PubMed HealthSearch

Biomedical subjects

A S Douglas

Publications and source records attributed to A S Douglas.

13 recordsLinked to original sources

Circannual rhythm of arterial and venous thromboembolic disease.

This study confirms previous reports of a seasonal variation in morbidity and mortality from coronary and cerebral arterial disease; these disorders are much less common in summer (e.g. July and August) than in winter (e.g. December and January). In coronary disease the shape of the curve for the annual morbidity is different from that for annual mortality and possible reasons for this are discussed. A similar circannual rhythm has been shown for venous thrombo-embolic disease.

Coronary Disease

Individualisation of oral anticoagulant therapy.

The hepatic synthesis of vitamin K dependent coagulation factors is modified by oral anticoagulant drugs, resulting in the release of functionally deficient coagulation factors into the circulation and consequently anticoagulation. Since their introduction into clinical medicine over 30 years ago, both clinical and scientific evidence has demonstrated the value of oral anticoagulants in the treatment and prophylaxis of venous thrombosis. In the treatment of arterial disease, however, both the indications for and usefulness of oral anticoagulants remain very much in doubt despite their widespread use in the 1950s and 1960s and in numerous clinical trials. The initiation and continuation of oral anticoagulant therapy is a co-operative venture involving the patient, the clinician and the laboratory. The clinician must have a thorough knowledge of the indications for and contraindications to the use of these drugs, and regular, accurate laboratory control is essential if haemorrhage, the major side effect, is to be avoided or reduced to a minimum. The patient must bear the responsibility for regular clinic attendance, abstinence from proprietary medications, and must immediately seek medical advice if any sign of haemorrhage occurs.

Age Factors

Familial thrombosis: inherited deficiency of antithrombin III.

Several members of a family living on the west coast of Scotland and on one of the islands off the coast had serious thrombotic disease. The plasma antithrombin III (ATIII) concentrations were measured by both functional and immunological assay in all available members of the family. Concentrations were 25% to 66% of normal in 12 people, including all seven with thrombotic disease. The inheritance pattern was characteristic of an autosomal dominant disorder. Thrombotic disease generally affected the leg, mesenteric, and axillary veins, although one man who had died before the study began had had severe arterial atheroma. In women the first thrombotic symptoms usually occurred during pregnancy. None of these patients have developed thrombotic symptoms until they were at least 18, so four younger members of the family who have ATIII deficiency but no thrombotic disease may eventually develop symptoms.

Adolescent

The contribution of plasma protease inhibitors to antiplasmin activity in man.

1. Human plasma contains a variety of proteins that are capable of inhibiting plasmin activity. Whole plasma possesses 'rapid' and 'progressive' plasmin-neutralizing activity: this study assesses the contribution of individual protease inhibitors to this plasmin-neutralizing property of plasma. 2. Rapid and progressive antiplasmin activities of human plasma correlate with alpha2-macroglobulin and alpha1-antitrypsin concentrations respectively. 3. Fluctuations in the amounts of the other measured inhibitors (antithrombin III, Cl in activator and inter-alpha-tryspin inhibitor) did not influence the measured antiplasmin activity.

Antithrombins