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Biomedical subjects

S R Shane

Publications and source records attributed to S R Shane.

17 recordsLinked to original sources

Factor VIII activity in normal volunteers receiving oral thyroid hormone.

We have previously reported that plasma factor VIII levels are elevated in hyperthyroidism and present here the effects of oral thyroid hormone and oral beta-adrenergic blockade on factor VIII in normal male volunteers. Oral levothyroxine in 14 volunteers and oral liothyronine in nine volunteers produced significant percentage increases in resting pulse and factor VIII-related activities (factor VIII coagulant activity, factor VIII-related antigen, and ristocetin co-factor activity). The addition of oral beta-adrenergic blockade significantly reduced or prevented elevations in resting pulse but not increases in factor VIII-related properties. These findings are discussed with reference to possible regulatory mechanisms for plasma factor VIII levels related to alterations in thyroid function.

Administration, Oral

Factor VIII activity and thyroid function.

Plasma factor VIII coagulant activity is decreased in hypothyroid patients and increased in hyperthyroid patients. We studied 21 untreated hypothyroid patients. Factor VIII coagulant activity was mildly decreased in association with significant depression of factor-VIII-related antigen and ristocetin cofactor activity in five patients. Factor-VIII-related properties significantly increased with oral thyroid replacement therapy in seven of 10 patients. Twenty-two untreated hyperthyroid patients were similarly evaluated. In 21 of these patients significant increases were noted in factor VIII coagulant activity, factor-VIII-related antigens, and ristocetin cofactor activity. Elevated factor-VIII-related properties returned to normal in all of 10 patients treated with radioactive iodine or propylthiouracil. We discuss the relation between thyroid function and factor-VIII-related properties in both hypothyroid and hyperthyroid patients.

Adult

Pulmonary toxicity from carmustine (BCNU): a case report.

A patient who had a pneumonectomy for lung carcinoma was treated with carmustine when brain metastases developed. His pulmonary function was mildly compromised prior to the pneumonectomy by many years of smoking. After six months of carmustine therapy [total dose: 2,250 mg (1,200 mg/m2)] he developed interstitial pulmonary fibrosis with histologic changes consistent with drug toxicity. With seven previously reported cases of this drug-effect and the addition of our case, carmustine must be added to the list of cancer chemotherapeutic agents that can cause pulmonary toxicity.

Autopsy

Relationship of free fatty acids and magnesium in ethanol withdrawal in dogs.

A group of dogs was conditioned to drink 4-6 g ethanol/kg/day for long periods. Ethanol ingestion was interrupted at monthly intervals in order to study some metabolic changes of the withdrawal period. Plasma long chain free fatty acids (FFA) increased by a maximum mean of 1.4 meq/liter (threefold), and magnesium (Mg) decreased by a maximum mean of 0.4 meq/liter (75% of control during the first 24 hr of simple ethanol withdrawal. Because magnesium salts of FFA are very insoluble, these divergent changes of Mg and FFA suggest that lipolysis may be responsible for the hypomagnesemia that occurs in ethanol withdrawal. In order to control lipolysis, glucose-insulin, glucose alone, and fructose alone were given intravenously for a 4-hr period beginning 14 hr after withdrawal. FFA fell by a maximum of 65% or 0.44 meq/liter and Mg fell by a maximum of 0.31 meq/liter during the glucose-insulin infusions. Nicotinic acid (10-20 mg/kg) in saline produced an identical drop in FFA and a slight rise in Mg. After stopping the nicotinic acid infusion, a sharp rebound rise in FFA and a sharp fall in Mg occurred similar to the simple withdrawal experiments. The sharp divergent changes in FFA and Mg after cessation of nicotinic acid infusion support the prime role of FFA-effecting movements of Mg and the thesis that FFA bind Mg. Control of lipolysis is theoretically sound in therapy of the ethanol withdrawal syndrome.

Alcoholism

Circadian rhythms of electrolyte and 17-hydroxycorticosteroid excretion in hyperthyroidism and hypothyroidism.

The circadian rhythms of excretion of sodium, potassium, calcium, magnesium, phosphorus and 17-hydroxycorticosteroid (17-ohcs) were determined in five normal subjects, in six patients with hyperthyroidism and five with hypothyroidism. Constant diets with identical 3-hourly feedings were employed, and urine collections were made every 3 hrs during a 3-day study period. The circadian patterns of urinary excretion of sodium, potassium and 17-OHCS were similar in all three groups with distinct daytime peaks and nighttime nadirs. The total quantities of the ions and 17-OHCS excreted were greater in hyperthyroid than in hypothyroid patients with the greatest difference noted with the 17-OHCS. The rhythms for calcium, magnesium and phosphorus excretion were accentuated in hyperthyroid patients but similar to those in normal subjects with early morning calcium and magnesium peaks and a phosphorus peak approximately 12 hrs later. While a similar although blunted circadian pattern for calcium and perhaps magnesium excretion was noted in hypothyroid patients, their phosphorus rhythms were distorted and rather flat. These latter results confirm the observation of MINTZ et al. and are compatible with their interpretation that thyroid hormone is permissibly necessary for the expression of a normal phosphaturic rhythm and that the circulating level of thyroid hormone influences the amplitude of the phosphaturic rhythm.

17-Hydroxycorticosteroids

Magnesium deficiency in alcohol addiction and withdrawal.

The earliest description of clinical magnesium deficiency was reported in 1934. In 1954, Flink reported alcoholism as a cause of magnesium deficiency. This has been confirmed by low serum and tissue levels, balance studies, low exchangeable 28Mg and parenteral Mg retention tests. Alcohol causes urinary Mg wastage, but other mechanisms related to alcoholism contribute to the magnesium deficiency including malnutrition, gastrointestinal losses, phosphate deficiency, acidosis and/or alkalosis, vitamin D deficiency and free fatty acidemia associated with alcohol withdrawal. Mg replacement therapy is recommended to prevent some of the serious sequelae of magnesium deficiency.

Alcohol Withdrawal Delirium