Aspirin kinetics and platelet aggregation in man.

Our aims were (1) to determine the effect of six commercially available aspirin (ASA) preparations on in vitro platelet aggregation, and (2) to relate changes in platelet function to ASA kinetics. Each of six subjects took a single dose of one of the following preparations--600 mg Asproclear, 600 mg Bufferin, 600 mg Bi-prin, 600 mg compressed ASA, 650 mg Ecotrin, or 650 mg S.R.A.--in random order every 3 wk. Venous blood was drawn before and at 2, 4, 6, and 24 hr after ASA dosage to measure platelet aggregation in response to collagen and adenosine diphosphate and, at more frequent intervals, to characterize ASA kinetics. Asproclear, Bufferin, Bi-prin, and compressed ASA yielded peak plasma ASA levels of 28 to 56 mumol/l (5 to 10 mg/l) within 15 to 60 min and peak salicylic acid (SA) levels of 72 to 290 mumol/l (10 to 40 mg/l) within 2 hr. Ecotrin and S.R.A. yielded plasma SA levels of 14 to 87 mumol/l (2-12 mg/l) within 4 to 24 hr and no measurable ASA at any time after dosing. Platelet aggregation was inhibited to an equal extent by all preparations. The time course for this inhibition was the same for all preparations but Ecotrin (which led to a more delayed effect). There was significant recovery of collagen-induced platelet aggregation at 24 hr with all preparations but Ecotrin. With Ecotrin and S.R.A. there was inhibition of platelet aggregation in the absence of measurable circulating ASA. We postulate that this was due to acetylation of cyclooxygenase in the portal circulation and that inhibition of peripheral cyclooxygenase may be spared.

Is there an HLA antigen association with duodenal ulcer?

To assess the influence of ethnic origin on the incidence of HLA antigens in duodenal ulcer, we typed 160 white Australian patients (including 22 born in Greece or Italy) and 320 blood donor controls for the HLA-A and -B loci. 5 of the 22 (22.7%) southern European patients, but only 19 of the 138 (13.8%) of the remaining duodenal ulcer patients were found to have antigen B5 compared with 27 (8.4%) of the controls. HLA-B12 was found in 55 (34.4%) duodenal ulcer patients (including 6 of the 22 southern European patients) and 117 (36.6%) controls. No significant association of duodenal ulcer with HLA-B5 or HLA-B12 was found when differences in racial origin of patients were taken into account.

Matching for HLA antigens of A, B, and DR loci in renal transplantation by Eurotransplant.

79 patients and their respective cadaveric kidney donors were typed for HLA-A, HLA-B, and HLA-DR antigens using frozen stored spleen lymphocytes and fresh peripheral-blood lymphocytes. The kidney-graft survival-rate at 3 to 18 months was highest when donor and recipient shared one or two DR antigens and three or four A and B antigens. The graft-survival rate was significantly higher (87 +/- 6%) at 18 months in these patients than in less well matched patients (48 +/- 9%).

Cimetidine treatment of duodenal ulceration: short term clinical trial and maintenance study.

Eighty-five patients with endospcopically confirmed duodenal or pyloric canal ulcers entered a double blind trial with 1200 mg of cimetidine per day or placebo for 6 weeks. Eighty-four per cent of patients treated with cimetidine and 38 percent of those receiving placebo healed their ulcers (P less than 0.001). Measurement of basal acid output and maximal acid output before and after treatment showed no significant change but patients who failed to heal their ulcers had a higher basal acid output and maximal acid output than those who healed. Patients who smoked or drank alcohol had the same healing rate as abstainers. Sity-seven patients with duodenal ulceration healed by a 6-week course of cimetidine were randomly allocated to 400 mg of cimetidine twice daily or placebo in the maintenance trial. Actuarial analysis of the number of relapses in each group demonstrates that cimetidine is highly effective in preventing relapse.

An estimation of the recombination fraction between the MLC locus and the FOUR locus.

Thirty-nine families with 167 children were typed for HL-A and studied in the MLC test. Two maternal recombinations between the FOUR and the MLC locus in two different families were found. An estimate of the recombination fraction between the FOUR and the MLC locus was calculated.