Penicillin skin testing: a way to optimize antibiotic utilization.
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Biomedical subjects
Publications and source records attributed to L Kabbash.
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A total of 317 patients received loratadine, 10 mg once daily, terfenadine 60 mg twice daily, or placebo in a 14-day, double-blind, randomized study in seasonal allergic rhinitis. Four nasal and four nonnasal symptoms were evaluated. At the end point evaluation, mean total scores of combined nasal and nonnasal symptoms decreased from baseline (improved) 46%, 44%, and 35%, respectively, for loratadine, terfenadine, and placebo. The difference between loratadine and placebo treatment was significant (p = 0.03). Loratadine was particularly effective compared with placebo in relieving nasal discharge, sneezing, and itching/burning eyes. Therapeutic response to treatment was good or excellent in 66 (64%) of 103 loratadine-treated patients, 58 (56%) of 104 terfenadine-treated patients, and 48 (47%) of 102 placebo-treated patients. Adverse experiences reported during the study were usually mild or moderate and were not significantly different among the three treatment groups. Sedation (somnolence) was reported by 10 loratadine-treated patients, seven terfenadine-treated patients, and eight placebo-treated patients. Loratadine, 10 mg once daily, was comparable to terfenadine, 60 mg twice daily, and significantly superior to placebo in the symptomatic relief of seasonal allergic rhinitis.
Human polymorphonuclear leukocytes (PMN) released large quantities of hydrogen peroxide in response to tumor necrosis factor, but only when the cells were adherent to surfaces coated with extracellular matrix proteins. The PMN did not respond when exposed to cytokines and matrix proteins in suspension, or when exposed to cytokines while adherent to surfaces coated with stearic acid. PMN from children with genetic deficiency of the CD11/CD18 integrins underwent a normal respiratory burst upon adherence to uncoated polystyrene, but not in response to tumor necrosis factor when tested on polystyrene that was coated with serum, fibronectin, vitronectin, fibrinogen, thrombospondin, or laminin. Anti-CD18 antibodies, alone of sixteen antibodies tested, induced a similar defect in PMN from normal donors, when the PMN were tested on surfaces coated with serum, fibrinogen, thrombospondin, or laminin; no defect was induced by the anti-CD18 monoclonal antibody IB4 in normal PMN tested on surfaces coated with fibronectin or vitronectin. Thus, for cytokines to induce a respiratory burst in PMN, the cells must be able to use CD11/CD18 integrins and must interact with matrix proteins in the solid phase. CD11/CD18, which is already known to serve as a receptor for fibrinogen, may also be a receptor for thrombospondin and laminin. Finally, receptor(s) exist on PMN for fibronectin and vitronectin which are not blocked by the anti-CD18 antibody IB4 but which are nonetheless CD11/CD18 dependent.
Recent reports of reticuloendothelial system Fc receptor function using anti-Rh(D) coated red blood cells (RBC) provide conflicting data regarding the degree of abnormality in systemic lupus erythematosus (SLE). The effect of different sensitizing doses of anti-Rh(D) on Fc receptor function was evaluated in 10 controls and 9 patients with SLE (5 with renal disease, 4 without) using 1 microgram anti-Rh(D) (6,700 molecules anti-Rh(D)/RBC by saturation analysis) and 0.125 microgram anti-Rh(D) (1,100 molecules/RBC). At the lower sensitizing dose the sensitivity of the assay was significantly increased. To correctly interpret the significance of studies of Fc receptor function from different centers, it is necessary to know the exact sensitizing doses used for each study.
Reticuloendothelial system Fc receptor function was measured in 10 patients with systemic lupus erythematosus (SLE) taking corticosteroids, 10 SLE patients not receiving corticosteroids and in 19 controls, 9 of whom were corticosteroid-dependent asthmatics and 10 of whom were healthy. Clearance studies were performed using autologous 51 Cr-labeled erythrocytes that had been sensitized with human IgG anti-Rh(D) [6,700 molecules/cell]. The clearance curves could be split into a fast (t1/2 fast) and a slow (t1/2 slow for any of the groups of patients. The results were correlated with serum C3, C4, DNA-binding, fluid phase 125I-Clq binding, a disease activity index, corticosteroid dose and duration of therapy with corticosteroids. The only significant correlation was an inverse correlation of C4 with the t1/2 slow in SLE patients not on corticosteroids (r=- 0.71, p less than 0.05). The t1/2 slow of the 3 SLE patients with active nephritis (86 +/- 40 min) was significantly different from the 17 SLE patients with inactive nephritis or normal renal function (37 +/- 5 min) (P less than 0.05). We conclude that there is no overall defect of Fc receptor function in our patients with SLE although there is decreased clearance in patients with active lupus nephritis.