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PubMed1983

[Cerebrovascular complications of thrombocytosis].

Cerebrovascular complications of thrombocytosis may be the presenting symptoms of the disease (thrombocythemia or secondary thrombocytosis). In the light of 3 recently studied cases, the clinical, pathogenic and therapeutic aspects are emphasized. Early diagnosis is fundamental if the occurrence of permanent neurologic dysfunction is to be avoided.

Aged↗
PubMed1983

Decrease in renal function due to sulphinpyrazone treatment early after myocardial infarction.

Twenty-nine patients with recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group (n = 15) who received sulphinpyrazone, 4 x 200 mg daily for 7 days. Renal function significantly and transiently deteriorated in the sulphinpyrazone group compared to the placebo group. In the sulphinpyrazone group the 24 hour-urinary prostaglandin E2 and kallikrein excretion were suppressed. These data suggest that the decrease in renal function caused by sulphinpyrazone early after myocardial infarction could be mediated by an inhibition of renal prostaglandin and/or kallikrein-kinin synthesis.

Acute Kidney Injury↗
PubMed1980

Antithrombotic therapy for vascular prosthesis: an experimental model testing platelet inhibitory drugs.

Although Dacron vascular grafts are widely used, they are thrombogenic and rapid blood flow maintains patency. When blood flow is suboptimal, antithrombotic therapy may prevent early occlusion. We evaluated the effect of three platelet inhibitory drugs: acetylsalicylic acid (ASA), dipyridamole (DPM), sulphinpyrazone (SPZ), and a combination of ASA plus DPM on platelet adherence to woven Dacron in an artificial circulation. Heparinized blood from 18 volunteers was divided equally for test and control circuits, and to the test each drug was added in therapeutic concentration. The experiment was repeated ex vivo using blood donated by six volunteers after each had taken, separately for 1 week: (1) no drug; (2) ASA, 300 mg, three times a day; (3) DPM, 100 mg, four times a day; (4) SPZ, 200 mg, four times a day; (5) ASA, 300 mg, plus DPM, 75 mg, combined, three times a day. Platelet count, adhesion and aggregation were measured during the 60-minute perfusion, and scanning electron miscroscopy of the graft's luminal surface was performed. ASA was the most effective single agent, significantly impairing platelet function and reducing consumption of platelets by the graft. DPM reduced platelet adherence only in the ex vivo experiment, and its addition to ASA imparted no further influence. Sulphinpyrazone had little effect in either experiment. Antithrombotic therapy with ASA and DPM requires clinical evaluation.

Aspirin↗
PubMed1980

Inhibition of thrombocytopenic episodes caused by the Arthus reaction, the sub-lethal Forssman reaction and ADP.

Through the use of 51Cr-labelling about 50% of circulating platelets were shown to be permanently removed from the circulation subsequent to the Arthus reaction but not after the sub-lethal Forssman reaction or the repeated injection of ADP to guinea pigs. Oral administration of ticlopidine inhibited the transient thrombocytopenia caused by ADP. Cyclooxygenase inhibitors including sulphinpyrazone and its thioether metabolite inhibited the thrombocytopenia of the Arthus reaction but only sulphinpyrazone effectively inhibited the thrombocytopenia of the sub-lethal Forssman reaction.

Adenosine Diphosphate↗
PubMed1981

Platelet and coagulation function in patients with abnormal cardiac valves treated with sulphinpyrazone.

Eight patients on warfarin with rheumatic heart disease and prosthetic cardiac valves were selected for study on the basis of persistently elevated plasma beta-thromboglobulin (beta-tg) and platelet factor 4 (PF4) concentrations. Platelet mean lifespan and fibrinogen half life were short, and positively correlated, and both were inversely related to the plasma concentration of the platelet specific proteins. Antithrombin III (ATIII) levels were also reduced. Treatment with sulphinpyrazone resulted in lengthening of both platelet and fibrinogen survival, a rise in ATIII but no change in the beta tg or PF4 concentrations. It is concluded that patients with abnormal cardiac valves and raised plasma levels of beta tg or PF4 have, despite warfarin, a consumption coagulopathy that can be inhibited by sulphinpyrazone.

Adult↗
PubMed1984

An approach to hyperuricemia and gout.

Arthrocentesis and patient and family histories make gout relatively easy to diagnose. The next step is to distinguish between primary and secondary hyperuricemia. Hyperuricemia results from either impaired renal excretion or excessive production of uric acid--or both. Determining the cause guides the choice of therapy.

Allopurinol↗