation between treated and control mice. None of the animals died due to drug related events or showed signs of asparaginase induced toxicity. CONCLUSION: Our data provide the first direct evidence that L-asparaginase is a potent antiarthritic agent and may represent an effective second line agent for future treatment studies in juvenile and adult rheumatoid arthritis.

Animals↗
PubMedDate not supplied

Aspirin and fenoprofen (Nalfon) in the treatment of juvenile rheumatoid arthritis results of the double blind-trial. A segment II study.

We compared efficacy and safety of aspirin (ASA) and fenoprofen in the treatment of JRA. Ninety-nine children with JRA were given ASA or fenoprofen in a 12-wk, multicentered, double-blind, parallel study. Initial fenoprofen dosage was 900 mg/m2/d increased to 1800 mg/m2/d (3200 mg/d-max). Initial ASA dosage was 1500 mg/m2/d increased to 3000 mg/m2/d (5450 mg/d-max). Adverse reactions forced removal of 14% of ASA treated patients from the trial, whereas no fenoprofen patient was removed for this reason. Forty of 50 ASA patients, and 47 of 49 fenoprofen patients completed at least 10 wk of therapy and analysis showed that the 2 drugs were nearly identical in efficacy, but toxicity was considerably less among fenoprofen treated patients.

Arthritis, Juvenile↗
PubMedDate not supplied

Ketoprofen (Orudis) in the treatment of juvenile rheumatoid arthritis. A segment I study.

The study objective was to establish a safe and efficacious dose of ketoprofen in children with JRA during a 4-week, open-labeled, non-controlled trial. Initial dosage was 100 mg/m2/d, gradually increased up to 200 mg/m2/d, not to exceed 320 mg/d. One patient was removed from the study due to hematuria. Clinical improvement was observed in 50% or more of the patients in 8 of the 15 indices assessed. Statistical improvement was detected in the number and severity of joints with pain on motion, the duration of morning stiffness, and the time required to travel 50 feet (p less than .035). Significant laboratory changes included decreases in the mean hemoglobin and hematocrit, and increases in ESR and BUN (p less than .03). Twenty patients experienced a total of 39 adverse effects and of these, 6 were judged to be attributable to ketoprofen. These preliminary data suggest ketoprofen's efficacy and safety is comparable to that of other nonsteroidal antiinflammatory drugs.

Arthritis, Juvenile↗