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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Psychotropic drugs are frequently employed to treat the wide range of neuropsychiatric syndromes that patients infected with the human immunodeficiency virus (HIV) may develop. In order to administer these agents properly, physicians should take certain factors into account: the central nervous systems of these patients are often impaired, the patients tend to suffer from medical illnesses, and they may be taking various other drugs. The possible interactions between substances taken by these patients may sometimes make it necessary to adjust the dosage of psychotropic agents administered. In addition, some of the antimicrobial, antifungal and antiviral agents used in the management of HIV infection may have adverse effects that include neuropsychiatric symptoms. The use of antipsychotic agents in these patients frequently results in the development of extrapyramidal symptoms. Tricyclic antidepressants are not well tolerated by patients with AIDS, due to the anticholinergic effects of these agents. The new antidepressants, which have fewer and milder adverse effects, are safer and have shown their efficacy in the treatment of the depressive episodes often seen in HIV-infected patients. Benzodiazepines must be prescribed with caution in patients with HIV infection and organic brain syndrome, since they can produce amnesia, confusion, lack of inhibition and paradoxical reactions. The indications for the use of psychostimulants in certain clinical situations, such as HIV-associated dementia and depression, is open to debate. Opiates are indicated in pain treatment, and in methadone maintenance programmes. Lithium and carbamazepine are advisable only in very restricted situations.
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PMID:Use of psychotropic drugs in patients with HIV infection. 751 59

Lithium is the recommended treatment for the prophylaxis of bipolar affective disorder. The drug is also effective in the prophylactic treatment of recurrent unipolar depression, although many psychiatrists prefer to use antidepressant drugs for this indication. The efficacy of lithium is well established in the short term treatment of mania, although neuroleptic drugs are required at the start of treatment for more severely disturbed patients. Lithium augmentation of antidepressant drugs is increasingly popular for the treatment of resistant depression. It is now common practice to maintain serum lithium concentrations in the range 0.5 to 0.8 mmol/L, which is generally as effective as higher concentrations while reducing the incidence of adverse effects and intoxication. Some individuals may nevertheless require higher serum concentrations. Most adverse effects such as tremor and gastrointestinal upset are usually minor and often transient. There is no good evidence of nephrotoxicity with long term treatment, but persistent polyuria can occur. Hypothyroidism, with or without goitre, can occur uncommonly during long term lithium therapy. Prescribers should be alert to, and patients should be educated about, the predisposing factors and early symptoms relating to lithium intoxication. Specialist mood disorder clinics can facilitate safer and more effective lithium treatment.
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PMID:Lithium. Current status in psychiatric disorders. 769 9

Lithium is frequently used in the management of several psychiatric disorders including acute mania, bipolar (manic-depressive) disorder, and recurrent depression. We describe a patient in whom hidradenitis suppurativa developed while the patient was receiving lithium. The cutaneous side effects of lithium are reviewed. The most frequent are psoriasis, acneiform lesions, folliculitis, alopecia, and a maculopapular/macular eruption. Many of these side effects respond less readily to conventional therapy while the patient is receiving lithium.
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PMID:Lithium therapy associated with hidradenitis suppurativa: case report and a review of the dermatologic side effects of lithium. 782 46

In the mouse forced swimming test (FST) pretreatment with a subactive dose of lithium (1 mEq/kg), given IP 45 min before the test, facilitated the antidepressant activity of iprindole, fluoxetine, and moclobemide (given IP 30 min before the test). These antidepressants (ADS) were not active alone in the FST in this study. Moreover, when subactive lithium was combined with a wide range of ADS, each given at subactive doses, those ADS with serotoninergic properties (e.g. imipramine, citalopram, paroxetine, fluoxetine, trazodone, mianserin, and moclobemide) significantly reduced immobility times. ADS acting primarily on noradrenaline (NA) or dopamine (DA) systems (desipramine, maprotiline, viloxazine, and bupropion) did not significantly decrease immobility when given in combination with lithium. This was also the case for RO 16 6491 [a reversible, B specific monoamine oxidase inhibitor (MAOI)], nialamide, and pargyline (both irreversible, mixed MAOIs). The anti-immobility effect of iprindole in combination with lithium suggests either a direct or indirect action on the serotonin (5HT) system by this ADS whose mechanism of action remains obscure. These results, using an animal behavioral model of depression and combining our present knowledge of the acute action of various ADS, support the hypothesis that the potentiation by lithium of ADS is via direct 5HT mechanisms, indirectly via a NA/5HT link, and/or by second messenger systems. Lithium may also facilitate the expression of antidepressant activity of ADS not active by themselves in the FST.
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PMID:Additive effects of lithium and antidepressants in the forced swimming test: further evidence for involvement of the serotoninergic system. 786 13

The addition of lithium to antidepressants as a strategy for the management of depressed patients not responding to a tricyclic antidepressant was derived from the observation in animals that long-term administration of tricyclic antidepressant drugs enhances the sensitivity of postsynaptic neurones. Lithium administration increases the function of 5-HT neurones and thus might lead to amelioration of the non-responding depression. There have now been a substantial number of studies of lithium augmentation in non-responding depressed patients and a positive effect is consistently reported. The combination of lithium with a variety of antidepressants has not been associated with excessive reports of serious adverse events and therefore appears to be a useful approach to patients with a poor response to antidepressants.
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PMID:Lithium addition in treatment-resistant depression. 793 Apr 94

Depression is one of the most prevalent disorders seen in primary care. About 50% of depression is treated in general medical settings. Although depression is highly treatable, incomplete response to a single antidepressant is common. We describe two clinical cases in which antidepressant augmentation was a therapeutic option and lithium carbonate was an appropriate choice. A brief review of the practical aspects of the clinical pharmacology of lithium is included. Lithium is a well-tolerated, safe, and effective medication for antidepressant augmentation.
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PMID:Antidepressant augmentation with lithium. 793 Nov 18

Research on bipolar disorder continues to indicate that recurrent episodes of mania and depression have a deteriorative effect on patient functioning, response to treatment, and prognosis. Lithium is the treatment of choice for both acute affective episodes and long-term maintenance, but not all patients respond adequately to lithium therapy. Alternatives or adjuncts to lithium in acute mania include carbamazepine, valproate, electroconvulsive therapy (ECT), and clozapine. For acute depression, antidepressants often are added to lithium treatment or used alone; nonpharmacologic options include ECT and light therapy. Studies suggest that carbamazepine and valproate may be as effective as lithium in maintenance therapy and that thyroid supplementation may increase response in rapid-cycling patients. Using psychosocial intervention in addition to maintenance pharmacologic treatment may increase medication compliance, decrease hospitalizations, and increase overall functioning.
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PMID:Treatment of bipolar disorder: how far have we come? 797 26

Nearly one percent of adults in the United States suffer from bipolar disorder, a severe, chronic, and life-threatening disease. This disorder involves periodic episodes of mania and depression. At least 80 percent of patients who have an initial episode of mania will have one or more subsequent episodes. Because recurring episodes have a cumulative deteriorative effect on functioning and treatment response, the sooner bipolar patients are diagnosed and treated, the better their changes are for recovery. With optimal treatment, a bipolar patient can regain approximately 7 years of life, 10 years of effective major activity, and 9 years of normal health, which otherwise would have been lost due to the illness. For treatment purposes, bipolar disorder is divided into three stages: acute mania, acute depression, and maintenance. Lithium is the standard treatment for acute mania, and its effectiveness is solidly supported by experimental evidence. Rigorous studies over the past 40 years involving hundreds of patients have repeatedly shown the efficacy of lithium therapy, with approximately 80 percent of subjects responding favorably. For those who do not, several other drugs and nonpharmacologic therapies are available that have shown high success rates in well-standardized trials. The anticonvulsant drug carbamazepine has been associated with improved symptoms in approximately 60 percent to 70 percent of subjects in double-blind trials comparing it against placebo, neuroleptics, and/or lithium. Valproate, another anticonvulsant, has been shown to be comparable to lithium and superior to placebo in treating acute mania in several double-blind, placebo-controlled trials. Electroconvulsive therapy (ECT) is another effective treatment for acute mania, with a positive response rate of approximately 80 percent. Acute bipolar depression has been successfully treated with a number of agents, including monoamine oxidase inhibitors (e.g., tranylcypromine), lithium, tricyclic antidepressants, and second-generation antidepressants (e.g., bupropion). Nonpharmacologic approaches such as ECT, sleep deprivation, and light therapy have been effective as supplemental therapy in many patients. For maintenance therapy, lithium is again the drug of choice. Clinical research has shown that maintenance lithium lessens the frequency and severity of episodes of mania and depression in bipolar patients and helps stabilize mood between episodes. Long-term lithium treatment also reduces the risk of mortality for bipolar patients: without treatment, mortality is two to three times higher than that of the general population; with treatment, it is not significantly different. Several other drugs have been studied as alternatives or adjuncts to lithium therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Report on efficacy of treatments for bipolar disorder. 808 77

Lithium (Li) reduces brain inositol levels by inhibiting the enzyme inositol monophosphatase. The enzyme inositol-1-phosphatase was measured in human red blood cells of controls, Li-free bipolar patients, and Li-treated bipolar patients and was found to be reduced by 80% in Li-treated bipolars, thus supporting the concept that chronic Li at therapeutic concentrations inhibits this enzyme. Two behaviors in rats caused by Li, reduction of rearing, and Li-pilocarpine seizures, are reversed by intracerebroventricular replenishment of inositol. The reversal is stereospecific to the naturally occurring myo-inositol; whereas the stereoisomer L-chiro-inositol is ineffective. The reversal is dose-dependent, requiring a dose consistent with known quantities of brain inositol depletion; and is time-dependent, as inositol must be given 1-8 h before stimulation. High-dose peripheral inositol also reverses the limbic seizures induced by Li-pilocarpine, and using gas chromatography was shown to increase brain inositol levels that had been reduced by Li treatment. Low-dose inositol could be shown to reverse a peripheral Li-induced side effect, polyuria/polydipsia, in rats and in patients treated with Li. A higher dose of inositol markedly reduced Hamilton Depression Ratings in 9 of 11 unipolar major depressive disorder patients previously unresponsive to tricyclics, in an open design, but had no effect on chronic schizophrenics in a controlled double-blind randomized crossover trial. A new inositol monophosphatase inhibitor, a fungal product originally discovered as a complement inhibitor, was found to act like Li and lower the seizure threshold for subconvulsant doses of pilocarpine. These data suggest that inositol monophosphatase inhibition is a key mechanism of Li's therapeutic action and that design of new inositol monophosphatase inhibitors may be a practical strategy to create new compounds with Li-like therapeutic effects.
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PMID:Ziskind-Somerfeld Research Award 1993. Biochemical, behavioral, and clinical studies of the role of inositol in lithium treatment and depression. 811 Sep 11

Lithium oxybutyrate was studied for effects on the circadian pattern of reserpine-induced depression ("open field") in relation to the time of the drug use. Reserpine given in a single dose of 0.75 mg/kg caused a reduction of diurnal frequencies, inversion of rhythm acrophases, decrease in their mesors and amplitudes. Lithium oxybutyrate given after rhythm acrophases in reserpine-treated animals recovered the lost 24-hour harmonics phase relations between them, but when used before acrophases it did not only fail to prevent the animals from the exhausting action of reserpine, but aggravated the course of depression.
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PMID:[Lithium oxybutyrate correction of the circadian pattern of reserpine-induced depression]. 818 9


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