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Biomedical subjects

S Ardeman

Publications and source records attributed to S Ardeman.

At least 19 recordsLinked to original sources
PubMed1981

Coagulation inhibitor in hypothyroidism.

A patient was referred for investigation of heavy bleeding after surgery. He showed several features of hypothyroidism but no goitre. Primary autoimmune hypothyroidism was confirmed by the finding of a low serum thyroxine concentration and a high thyrotropin concentration. Factor VIII concentration was low, and a mild coagulation inhibitor was found. The patient was treated with thyroxine and returned to normal health within a few months. The inhibitor found in this patient may have been specific for factor VIII, but the presence of coagulation inhibitors should be considered in patients with hypothyroidism.

Adult↗
PubMed1978

Secretion of intrinsic factor and hydrochloric acid after 12 weeks' treatment with cimetidine.

A sample of 16 patients had pentagastrin stimulation studies performed before starting a 12 week course of cimetidine, and again 12 hours after completing the course. Basal and pentagastrin stimulated intrinsic factor secretion was assayed in 13 patients. There was no significant difference in the pattern of secretion after 12 weeks' treatment with cimetidine. The basal and peak acid outputs of all 16 patients were measured. No significant difference was found in the pattern of acid secretion after treatment. It appears that parietal cell secretory function is restored to normal within 12 hours of discontinuing a prolonged course of cimetidine.

Cimetidine↗
PubMed1972

Folate deficiency after anticonvulsant drugs: an effect of hepatic enzyme induction?

Serum and red cell folate levels were reduced in 59% and 58% respectively of 75 children with epilepsy attending a residential school. The degree of folate deficiency was significantly related to increased hepatic microsomal enzyme activity, assessed from increased urinary excretion of D-glucaric acid and also correlated with the daily dose of anticonvulsant taken. Anticonvulsant drugs are known to have inducing properties, and since folate is required as a cofactor in drug hydroxylations it is suggested that folate depletion results from increased demand for the cofactor after induction of drug-metabolizing enzymes. As folate deficiency may ultimately limit drug metabolism this hypothesis would explain why blood phenytoin levels decrease and fit control may worsen after correction of folate deficiency in epileptic patients.

Adipates↗