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Biomedical subjects

A A Albala

Publications and source records attributed to A A Albala.

At least 19 recordsLinked to original sources
PubMed1989

Comparison of early and delayed inpatient dexamethasone suppression tests.

Ninety-five inpatients completed a dexamethasone suppression test (DST) within 72 hours after admission and again after at least 1 week of medication-free hospital care. The frequency of cortisol nonsuppression in patients with endogenous depression (ED) was high and not significantly different at both tests. In patients with diagnoses other than ED, the higher rate of cortisol nonsuppression at the first DST was associated with a significant decrease in test specificity. Change in postdexamethasone cortisol levels at repeat testing was associated with a decrease in depressive symptomatology, but was not related to weight change during hospitalization.

Adult↗
PubMed1986

Prolactin response to TRH in depression.

We studied the prolactin response to TRH in 53 unmedicated psychiatric inpatients. The prolactin response of females was significantly greater than the response of male subjects. There was no significant difference in the prolactin response to TRH between depressed patients and those with other psychiatric diagnoses. There was no significant relationship between the prolactin response to TRH and the severity of depression, the TSH response to TRH or the resistance to suppression of cortisol secretion by dexamethasone.

Adrenal Cortex↗
PubMed1985

Opioid regulation of hypothalamic-pituitary-adrenal function in depression.

A morphine infusion paradigm was used to investigate opioid mechanisms in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis in depression. The subjects were unmedicated psychiatric inpatients and healthy volunteers. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion was associated with a diagnosis of major depression and abnormal dexamethasone suppression test results. Our data suggest that the hyperactivity of the HPA axis observed in depression is abnormally resistant to opioid inhibition as well as glucocorticoid feedback.

Adult↗
PubMed1985

Prolactin response to morphine in depression.

Twenty-two unmedicated inpatients with major depression and 18 healthy volunteers of either sex were given an intravenous injection of 5 mg morphine. Blood samples were drawn immediately before and at intervals for 3 hrs after the injection and assayed for prolactin. Morphine stimulated prolactin secretion. The prolactin response of females was significantly greater than the response of male subjects. There were no significant differences in the prolactin response to morphine between depressed and healthy subjects. The implications of these findings for the hypothesized role of the opioid system in the pathophysiology of depression are discussed.

Adult↗
PubMed1985

Hormone response to repeated electroconvulsive therapy: effects of naloxone.

Plasma prolactin (PRL), cortisol, and growth hormone (GH) were measured before, and at 15-min intervals for 1 hr after, electroconvulsive therapy (ECT). This was repeated over a series of 6 consecutive treatments for each of 12 depressed drug-free inpatients. Patients received naloxone, 2 mg or 20 mg, by intravenous infusion before the third and fifth treatment. ECT was consistently followed by a release of PRL and cortisol, although two patterns of PRL response could be distinguished. In eight patients, the PRL response did not change significantly with repeated ECT, whereas in four patients, the plasma PRL increased tenfold after the first treatment and decreased after each successive treatment. The GH level varied widely, with no evidence of a reliable response to ECT. Opiate receptor blockade with low- or high-dose naloxone did not alter the release of PRL or cortisol after ECT. These findings demonstrate a reliable PRL and cortisol response to ECT, but do not support a role for endogenous opiates in these hormonal changes.

Adult↗
PubMed1985

Cortisol escape from morphine suppression.

Twenty-one unmedicated, sequentially admitted psychiatric patients of either sex and four male healthy volunteers were given an intravenous injection of 2.5 mg morphine. Blood samples were drawn immediately before and at 30-minute intervals for 3 hours after the injection and assayed for cortisol. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion (escape) was more frequent in patients with a diagnosis of major depressive disorder and with abnormal dexamethasone suppression test results. The sensitivity of this infusion paradigm for the diagnosis of major depressive disorder was 40%, and the specificity was 82%. The implications of these findings for the pathophysiology of depression are discussed.

Adult↗
PubMed1984

Morphine inhibits cortisol and stimulates prolactin secretion in man.

The role of opioids in endocrine regulation has been the subject of numerous studies. Surprisingly, however, the acute endocrine effects of morphine on basal hormonal levels in man have not been adequately documented. We report here the effects of intravenous morphine (5 mg) on plasma cortisol and prolactin. Fourteen healthy volunteers (nine male, five female) received morphine at 0930 hr. Blood samples were collected immediately before and 30, 60, 90, 120 and 180 min after the injection. In six of the male subjects the procedure was repeated with a placebo (normal saline) injection. Morphine stimulated prolactin release. There was a trend for a greater response in females compared to male subjects. Cortisol secretion was markedly suppressed by morphine. In sharp contrast to the results obtained with placebo, cortisol levels following morphine declined progressively at a rate consistent with the half-life of cortisol. This downward trend of cortisol values continued uninterrupted for the duration of the experiment in all 14 subjects. These results are consistent with the presence of an inhibitory opioid mechanism in the human hypothalamo-pituitary-adrenal axis.

Adrenal Cortex↗
PubMed1983

Escape from dexamethasone suppression: possible role of an impaired inhibitory opioid mechanism.

Several lines of evidence indicate that the activity of the hypothalamus-pituitary-adrenal (HPA) axis in depression is disinhibited. Escape from dexamethasone suppression, although not limited to is more frequent in patients with endogenous depression compared to normals or patients with other psychiatric diagnoses. Norepinephrine, serotonin and acetylcholine have been implicated in the pathophysiology of this neuroendocrine abnormality. Morphine, 5 mg intravenously, suppressed cortisol secretion in healthy volunteers (n = 4) and the majority of 32 psychiatric inpatients. However, patients with endogenous depression and abnormal dexamethasone suppression test results show early resumption (escape) of cortisol secretion following the initial suppression induced by morphine. It is concluded that the pathophysiology of this neuroendocrine abnormality is not limited to classical neurotransmitter-HPA axis interaction but that it also involves opioid inhibitory mechanisms.

Depressive Disorder↗
PubMed1981

A specific laboratory test for the diagnosis of melancholia. Standardization, validation, and clinical utility.

Four hundred thirty-eight subjects underwent an overnight dexamethasone suppression test (DST) to standardize the test for the diagnosis of melancholia (endogenous depression). Abnormal plasma cortisol concentrations within 24 hours after dexamethasone administration occurred almost exclusively in melancholic patients. The best plasma cortisol criterion concentration, above which a DST result may be considered abnormal, was 5 microgram/dL. The optimal dose of dexamethasone was 1 rather than 2 mg. Two blood samples obtained at 4 and 11 PM after dexamethasone administration detected 98% of the abnormal test results. This version of the DST identified melancholic patients with a sensitivity of 67% and a specificity of 96%. Baseline nocturnal plasma cortisol concentrations were not useful. Abnormal DST results were found with similar frequency among outpatients and inpatients with melancholia; but they were not related to age, sex, recent use of psychotropic drugs, or severity of depressive symptoms. Extensive evidence validates this practical test for the diagnosis of melancholia.

Adolescent↗
PubMed1981

Dexamethasone suppression test and selection of antidepressant medications.

Endogenous depressives with abnormal dexamethasone suppression tests (DSTs) respond better to somatic antidepressant treatments than those with normal DSTs. Whether the DST also aids in the selection of specific antidepressants has not been determined. A pilot report suggested that patients with abnormal DSTs might be noradrenaline-deficient and respond preferentially to imipramine or desipramine, whereas those with normal DSTs might be serotonin-deficient and respond best to amitriptyline or clomipramine. Attempting to replicate this observation, we studied 26 patients diagnosed with Research Diagnostic Criteria as major depressive disorder, endogenous subtype, and with DSM-III as having melancholia. All were drug-free during baseline evaluation. All had abnormal DST results, with post-dexamethasone plasma cortisol levels exceeding 5 microgram/dl. We treated subjects with either imipramine or amitriptyline and compared clinical response with weekly Hamilton Depression Rating Scales, completed by raters blind to both DST results and the research question. Thereapeutic plasma levels were documented. We found no significant differences in treatment response between the subgroups. Twenty of the 26 subjects did well. The imipramine-treatment group failed to have either earlier response or better final outcome. These data fail to replicate suggestions that DST results assist in the selection of either imipramine or amitriptyline.

Amitriptyline↗
PubMed1981

Changes in serial dexamethasone suppression tests among unipolar depressive receiving electroconvulsive treatment.

An abnormal dexamethasone suppression test (DST) identifies endogenous depressive with 95% confidence. The DST normalizes with successful treatment. Serial DSTs throughout treatment could provide useful information on (i) whether they biologically monitor clinical response, (ii) when DST normalization does occur, and (iii) whether early normalization predicts clinical outcome. We studied six inpatients who had abnormal DSTs on admission and serial DSTs during and after a course of ECT. All were diagnosed as unipolar major depressive disorder, endogenous (RDC). Clinical improvement was monitored with weekly Hamilton Rating Scales. Five of six abnormal DST patients converted to a normal test and showed significant clinical improvement. On patient failed to normalize and also had a poor outcome. All DST normalizations occurred by the fourth to sixth ECT. Additional ECTs resulted in further reduction in DST plasma cortisol values. All normalizers experienced progressive clinical improvement, and the DST successfully monitored these changes. DST conversion occurred early in treatment. Early DST normalization may have predictive value for good treatment response.

Depressive Disorder↗
PubMed1981

Speech pause time: a marker of psychomotor retardation among endogenous depressives.

Speech pause time (SPT)-the silent interval between phonations during automatic speech-is elongated during depressive episodes among endogenous depressives. Phonation time is unchanged. To follow up and expand earlier small-scale studies of these psychomotor findings we conducted a prospective determination of SPT among 24 unipolar (UP) depressives, 12 bipolar (BP) depressives, and 19 nondepressed controls. SPT was lengthened among both UP and BP depressives during their episodes. This elongation disappeared with clinical improvement. Nondepressed controls did not have longer SPT. During states of clinical remission, depressives and controls had comparable SPT values. Replications are required, but the measurement of SPT appears to be a useful, objective technique for identifying and monitoring psychomotor deceleration among depressives.

Bipolar Disorder↗