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Biomedical subjects

A L Pottash

Publications and source records attributed to A L Pottash.

At least 19 recordsLinked to original sources
PubMed1987

Eating disorders and cocaine abuse: a survey of 259 cocaine abusers.

A structured clinical interview designed to diagnose eating disorders was administered to 259 consecutive callers to the National Cocaine Hotline who met DSM-III criteria for cocaine abuse. Thirty-two percent of those surveyed met DSM-III criteria for either anorexia nervosa, bulimia, or both disorders. The prevalence rates for each of these disorders in this sample appeared elevated even when narrow diagnostic criteria were applied. The data suggest that drug abusers should be screened carefully for the presence of an eating disorder and that abnormalities of eating behaviors seen among these individuals should not be attributed simply to drug use.

Adolescent↗
PubMed1986

Evaluating depression in alcoholics.

The persistence of untreated depression was evaluated in 49 severely depressed alcoholics. After 2 weeks of sobriety, 80% of patients with initial major depression by Research Diagnostic Criteria were no longer depressed. These patients improved without antidepressant medications, suggesting the need for a 2-week period of sobriety before psychopharmacotherapy for depression is instituted. Many severe depressions in actively drinking or recently sober alcoholics may represent alcohol-induced organic affective syndromes which, unlike major depressive illness, remit spontaneously with sobriety.

Adult↗
PubMed1986

Central stimulant abuse: neurochemistry and pharmacotherapy.

This paper reviews certain clinical and neurochemical aspects of cocaine abuse. Once entrenched patterns of addiction have developed, cocaine addicts suffer progressive financial, medical, psychiatric and psychosocial deterioration that results, to some extent, from cocaine-induced neurochemical alterations in the brain. While cocaine produces euphoria through its stimulatory effect on dopamine neurons, several lines of evidence suggest that dopamine depletion occurs after chronic cocaine abuse. The dopamine neurotransmitter system is therefore a natural starting point for understanding the biology of cocaine addiction and selecting suitable adjunctive pharmacological agents. Furthermore, the dopamine depletion hypothesis implies that cocaine is "physically" addictive and provides a biological framework for understanding this disease and refining present therapeutic approaches.

Antipsychotic Agents↗
PubMed1985

Number of cortisol time-points and dexamethasone suppression test sensitivity for major depression.

Failure to suppress cortisol secretion after administration of dexamethasone has been reported to be a diagnostic marker for major depression and to have prognostic implications when repeated after antidepressant treatment. The pulsatile pattern of cortisol secretion suggested to us that increasing the number of post-dexamethasone cortisol determinations might significantly increase the sensitivity of the dexamethasone suppression test (DST) for major depression. With a conventional two-point DST (1600 h and midnight), 5% of 20 normal volunteers, 8% of 13 inpatients with non-major depressions, and 31% of 65 inpatients with primary major depression failed to suppress. With six post-dexamethasone points (0800 h, 1200 h, 1600 h, 2000 h, 2200 h, midnight), the respective percentages were 10, 15 and 44%. The additional points increased the sensitivity from 31 to 44%, mostly by identifying more major depressives with a "late escape" pattern. If a clinician is using the DST to establish a marker for major depression that can be repeated to monitor response to treatment and the likelihood of relapse, then perhaps the increased sensitivity of the six-point DST would be helpful, despite a modest decrease in specificity from 94 to 88%.

Adjustment Disorders↗
PubMed1984

Specificity of the DST and the TRH test for major depression in alcoholics.

The authors examined dexamethasone suppression test (DST) and thyrotropin-releasing hormone (TRH) test results in 32 chronic alcoholics without depression or hepatic disease to see if alcoholism alone might lead to positive test results. After 3 weeks of sobriety there were no DST abnormalities, but blunted TRH test results were observed in eight of the 32 alcoholics. More of the 15 patients also tested during alcohol withdrawal than of the 20 normal subjects or the 32 alcoholics without alcohol withdrawal had DST and TRH test abnormalities. When performed after 3 weeks of sobriety, the DST but not the TRH test has potential as a specific laboratory adjunct in the diagnosis of depression in alcoholics.

Adult↗
PubMed1984

Comparison of the dexamethasone suppression test and the cortisol suppression index.

Among 50 inpatients, the sensitivity and specificity of the dexamethasone suppression test (DST) were 51.7% and 85.7%, respectively. For the cortisol suppression index they were 10.3% and 91% at 8:00 a.m. and 51.7% and 57.1% at 4:00 p.m. Thus, the cortisol suppression index does not appear to be an adequate substitute for the DST.

Adolescent↗
PubMed1984

Psychopharmacologic treatment of depression.

The authors emphasize the favorable response of most patients with major depression to appropriate pharmacotherapy, and present a decision-tree approach to the pharmacotherapy of major depression. Also discussed are use of contemporary clinical nosology and neuroendocrine diagnostic tests to identify candidates for pharmacotherapy and/or ECT, use of secondary tricyclics because of their lower incidence of side-effects, monitoring plasma levels of antidepressants to achieve therapeutic levels, and potentiating tricyclic nonresponders with T3 or lithium.

Affective Disorders, Psychotic↗
PubMed1983

The TRH test and urinary MHPG in unipolar depression.

Twenty-five men and 26 women with major unipolar depression were evaluated by the TRH test and urinary MHPG excretion. A significant positive correlation between TSH response to TRH and urinary MHPG was found in the men, though not in the women. These findings suggest that at least for depressed men, central norepinephrine deficiency may be the neurobiological substrate of blunted TSH responses to TRH.

Adolescent↗
PubMed1983

The thyrotropin-releasing hormone and dexamethasone suppression tests in the familial classification of depression.

Eighty-eight depressed patients who had received a dexamethasone suppression test (DST) and thyrotropin-releasing hormone (TRH) test were divided into four subgroups based on family history of psychiatric illness. Nonsuppression on the DST was found in 46% of familial pure depressive disease (FPDD) patients, 38% of sporadic depressive disease (SDD) patients, 38% of depressive spectrum disease (DSD) patients, and 50% of mixed depressive disease patients (patients with both a first degree relative with alcoholism and one with depression). A blunted thyroid-stimulating hormone response to TRH was found in 50% of FPDD patients, 56% of SDD patients, 47% of DSD patients, and 56% of mixed depressive disease patients. Neither the DST nor TRH test was found to distinguish significantly among the four familial subgroups of depression.

Adult↗