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Biomedical subjects

J H Winter

Publications and source records attributed to J H Winter.

48 records · Page 3Linked to original sources
PubMed1982

Treatment of venous thrombosis in antithrombin III deficient patients with concentrates of antithrombin III.

Two patients with familial antithrombin III deficiency developed deep venous thrombosis of the lower limb. The diagnosis of venous thrombosis was made by the indium labelled platelet technique which also allowed for the daily assessment of thrombus size. Each patient received treatment with Warfarin, subcutaneous heparin, and infusions of antithrombin III concentrates. The authors conclude that infusions of antithrombin III concentrates may be of value in limiting the extent of acute thrombosis in patients with a severe deficiency of this protein and may help prevent pulmonary embolism. The haemorrhagic risk of continuing modest doses of heparin with high dose ATIII therapy appears small. In addition to its value in the diagnosis of venous thrombosis the indium platelet technique may give an early indication of thrombus extension and may thus indicate the effectiveness of treatment.

Adult↗
PubMed1982

Familial antithrombin III deficiency.

Antithrombin III is the major physiological inhibitor of the coagulation mechanism and a deficiency of this protein results in a marked predisposition to venous thromboembolic disease. Three Scottish families with a deficiency of this protein are described and other reported families are reviewed. The properties, functions and methods of assay of antithrombin III are outlined; the molecular abnormalities, inheritance, clinical and laboratory characteristics of antithrombin III deficiency are described, and the use of antithrombotic drugs and human antithrombin III concentrates in this deficiency is discussed.

Adolescent↗
PubMed1981

Transfusion studies in patients with familial antithrombin III (ATIII) deficiency: half-disappearance time of infused ATIII and influence of such infusion on platelet life-span.

Two patients with familial ATIII deficiency received infusions of a concentrate of ATIII prepared from human plasma. Serial plasma samples were assayed for their functional and immunological content of ATIII. The rates of disappearance of ATIII activity found in this study suggest that, initially, frequent infusions are necessary to maintain normal levels of ATIII activity in patients with a severe deficiency. In one patient platelet survival did not appear to be influenced by ATIII infusions.

Adult↗
PubMed1981

Oral anticoagulants.

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Administration, Oral↗
PubMed1979

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↗