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Biomedical subjects

M Solter

Publications and source records attributed to M Solter.

28 records · Page 2Linked to original sources
PubMed1978

Relative increase of serum reverse T3 in patients with hypothyroidism.

In 17 hypothyroid patients serum T3: rT3 ratio was 7.5 /+- 1.1 which was significantly lower than in control subjects (12.2 /+- 0.6; p less than 0.001). The data suggest that in hypothyroidism the organism might shift conversion of T4 from biologically active T3 to biologically inactive rT3 which may not be a defense mechanism of the body, as it was found in chronic systemic illness.

Adult↗
PubMed1975

Treatment of reactive hypoglycemia with buformin.

The therapeutic effect of short-term buformin (l-butylbiguanide) treatment was investigated in 12 patients with reactive hypoglycemia. Eleven of them were classified as having idiopathic reactive hypoglycemia, nine obese and two nonobese. None of these patients had a degree of hyperglycemia during glucose tolerance tests which would indicate diabetes mellitus. In one patient reactive hypoglycemia was related to chemical diabetes. The diagnosis of reactive hypoglycemia was established on the basis of patient's hypoglycemic reaction and low blood glucose levels during 6-hour oral glucose tolerance tests. The patient's received 200 mg of buformin daily for 7 days and its therapeutic effectiveness was assessed by repeat testing. Buformin treatment resulted in significant increase of blood glucose values between 180 and 360 min after oral glucose challenge and in considerable improvement of hypoglycemia in nine obese patients with idiopathic reactive hypoglycemia and in the patient with chemical diabetes. Buformin also significantly reduced maximal insulin response and incremental insulin areas. In two nonobese patients hypoglycemic reaction was deteriorated after buformin therapy.

Adult↗
PubMedDate not supplied

Glucose-insulin interaction in obese individuals with asymptomatic reactive hypoglycemia.

The interrelationship of glucose and insulin was investigated in obese nondiabetic subjects with asymptomatic reactive hypoglycemia. Results were compared to those obtained from obese control subjects and normal individuals. The diagnostic criteria for asymptomatic reactive hypoglycemia were the appearance of blood glucose values of 40 mg/dl and below during the postabsorptive phase of a 6-h OGTT and the absence of related symptoms. The blood glucose nadir occurred earlier in obese hypoglycemics than in obese controls. Maximum insulin response was similar in both obese groups, but occurred significantly later in obese hypoglycemics than in obese subjects without hypoglycemia and normal subjects. In obese hypoglycemics the blood glucose nadir was inversely proportional to the time of the insulin peak (i.e. the later the insulin peak the lower the blood glucose nadir) but correlated poorly to maximum insulin values. Delayed insulin response was found to be the major abnormality in asymptomatic reactive hypoglycemia and a probable cause of the decreased ability to maintain post-hyperglycemic glucose homeostasis. Decreased glucose tolerance in some obese hypoglycemics pre-treated with prednisolone suggests that asymptomatic reactive hypoglycemia could be the manifestation of an early diabetic stage.

Adult↗
PubMedDate not supplied

[Euthanasia].

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Ethics, Medical↗