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B Dew

Publications and source records attributed to B Dew.

6 recordsLinked to original sources

Dose-response studies with thyrotropin-releasing hormone: evidence for differential pituitary responses in men with major depression, alcoholism, or no psychopathology.

A reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been reported in both alcoholic and depressed men. To discern whether the pathophysiological basis of a reduced TSH response is similar in these two disorders, the present study compares the dose-response patterns of TSH and prolactin (PRL) to TRH in depressed, alcoholic, and control men. Four doses of TRH (25, 100, 500, and 800 micrograms) were given at several day intervals to 6 men with major depression, 8 men with alcohol dependence, and 7 control men. Examination of the pattern of TRH-induced TSH and PRL response revealed differences for each paired group comparison: depressed versus control, depressed versus alcoholic, and alcoholic versus control. Compared with controls, depressed men had low TSH and low PRL responses to TRH, whereas alcoholic men had low TSH responses and normal PRL responses. Levels of neither thyroid hormones, cortisol, or sex steroids, nor age or body size, explained these differences. These findings suggest that the pathophysiological basis of a reduced TSH response to TRH is different in alcoholism, compared with depression.

Adult

Dose-response studies with protirelin.

BACKGROUND: A reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (protirelin [TRH]) has been found consistently in a portion of patients with major depression. One hypothesis to explain this observation is that pituitary TRH receptors are down-regulated in major depression. One prediction stemming from this hypothesis is that prolactin (PRL) as well as TSH responses to TRH should be attenuated. To adequately test the pattern of protirelin-induced TSH and PRL responses with a protirelin dose-response design is necessary. METHODS: Four doses of protirelin (25, 100, 500, and 800 micrograms) were infused in an ascending schedule at intervals of 3 to 7 days in patients with major depression and in control subjects. Seven women and six men with major depression were compared with age- and gender-matched controls (five women and seven men). The TSH and PRL responses were measured at regular intervals following each dose of protirelin. RESULTS: No significant group differences in baseline levels of thyroid hormones or cortisol were present. Depressed men exhibited significant reductions in both TSH and PRL responses to protirelin across all doses compared with control men. Depressed women exhibited significant reductions in TSH responses but not in PRL responses compared with control women. CONCLUSIONS: The findings that men with major depression exhibit reductions in both protirelin-induced TSH and PRL responses support the hypothesis that TRH receptors are downregulated in depression. The findings in women are less clear and may represent the greater variance in the protirelin-induced PRL responses found in women.

Adult

Pituitary sensitivity to thyroid hormones in depressed patients.

To evaluate the feedback control of thyroid hormones on TSH release, 18 normal subjects and 16 depressed patients received two TRH injections: on days one and nine. Forty eight hours before the second TRH injection subjects and patients received either T3, 100 micrograms orally, or matched placebo. T3 administration resulted in a highly significant and similar reduction of delta max TSH and FT4-index levels in both subjects and patients whereas serum T3 levels were unchanged. These data suggest that the pituitary response to the negative feedback signal of T3 is intact in depressed patients.

Adult

Plasma levels of exogenous thyrotropin-releasing hormone (TRH) in normal subjects: relationship to endocrine and behavioral effects.

Plasma levels of exogenous TRH were measured in eleven normal subjects. They were assessed as to their possible associations with the TRH disappearance rate in vivo, with the TSH and prolactin response, and with the behavioral (and side) effects of TRH. Max. levels of plasma TRH occurred consistently two minutes after injection of TRH (0.5 mg). They ranged from 8.1 to 75.1 ng/ml and were negatively correlated with the in vivo TRH disappearance rate. The latter, in turn, was positively correlated with such factors as height and body surface. Max. plasma TRH levels were not related to the magnitude of the TSH or prolactin response, or to the occurrence of behavioral effects. Nor were they related to the TRH-induced side effects although these effects occurred during the time of increasing TRH plasma levels.

Adult