Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper is a brief review which deals with research findings, clinical issues, and strategies in the pharmacotherapy of alcoholism. The pharmacotherapy is presented according to different clinical phases of the alcoholic process. The acute intoxicated patient receives supportive treatment, to be clinically observed to prevent severe respiratory depression, aspiration of vomitus, and severe alcohol withdrawal syndrome. Benzodiazepine therapy is the mainstay in treating alcohol withdrawal syndrome. Disulfiram is the only chemical used in the United States to deter the alcoholic patient from further alcohol drinking. Although there is not a specific agent for alcoholism per se during the sobriety state, the alcoholic patients' concurrent underlying psychiatric conditions (such as schizophrenia, anxiety, and depression) should be treated properly and adequately.
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PMID:Pharmacotherapy of alcoholism: the American current status. 204 13

This article deals with common issues encountered in elderly persons who are medically ill. Agitation and delirium, including alcohol withdrawal syndrome, are frequently encountered problems, and useful intervention strategies are presented. Depression in this population is discussed, and a brief review of the use of antidepressants is given. Finally, the approach to and management of anxiety, with special focus on the intensive care unit setting, is summarized. Principles of pharmacotherapy in the elderly are reviewed.
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PMID:Perioperative psychiatric considerations in the elderly. 219 18

In rats with the persistent alcohol motivation the electrophysiological sleep pattern was studied during ethanol intake, after 24 and 48 hours of alcohol withdrawal. It was established that during the voluntary ethanol intake rats may be divided into two groups: with comparative deficit (1st group) and comparative abundance (2nd group) of REM sleep. Alcohol withdrawal caused differential alterations of sleep-wakefulness cycle: in the 1st group of rats REM sleep was more suppressed while in the 2nd group--more increased in comparison to those during ethanol intake. In all animals the SWS depression, increase of awakenings, the aggravation of falling asleep and decrease of sleep depth were observed. DSIP (0.1 mg/kg, i.p. 1 hour before sleep recording) was found to regulate sleep disorders caused by ethanol withdrawal. It makes the neuropeptide possible to be recommended for ethanol withdrawal syndrome treatment in clinical practice.
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PMID:[Effects of delta sleep-inducing peptide on electrophysiological parameters of sleep during alcohol withdrawal in rats]. 226 15

The effect of gamma-hydroxybutyric acid (GHB) on ethanol withdrawal syndrome in alcoholics was investigated in a randomised double-blind study. Patients with withdrawal symptoms were treated either with GHB (orally in a syrup preparation) (11 patients) or with the syrup alone (12). GHB treatment (50 mg/kg) led to a prompt reduction in withdrawal symptoms, such as tremors, sweating, nausea, depression, anxiety, and restlessness. The only side-effect was dizziness. GHB may be useful in the management of alcohol withdrawal syndrome in man.
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PMID:Gamma-hydroxybutyric acid for treatment of alcohol withdrawal syndrome. 257 Oct 21

TRH and naloxone influence on the clinical hormonal manifestations of the alcohol withdrawal syndrome (AWS) was studied. The results obtained were suggestive of the association of the pathogenesis of symptoms like frustration, skin hyperemia, tachycardia, and raised BP with function of the peptidergic system. It should be noted that symptoms like depression, sleep disturbances and headaches happened to be more sensitive to TRH while sweating is more sensitive to naloxone. A positive therapeutic effect of naloxone in the early period of AWS was likely to result from lowered function of the opiate system. The data obtained led to a preliminary conclusion of a close interrelationship and involvement of the hormonal, peptidergic and opiate systems in AWS pathogenesis, this being an important factor for the understanding of alcohol-induced abnormalities and for the choice of pathogenetically founded therapeutic methods.
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PMID:[Participation of the peptidergic and endogenous opiate systems in the pathogenesis of early manifestations of the alcohol abstinence syndrome]. 283 19

Urinary cyclic adenosine monophosphate (AMP-c) was measured morning and evening in 35 patients with alcohol withdrawal syndrome (AWS). 65% of the patients revealed a higher night time than day time concentration of AMP-c in the urine, reflecting increased sympathetic adrenergic activity. The circadian rhythm was lost in 88.55% of the 35 patients. The pathogenic factors and mechanisms involved in AWS are discussed and the contribution of sympathetic adrenergic hyperactivity to the onset of the withdrawal syndrome with its concomitant depression of the cholinergic and GABAergic systems is emphasised. Finally it is suggested that insomnia and the loss of REM sleep may also contribute to the onset of the condition.
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PMID:[Changes in the circadian rhythm of urinary cyclic adenosine monophosphate during the alcoholic withdrawal syndrome and related neurobiological correlations]. 299 62

Alterations in central dopamine function have been identified in depression and in alcohol withdrawal. Attempts to determine the magnitude and direction of the central dopamine alteration in alcohol withdrawal have produced conflicting results. In this study serum prolactin (PRL) was used as an indicator of central dopamine activity since dopamine is the most important factor in the control of prolactin secretion from the pituitary. Increased serum PRL levels were found during alcohol withdrawal and they correlated significantly with high scores on the Hamilton Depression Rating Scale (HDRS). No significant correlations were identified with The Brief Psychiatric Rating Scale (BPRS), the 'Mini-Mental State' of Folstein (MMS), The Beck Depression Inventory (BDI) or The Modified Gross Alcohol Withdrawal Selective Severity Assessment Scale (GAWSSA). The authors concluded that the transient depressive symptomatology typically found in detoxifying alcoholic patients may be, in part, the result of a central hypodopaminergic state.
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PMID:Serum prolactin correlates with depressed mood during alcohol withdrawal. 375 69

Tiapride was used in 55 chronic alcoholics. It has a sedative effect on the anxiety, aggressiveness and agitation observed during the alcohol withdrawal syndrome. It is also effective against tremor, insomnia and fatigue. Fatigue or depression do not occur as side-effects. Tiapride induces a psychological feeling of wellbeing which is heightened by continuation of detoxication and general management.
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PMID:[Tiapride in detoxication of chronic alcoholics (author's transl)]. 627 32

Panic disorder (PD) is a common psychiatric illness, which has many complications such as major depression, increased suicide risk, agoraphobic avoidance behaviour, alcohol abuse and dependence. A number of studies have now documented increased rates of anxiety disorders among alcoholics and of alcoholism among patients presenting with anxiety disorders. In general, it appears that PD is more prevalent in alcoholics than would be expected on the basis of general population rates. Alcohol withdrawal is clearly associated with severe anxiety symptoms. It is suggested that repeated withdrawal episodes may trigger panic through a kindling process by causing subconvulsive stimuli with increasing amounts of electrical excitability or even spontaneous seizures. Serotonergic medications are effective in treating PD and depression. They also diminish interest in drinking in ethanol-dependent patients. Serotonergic agents can also affect conditioning and learning as well as behavioral control and self-administration. The treatment of panic patients with depressive and alcohol problems usually requires long-term treatment.
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PMID:Alcohol and depression in panic disorder. 791 95

Alcohol withdrawal syndrome (AWS) may result in nausea, vomiting, diarrhea, weakness, sweating, tremors, tachycardia, hypertension, agitation, delirium, hallucinations, seizures, and death beginning 6 hours after alcohol cessation in alcoholics. Benzodiazepines are cross-tolerant with ethanol and are considered first-line therapy for treating AWS. Chlordiazepoxide and diazepam are first metabolized by hepatic oxidation, then glucuronidation. Lorazepam and oxazepam undergo only hepatic glucuronidation. Benzodiazepine oxidation is decreased in persons with liver disease and the elderly. Accumulation with resultant excessive sedation and respiratory depression may be significant when administering chlordiazepoxide or diazepam to patients with impaired oxidative metabolism. Lorazepam and oxazepam metabolism is minimally affected by age and liver disease. Chlordiazepoxide and diazepam are erratically absorbed by the intramuscular route. Lorazepam is predictably absorbed by the intramuscular route. Oxazepam is not available in parenteral form. Lorazepam appears to be the safest empiric choice among the various benzodiazepines for treating AWS in the elderly and in patients with liver disease, or those who require therapy by the intramuscular route.
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PMID:Benzodiazepines for alcohol withdrawal in the elderly and in patients with liver disease. 870 Jul 92


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