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Biomedical subjects

J C Garbutt

Publications and source records attributed to J C Garbutt.

At least 37 records · Page 2Linked to original sources
PubMed1992

Evidence for normal feedback inhibition of triiodothyronine on the thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) in abstinent male alcoholics.

Disturbances in the hypothalamic-pituitary-thyroid (HPT) axis have been reported in abstinent, noncirrhotic alcoholics, including a reduction in thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) and reductions in triiodothyronine (T3). Some evidence has suggested that a portion of alcoholics may also exhibit a disturbance in the feedback inhibition of thyroid hormone on TSH release. To evaluate the function of the HPT axis negative feedback system in abstinent, noncirrhotic alcoholic men we compared the TSH response with TRH before and after a standard suppressive dose of T3. Ten alcoholic subjects were studied and compared with four control subjects from a previous study and to literature values. The mean percent reduction in TSH response in the alcoholic subjects of 74 +/- 7% was almost identical to the 71 +/- 9% reduction observed in normal subjects. The present findings indicate that noncirrhotic, abstinent alcoholic men exhibit normal suppression of the TSH response to TRH following T3.

Adult↗
PubMed1992

Neuroendocrine effects of intravenous clomipramine in depressed patients and healthy subjects.

OBJECTIVE: Neuroendocrine challenge paradigms have been used to asses serotonergic systems in depression, but limitations in the specificity of many of these tests have been noted. In this study, the neuroendocrine responses to acute intravenous administration of the serotonin (5-HT) reuptake inhibitor clomipramine were assessed in depressed patients and matched control subjects. METHODS: Thirty hospitalized patients who met DSM-III-R criteria for major depression, and 30 healthy control subjects who were matched for age, sex, and season of year for the time of study, received 12.5 mg of intravenously administered clomipramine. RESULTS: The depressed patients demonstrated significant blunting of prolactin responses to clomipramine, as well as trends toward blunted ACTH and cortisol responses. There was no difference between the patient and control groups in growth hormone responses, plasma clomipramine levels, or self-reports of side effects. CONCLUSIONS: These data support the hypothesis that depressed patients have abnormal neuroendocrine responses to the intravenous administration of the 5-HT reuptake inhibitor clomipramine. Further study is required to delineate the mechanisms responsible for the abnormal response to intravenously administered clomipramine in depression.

Adolescent↗
PubMed1991

Behavioral and endocrine interactions between thyrotropin-releasing hormone and ethanol in normal human subjects.

Thyrotropin-releasing hormone (TRH) has been shown to antagonize the depressant effects of ethanol in animals, but conflicting findings have been reported in humans. To test whether TRH counteracts any of a variety of ethanol-sensitive behavioral measures in normal human subjects and for an effect of ethanol on TRH-induced thyrotropin (TSH) and prolactin (PRL) response, we administered TRH (500 micrograms) or placebo over 1 min intravenously, 30 min after subjects had ingested 0.8 g/kg of ethanol or a placebo drink. Blood samples for TSH and PRL were drawn prior to and 15 and 30 min after injection. Eight male subjects were studied in a balanced, crossover design with each subject receiving placebo-placebo, TRH-placebo, placebo-ethanol, and TRH-ethanol. Whereas ethanol had significant and expected effects on subjective measures, memory, disinhibition, reaction time and time perception, TRH failed to counteract any ethanol effect, except for a small effect in one memory task. Similarly, no effect of ethanol on TRH-induced TSH or PRL response was found. Though the behavioral findings could be interpreted to indicate that TRH does not alter ethanol sensitive behaviors in humans it will be necessary to utilize higher dosages of TRH and/or TRH analogues before firmly drawing this conclusion.

Adult↗
PubMed1991

Dose-response studies with thyrotropin-releasing hormone (TRH) in abstinent male alcoholics: evidence for selective thyrotroph dysfunction?

A reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been reported in subjects with a history of alcoholism whereas prolactin (PRL) responses have generally been normal. One hypothesis proposed to explain the reduced TSH response is down-regulation of pituitary TRH receptors. If this is correct, PRL response should also be diminished. To account for the different dose-response characteristics of TSH/PRL we have given four dosages of TRH (25, 100, 500 and 800 micrograms) to eight noncirrhotic, male alcoholics abstinent from ethanol a minimum of 28 days and to seven male control subjects. Across the TRH dose range the alcoholic subjects exhibited reduced basal TSH (p = .01) and a reduced TSH response (p = .0023) but no differences in basal and stimulated PRL levels. Alcoholic subjects had higher basal T4, T3 and FT4I values than did control subjects but covarying for T4, T3 and FT4I did not change the significance of either TSH or PRL findings. No significant differences in estradiol, estrone, testosterone, cortisol or glucose were noted between groups. The present study confirms the observation of a lower TSH response to TRH in abstinent alcoholics and indicates that the lower response cannot be overcome by increasing TRH dosage. The similar PRL response between groups suggests normal lactotroph function in noncirrhotic abstinent alcoholics and argues against the pituitary TRH receptor down-regulation hypothesis.

Adult↗
PubMed1991

Serotonin, suicide, and aggression: clinical studies.

Both suicidal and aggressive, impulsive behaviors have been linked to putative dysregulation in central serotonergic systems. We review data examining the role of serotonin (5-HT) in suicide from postmortem studies and clinical investigations of suicide attempters, including our own preliminary work derived from neuroendocrine challenges with the 5-HT uptake inhibitor clomipramine. Various approaches to the study of 5-HT and aggressive, impulsive behavior, including cerebrospinal fluid studies, investigations of peripheral measures of 5-HT, and neuroendocrine studies utilizing 5-HT probes, are highlighted. Several important caveats, including the challenge of quantifying "suicidality" and "aggression" in reliable and valid ways, should be considered in interpreting the results of clinical studies of 5-HT and suicide and aggression.

Adolescent↗
PubMed1990

Subclinical hypothyroidism: a review of neuropsychiatric aspects.

The authors review current information about the prevalence, causes, course, and consequences of subclinical hypothyroidism. There is evidence that subclinical hypothyroidism may be associated with cognitive dysfunction, mood disturbance, and diminished response to standard psychiatric treatments. Recommendations are presented for the screening, evaluation and treatment of patients in whom subclinical hypothyroidism may be contributing to neuropsychiatric dysfunction.

Humans↗
PubMed1990

Abnormal neuroendocrine responsivity to clomipramine in depression.

We used a pharmacologic probe that measures the neuroendocrine response to acute, intravenous "challenge" with the serotonin re-uptake inhibitor, clomipramine, in our studies of the biochemical bases of depressive illness. In two studies conducted at different sites, depressed patients consistently demonstrated blunted prolactin responses to clomipramine, compared with healthy control subjects. In order to clarify the mechanisms that might account for this abnormal neuroendocrine response to clomipramine in depression, we administered a thyrotropin-releasing hormone (TRH) stimulation test to 7 depressed patients who had also received a clomipramine challenge test. Although these patients demonstrated blunted prolactin responses to clomipramine, their prolactin responses to TRH were robust. These observations suggest that the blunted prolactin response to clomipramine in depression is not attributable to diminished hormonal secretory capacity in anterior pituitary lactotrophs and may be a reflection of dysregulation in central serotonergic systems.

Adult↗
PubMed1989

TSH response to TRH in depression with and without panic attacks.

Low thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) has been repeatedly described in approximately 25% of patients with major depression. Panic disorder appears related to depression along several dimensions, including prevalence of low TSH response to TRH. The authors divided 46 patients with primary unipolar depression by gender and by presence or absence of concurrent panic attacks and compared their TRH test results with those of 106 normal control subjects, controlling for confounding variables. Depressed patients with panic had higher prevalence of low TSH response and significantly lower mean TSH response than depressed patients without panic. The latter were indistinguishable from normal control subjects.

Adult↗
PubMed1988

Lack of acute d-amphetamine effects on thyrotropin release.

Case reports have suggested that amphetamine abuse causes excessive secretion of thyrotropin (TSH) and thyroxine (T4). Such an amphetamine-induced effect might be noradrenergic-mediated in the hypothalamus. The current controlled study examined oral d-amphetamine effects on the hypothalamic-pituitary-thyroid axis in normal humans. No acute effects were seen on TSH, T3 or T4 levels. d-Amphetamine elevated cortisol levels at 180 min, as previously reported.

Adult↗
PubMed1988

Apparent complex partial seizures in a bipolar patient after withdrawal of carbamazepine.

A 64-year-old woman with long-standing bipolar illness was treated with carbamazepine and clonazepam with minimal success. Discontinuation of carbamazepine and clonazepam was followed by episodic amnesia, purposeless behavior, déjà vu, and confusion. Although her EEG was normal, the episodes were compatible with complex partial seizures and ceased after carbamazepine and clonazepam were reinstituted. This case raises the question of whether discontinuing carbamazepine and clonazepam can induce complex partial seizures in bipolar patients.

Bipolar Disorder↗
PubMed1987

Lack of effect of dopamine receptor blockade on the TSH response to TRH in borderline personality disorder.

We recently reported that some patients with borderline personality disorder (BPD) exhibit a blunted thyrotropin (thyroid-stimulating hormone; TSH) response to thyrotropin-releasing hormone (TRH). Because it is known that dopamine can inhibit the TSH response to TRH and that some patients with BPD show improvement with antipsychotic (dopamine-blocking) medication, we investigated whether haloperidol could reverse the blunted TSH response in BPD. Of 12 patients with BPD, three showed a blunted TSH response that did not normalize with haloperidol. Furthermore, there were no overall group changes in TSH response with haloperidol. The present study suggests that reductions in TSH response in BPD are not secondary to dopamine.

Adult↗
PubMed1987

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↗
PubMed1987

Evaluation of the diagnostic utility of the TRH-induced TSH response in psychiatric disorders.

To evaluate the diagnostic utility of TSH blunting, the TRH-induced TSH response was measured in 168 normal subjects and 176 psychiatric patients. It was blunted in some acutely depressed, alcoholic, and borderline patients, but not in schizophrenic patients. In both depression and alcoholism the fault also occurred during symptomatic recovery, though with reduced frequency. Although TSH blunting was useful in distinguishing between borderline and schizophrenic patients, its diagnostic utility in identifying or confirming an existing psychiatric disorder appears to be limited. TSH blunting is not specific for any particular psychiatric diagnosis, and its sensitivity generally is low. However, the fault has promising research utility, particularly for study of the biologic interface between depression, alcoholism and borderline personality disorder. Beyond this, further study of the possible trait nature of TSH blunting in both depression and alcoholism appears warranted.

Adult↗
PubMed1986

Is there paradoxical growth hormone response to thyrotropin-releasing hormone in depression?

Several investigators have reported a paradoxical growth hormone (GH) response to thyrotropin-releasing hormone (TRH) in depressed patients, but other studies have failed to confirm this. In the present study, the GH response to TRH was studied in depressed patients and normal subjects. The rate of paradoxical GH response to TRH in depression was no different than that observed in control subjects. This was the case whether the data was examined using mean values or using frequency of abnormal responses. Patients with blunted thyrotropin (TSH) responses did not differ in GH release from patients with normal TSH response. A variety of factors may have contributed to the earlier reports of a positive GH response to TRH, including the definition of paradoxical GH release and the fact that depressed patients exhibit more frequent spontaneous diurnal GH release than do normal subjects.

Adult↗