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PubMed1978

[Physiopathological bases for a rational therapy of gout].

Rational therapy of gout must be correlated with the two basic aetiopathogenetic factors, i.e. metabolic error and the inflammatory dysreactive moment. Due to its different action mechanism, the former is responsible for the typing of adult primary hyperuricaemia: a) hyperincorporating and hyperescretory forms; b) normo-incorporating and relatively or absolutely hypoexcretory forms; c) hyperincorporating and hyposcretory forms. It would be a mistake to treat the condition chemically without knowing the physiopathology of the metabolic error. On the basis of a preliminary typing assessment, rational chemical correction of the metabolic error in gout cases can be achieved with drugs that block the enhanced endogenous synthesis of uric acid (allopurinol, etc.) or correct the metabolite renal excretion defect. Therapy of the dysreactive-inflammatory component should involve non-steroid anti-inflammatory drugs. The disadvantages of using cortisones in gout treatment are stressed.

Allopurinol↗
PubMed1988

Secondary prevention of vascular disease by prolonged antiplatelet treatment. Antiplatelet Trialists' Collaboration.

Thirty one randomised trials of antiplatelet treatment for patients with a history of transient ischaemic attack, occlusive stroke, unstable angina, or myocardial infarction were identified. Six were still in progress, and the results of the remaining 25 were reviewed. They included a total of some 29,000 patients, 3000 of whom had died. Overall, allocation to antiplatelet treatment had no apparent effect on non-vascular mortality but reduced vascular mortality by 15% (SD 4%) and non-fatal vascular events (stroke or myocardial infarction) by 30% (4%). This suggested that with good compliance these treatments might reduce vascular mortality by about one sixth, other vascular events by about a third, and total vascular events by about a quarter. There was no significant difference between the effects of the different types of antiplatelet treatment tested (300-325 mg aspirin daily, higher aspirin doses, sulphinpyrazone, or high dose aspirin with dipyridamole), nor between the effects in patients with histories of cerebral or cardiac disease. Thus antiplatelet treatment can reduce the incidence of serious vascular events by about a quarter among a wide range of patients at particular risk of occlusive vascular disease. The balance of risk and benefit, however, might be different for "primary" prevention among people at low absolute risk of occlusive disease if antiplatelet treatment produced even a small increase in the incidence of cerebral haemorrhage.

Angina Pectoris↗