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Biomedical subjects

R A Hutton

Publications and source records attributed to R A Hutton.

At least 73 records · Page 4Linked to original sources
PubMed1979

Platelet function in beta-thalassaemia major.

Abnormal platelet aggregation was found in eight (44%) of 18 patients with beta-thalassaemia major and transfusional iron overload. The aggregation defect bore no correlation with the degree of hepatic fibrosis, liver function tests, whether or not splenectomy had been performed, the degree of iron overload, haematocrit, platelet count, serum vitamin E level, or leucocyte ascorbate concentration. Only three of the 18 patients showed prolonged bleeding times as well as abnormal platelet aggregation, and only one of these suffered clinically significant haemorrhage. The results show that a proportion of patients with beta-thalassaemia major have abnormal platelet function. It is possible, however, that the in vitro abnormality might be due partly to artefacts induced by manipulations required to remove the abnormal thalassaemic red cells, and this may explain the much lower incidence of significant haemorrhage.

Adolescent↗
PubMed1979

Platelet aggregation studies during transient hypoglycaemia: a potential method for evaluating platelet function.

The effect of acute hypoglycaemia on platelet function was examined in patients undergoing an insulin stress test. Enhanced platelet aggregation was observed in all cases but platelet count, platelet adenine nucleotides, and the plasma level of von Willebrand factor were unchanged overall. The onset of the hypoglycaemia-induced increase in platelet aggregation coincided with the lowest blood glucose levels recorded and with the clinical signs of adrenaline release. Increased platelet aggregation was maintained thereafter for the two-hour test period. There was no apparent correlation with changes in cortisol, growth hormone, and prolactin. No change in platelet function was observed after the administration of L-dopa. We suggest that the measurement of platelet aggregation during a standard insulin stress test may provide a means of evaluating platelet function in vivo and the influence of drugs thereon.

Adenine Nucleotides↗
PubMed1979

The hemostatic defect of chronic liver disease. Kinetic studies using 75Se-selenomethionine.

With the use of cohort labeling with 75Se-selenomethionine, simultaneous platelet, fibrinogen, and plasminogen survival studies were carried out in 8 patients with chronic alcoholic liver disease and in 5 normal subjects. Clinical features, liver function tests, coagulation and fibrinolytic system activities, and platelet function were also assessed. On the basis of platelet survival, the patients could be divided into two groups. Three patients had shortened platelet survival; they were all thrombocytopenic and had greater prolongation of the prothrombin time (PT) and activated partial thromboplastin time (PTT) than the other 5 patients. However, platelet turnover was decreased in all the patients, and there was no difference between the two groups with regard to fibrinogen or plasminogen survival nor in the in vitro evidence of disseminated intravascular coagulation (DIC). Fibrinogen survival was increased in 5 of the 8 patients. Plasminogen survival was normal in 6 patients and prolonged in 2 patients with very low plasminogen levels. The absence of increased fibrinogen turnover in the patients studied indicates that the abnormalities in coagulation tests were not due to consumption coagulopathy. The authors' studies suggest that, at least for patients with chronic stable alcoholic liver disease, the concept that the coagulopathy of liver disease is due to increased utilization of clotting factors should be revised with caution.

Blood Coagulation Disorders↗
PubMed1977

A chlorpromazine-induced inhibitor of blood coagulation.

An inhibitor of blood coagulation was detected in the plasma of four schizophrenic patients receiving long-term chlorpromazine therapy. The partial thromboplastin time (PTT) was prolonged in all four patients and the prothrombin time (tpt) was prolonged in one. The inhibitor which resembled in many respects that seen in patients with systemic lupus erythematosus (SLE), was shown to be associated with the tigM-rich fractions of the serum. None of the patients manifested a clinical bleeding tendency and in two, discontinuation of the chlorpromazine was followed by a decrease in the activity of the anticoagulant. While three of the patients had a positive antinuclear antibody test (ANA) and the fourth a false positive serology for syphilis, no further evidence for SLE was found.

Adult↗
PubMed1976

Defect of platelet function associated with chronic hypoglycaemia.

Two patients are described with chronic hypoglycaemia; the first having glucose-6-phosphatase deficiency (type I glycogen storage disease), and the second fructose 1:6-diphosphatase deficiency. Both cases were associated with a bleeding diathesis, a defect of platelet aggregation, and a deficiency of platelet adenine nucleotides. The effect on the platelet abnormalities of a period of normoglycaemia was studied in both patients. Correction of the platelet abnormalities occurred rapidly after stabilization of the blood glucose within the normal range. Normal function persisted for the duration of the normoglycaemia, facilitating diagnostic liver biopsy and surgical procedures. A biochemical explanation for the nucleotide deficiency is suggested.

Adenine Nucleotides↗
PubMed1973

Hereditary giant platelet syndrome: a disorder of a new aspect of platelet function.

The platelets of three patients with the hereditary giant platelet syndrome of Bernard and Soulier failed to aggregate in response to either ristocetin or bovine fibrinogen. The results of aggregation experiments using mixtures of platelets and plasma suggest that a reaction between a plasma factor deficient in von Willebrand's disease and a platelet component lacking in our patients, and leading to platelet aggregation independently of adenosine diphosphate (ADP), is essential for normal haemostasis.

Adenosine Diphosphate↗
PubMed1968

Haemostatic mechanism in uraemia.

The haemostatic mechanism was investigated in 20 patients with renal failure, of whom nine had evidence of a bleeding tendency. A defect of platelet function was the most common finding. The effect of dialysis on the bleeding state is briefly discussed, and a scheme for the routine investigation of haemostasis in renal failure is put forward.

Adolescent↗