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E L Toth

Publications and source records attributed to E L Toth.

28 records · Page 2Linked to original sources
PubMed1990

Age-related decline in interleukin 2 production in response to influenza vaccine.

Articles in the recent literature document an abnormal antibody response in elderly persons to influenza vaccination. Several studies have presented evidence to show that immune dysfunction in aged mice and humans may be due to a defect in the production of interleukin 2 (IL2) by helper T cells (TH). Cultures of peripheral blood mononuclear cells (PBMC) were prepared from blood samples taken at eight weeks after vaccination (0.5 mL of Armand-Frappier, 15 micrograms/0.5 mL each of A/Taiwan/1/86, A/Leningrad/360/86, and B/Ann Arbor/1/86 administered in the fall of 1987) from a group of elderly men and a young control group. Peripheral blood mononuclear cells were frozen in 10% dimethyl sulfoxide (DMSO) until all the cells were cultured. After stimulation with a 1/320 dilution of the same influenza vaccine, cultures of PBMC from young controls showed a significantly greater increase in IL2 production than the cultures of PBMC from the elderly group of patients. This was statistically significant at both day 3 (P less than .01) and day 5 (P less than .05) of culture using the Mann-Whitney U test. Previous experiments that have shown defective IL2 production related to aging have used potent mitogens such as concanavalin A and phytohemagglutinin to stimulate TH. This study provides evidence that defective IL2 production may also occur in response to physiologic antigenic stimulation and may be one explanation for the reduced efficacy of influenza vaccination in elderly persons.

Aged↗
PubMed1988

Lack of metabolic effects of a triphasic formulation containing norethindrone in normal women studied prospectively.

The glucose and insulin responses to oral glucose tolerance tests and lipid values in normal women taking a triphasic pill containing norethindrone (Ortho 7/7/7) were performed. After three months, no significant changes in these metabolic indices were found. These results confirm and expand the knowledge regarding the metabolic safety of norethindrone-containing triphasic formulations.

Adult↗
PubMed1988

Primary hypothyroidism presenting as growth delay and pituitary enlargement.

We report the case of a young boy being considered for pituitary surgery because of pituitary enlargement found during assessment of growth delay. There was no goitre but he was hypothyroid clinically and biochemically. The finding of an elevated TSH suggested primary thyroid disease with thyrotroph hyperplasia. Treatment with L-thyroxine resulted in prompt resolution of his pituitary enlargement and improvement in his visual fields.

Child↗
PubMed1988

Insulin action is altered in hyperthyroidism.

We have assessed insulin action in five hyperthyroid patients, pre- and post-radioactive iodine therapy using oral glucose tolerance tests, monocyte insulin binding and dose response curves generated with the euglycemic clamp technique. All patients had become euthyroid after radioactive iodine therapy with a decline in the plasma free T4 index level from 278 +/- 43 to 105 +/- 9. Fasting glucose was modestly, but significantly elevated in the thyrotoxic patients compared to when they were rendered euthyroid (p less than 0.05). Oral glucose tolerance tests showed no difference in either glucose or insulin values after the glucose load. Insulin receptor binding and affinity were similar regardless of their thyroid status. Hepatic glucose production in the basal state was elevated in the thyrotoxic patients, 61 +/- 5 mg/M2/min vs 49 +/- 3 mg/M2/min (p less than 0.05). At the lowest level of insulin infusion no difference in glucose disposal was found. At maximum insulin concentrations the glucose disposal rate was enhanced in the thyrotoxic patients, 686 +/- 19 vs 567 +/- 26 mg/M2/min (p less than 0.01). These results indicate that higher fasting glucose levels may result from increased hepatic glucose production in thyrotoxicosis, but as indicated by the oral glucose tolerance tests, this defect in insulin action is usually of minor significance. However, insulin responsiveness measured at pharmacological insulin levels is augmented in thyrotoxicosis.

Adult↗
PubMed1987

Insulin action does not change during the menstrual cycle in normal women.

Normal women have alterations in carbohydrate metabolism during pregnancy and when taking oral contraceptives, and clinical observations suggest that diabetic women need more insulin during menstruation. We, therefore, studied insulin action in normal women during the menstrual cycle in the follicular, luteal, and menstrual phases. Glucose tolerance was similar at all three times. Specific insulin receptor binding to monocytes did not change during the menstrual cycle. Euglycemic insulin clamp studies at four different insulin infusion rates (15, 40, 120, and 240 mU/M2 X min) showed no differences in insulin sensitivity or responsiveness throughout the menstrual cycle, and hepatic glucose output did not change. These studies suggest that if insulin action is impaired during menstruation in diabetic women it is because of factors that are not detected in normal women.

Adult↗
PubMed1984

Hereditary central diabetes insipidus: plasma levels of antidiuretic hormone in a family with a possible osmoreceptor defect.

A large Canadian kindred of Irish extraction extending from Quebec to British Columbia with autosomal dominant diabetes insipidus responsive to exogenous antidiuretic hormone (ADH) is described. Out of 121 individuals 34 have been identified as affected in seven generations. The disorder is characterized by variability in age at onset and in severity, and by apparently spontaneous abatement in old age. The affected subjects do not appear to manifest hypertension or its sequelae. In three individuals tested the plasma ADH level was very low in spite of adequate osmotic stimulation. However, the level rose in two of them when they were given furosemide, which suggests an osmoreceptor defect and a normal ADH response to volume change.

Adult↗