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Biomedical subjects

F S Halpern

Publications and source records attributed to F S Halpern.

At least 19 recordsLinked to original sources
PubMed1988

Prolactin responses to haloperidol in normal young women.

The prolactin (PRL) responses to intramuscular haloperidol (HPD) (0.5, 1.0, and 1.5 mg) were evaluated in six normal premenopausal women during the follicular and luteal phases of their menstrual cycles. These were compared to the PRL responses to these doses of HPD in normal young men. PRL responses to HPD did not differ between the follicular and luteal phases. The mean log-transformed PRL response to the lowest HPD dose (0.5 mg) in women was less than that in the men, but the women had greater PRL responses than the men to the higher haloperidol doses (1.0 mg and 1.5 mg).

Adult↗
PubMed1985

Three tests of cortisol secretion in adult endogenous depressives.

Seventy-nine drug-free adult patients fitting RDC criteria for major depressive disorder endogenous subtype (EMDD), and 64 normal adult volunteers, were studied at pretreatment with at least one of three tests of cortisol secretion. The tests were: 1) Mean half-hourly cortisol concentrations from 1 p.m. to 4 p.m. (1-4 PM CORT); 2) plasma cortisol response to 0.15 mg/kg of dextroamphetamine hydrochloride (DACT) in the afternoon; 3) dexamethasone suppression test (DST) using 1 or 2 mg. Thirty-six depressive and 27 volunteers underwent all three tests. Analysis of the data was performed for each test singly, for all pairs of tests and for all three tests in same subjects. Results show that the single most sensitive cortisol test for depressions is the DACT (72%), with a specificity of 88%. These tests may measure different underlying pathophysiologies associated with depression.

Adolescent↗
PubMed1982

Growth hormone response to dextroamphetamine in depressed patients and normal subjects.

The human growth hormone (HGH) response to dextroamphetamine sulfate (doses, 0.1 and 0.15 mg/kg) was determined in both the morning and evening in patients with endogenous and atypical depression and in normal young men and normal postmenopausal women. Although the HGH response was found to be reduced in endogenously depressed postmenopausal women, it was equally reduced in normal postmenopausal women and in patients with atypical depression. Depressed and normal men had larger HGH responses, but there were no differences between depressed and normal men. These results do not confirm an earlier report that the reduced HGH response to dextroamphetamine is specific to endogenous depression. The results do suggest the importance to control for other variables in studies of HGH responses in psychiatric patients.

Adult↗
PubMed1982

Diurnal hormonal responses to thyrotropin-releasing hormone in normal men.

Bolus injections of synthetic thyrotropin-releasing hormone (TRH) were administered to five young normal men in the morning (0900 hr) and the evening (1800 hr) on different days. Frequent blood samples for prolactin (PRL) and TSH analyses were collected before and after TRH infusion. Although there were no differences between the morning and the evening basal PRL levels, a significantly greater PRL response to TRH in the evening was observed (delta PRL, a.m. vs p.m., p less than 0.025). Since TRH stimulates PRL through a direct effect on the pituitary, our data suggest that there is a diurnal variation in the pituitary lactotroph responsiveness to TRH. On the other hand, a.m. and p.m. basal and TRH-stimulated TSH responses were virtually identical.

Adult↗
PubMed1981

Paradoxical cortisol responses to dextroamphetamine in endogenous depression.

Dextroamphetamine hydrochloride was administered intravenously (IV) in the morning and evening to 22 unmedicated patients with severe endogenous depressions and 18 normal control subjects. While the normal subjects generally had a sharp increase in plasma cortisol level by 30 minutes after drug administration, two thirds of the depressed patients showed instead a paradoxical suppression of cortisol levels by 60 minutes. Discrimination between normal subjects and depressives was greatest in the evening. These results are consistent with other reports of abnormal cortisol responses in depressed patients to smaller IV doses of dextroamphetamine and larger doses of methamphetamine hydrochloride. A defect in activation or noradrenergic alpha receptors may account, in part, for the abnormal cortisol responses. The dextroamphetamine cortisol test in other patient populations requires study before its diagnostic use in endogenous depression can be established.

Adolescent↗
PubMed1981

Clozapine: plasma levels and prolactin response.

Serial plasma clozapine levels and serum prolactin levels were determined in two schizophrenic patients receiving clozapine, a novel antipsychotic drug. Despite marked therapeutic response and substantial clozapine blood levels, prolactin levels obtained 11--12 h after the last oral dose were unaffected or only minimally elevated. This confirms previous evidence of clozapine's unusual characteristics.

Adult↗
PubMed1981

Relative insulin insensitivity and cortisol secretion in depressed patients.

Relative insulin insensitivity occurs in a substantial portion of patients with major endogenous depressions, and about half such cases also hypersecrete cortisol in the afternoon and evening. This study assessed the relation between these two abnormalities in 16 patients with major endogenous depression. Over several days, insulin tolerance tests (ITTs) were performed in the morning and evening, and measures of cortisol secretion taken: plasma cortisol at 0800, 1600, and 2300 hours, both before and after dexamethasone; baseline cortisol before ITTs; and mean 24-hour plasma cortisol concentrations (in 10 cases). After clinical recovery, some of these patients had repeat ITTs (n = 10) and repeat predexamethasone and postdexamethasone cortisol assessments (n = 9). Additionally two control groups of 15 normal subjects and of 12 schizophrenic patients received morning ITTs. None of the control subjects manifested insulin insensitivity. However, during illness, 8 of the 16 depressed patients manifested relative insulin insensitivity (glucose drop less than 50%, glucose nadir greater than 50 mg/dl); compared to the insulin responsive depressed group, the insensitive group had insignificantly greater afternoon and evening cortisol secretion by nearly all indices. After clinical recovery, hypoglycemic response for the entire group was significantly greater than during illness; this improvement was accounted for by the increased insulin responsivity of the previously insulin resistant subgroup. There was also substantial plasma cortisol reduction in the previously insulin resistant group after clinical recovery, but not in the insulin sensitive group.

Adult↗
PubMed1981

Endocrine responses to thyrotropin-releasing hormone in major depressive disorders.

The endocrine response to thyrotropin-releasing hormone (TRH) was studied in severely endogenously depressed patients during illness (n = 21) and after recovery (n = 18). The thyroid-stimulating hormone (TSH) response to TRH was blunted (deltaTSH less than 5 microIU/ml) in over one third of depressives during illness and remained blunted in most even after recovery. There was no correlation between multiple measures of cortisol secretion (the mean 24-hour plasma cortisol, dexamethasone suppression test, and plasma cortisol during the TRH procedure) and the TSH response during illness and after recovery. The TSH and prolactin (PRL) responses to TRH, as well as the baseline PRL, were significantly lower during illness. The role of possible abnormalities in dopamine and/or serotonin in depression contributing to these endocrine disturbances is discussed.

Adult↗
PubMed1981

The prolactin-stimulating potency of reserpine in man.

The prolactin (PRL) response to 0.5 mg i.m. of reserpine was compared to 0.5 mg i.m. of haloperidol in eight young men. The fact that reserpine was found to be a potent releaser of PRL--significantly greater than haloperidol--suggests a major role of storage pool dopamine in regulating PRL Secretion. Since the PRL response to neuroleptics is highly correlated with clinical potency, reserpine could be a potent antipsychotic, and further clinical trials are indicated.

Adult↗
PubMed1981

Cortisol secretion and dexamethasone response in depression.

The authors administered 2 mg of dexamethasone at 11:00 p.m. to 37 unmedicated hospitalized endogenously depressed patients and assessed their plasma cortisol response at 4:00 and 11:00 p.m. the next day. In addition, on nondexamethasone days 26 of these patients had mean 24-hour plasma cortisol concentration determinations from samples taken at 30-min intervals and 32 had plasma determinations from a single sample taken at 4:00 and 11:00 p.m. Mean 24-hour plasma cortisol concentration was elevated in 50%; only 7 of the 26 were dexamethasone resistant, and 6 of these 7 were hypersecretors. The authors suggest that dexamethasone resistance reflects the abnormality of cortisol hypersecretion in depression and that the 2-mg dexamethasone suppression test is a highly specific but not very sensitive indicator of hypersecretion.

Adult↗
PubMed1981

Failure of dopaminergic blockade to affect prolactin, growth hormone, and cortisol responses to insulin-induced hypoglycemia in schizophrenics.

The PRL, GH, and cortisol responses to insulin tolerance tests (ITTs) were evaluated in 12 medically healthy schizophrenic patients during a drug-free period and after 1 and 6 weeks of treatment with penfluridol, a potent, long acting, dopamine-blocking neuroleptic. Hypoglycemic responses were the same before and during penfluridol therapy. Although resting PRL levels were evaluated during initial penfluridol therapy (week 1), hypoglycemia provoked a further substantial PRL increment, not significantly different in magnitude from that induced by hypoglycemia during the drug-free period. However, there was a 54% reduction (P less than 0.05) in the increase in the area under the PRL curve during week 6 compared to the drug-free period. Regarding GH and cortisol, resting levels, areas under the curve, and maximal increments after ITT were essentially the same during weeks 1 and 6 of penfluridol treatment as in the drug-free period. The failure of 1 week of dopaminergic blockade to significantly alter the hormonal (PRL, GH, and cortisol) responses to ITT in the group as a whole suggests that dopamine-blocking mechanisms play little role in mediating these responses, at least in schizophrenic patients.

Female↗
PubMed1980

Dextroamphetamine and cortisol in depression. Morning plasma cortisol levels suppressed.

Dextroamphetamine sulfate administered intravenously in the morning to 11 unmedicated depressed patients suppressed previously elevated plasma cortisol levels to normal in 90 minutes, a fall of 33% from baseline. Ten other depressed patients, without amphetamine, maintained high cortisol levels during the same time period. In each of five normal young men, amphetamine identically administered stimulated a rise in cortisol between 15 and 30 minutes after infusion, an acute response absent in ten of the 11 depressed patients; by 90 minutes after amphetamine administration, plasma cortisol had fallen to normal and identical levels in both groups. Since noradrenalin normally inhibits hypothalamic corticotropin releasing factor (and adrenocorticotropic hormone) secretion, a noradrenergic deficit may account for cortisol hypersecretion in depression; amphetamine may transiently "correct" this deficit in depressed patients, thereby reducing their cortisol secretion.

Adult↗
PubMed1980

The effect of benztropine mesylate on the prolactin response to haloperidol.

The interaction between cholinergic and dopaminergic systems in regulating prolactin responses was investigated in normal men by administration of haloperidol (0.5 mg IM), with and without benztropine (1.0 and 2.0 mg IM). The acute prolactin response (at 30, 45, and 60 min) to haloperidol plus benztropine was significantly delayed compared to the response to haloperidol alone, in the same subjects. However, between 90 and 120 min after drug administration, prolactin responses achieved were similar in the three drug conditions. The results suggest a modest cholinergic-dopaminergic antagonism in the tuberoinfundibular system, apparent at low doses of neuroleptic and high doses of anticholinergic drugs.

Adult↗