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)

Bipolar affective disorder (manic-depressive disease) is a mental disturbance characterized by phases of both depression and mania. Mania is essential to the diagnosis and is characterized by elevated mood, flight of ideas, and increased psychomotor activity. Current psychiatric literature not only shows that this disease is familial but has also demonstrated, through linkage studies, that an X-linked dominant mode of inheritance adequately explains the strong prevalence of bipolar affective disorder in some families. The family discussed here shows many of the known clinical aspects of bipolar affective disorder. It serves as an example consistent with the X-linked dominant mode of inheritance. Knowledge of the genetic background of this disease aids the family physician by helping to identify members of the family likely to have acquired this condition. The family physician can then look for future problems in them and in their offspring, leading to earlier diagnosis and more effective management. Thus, a member of a bipolar family with supposed unipolar illness (depression only) might be better served with the prophylactic use of lithium carbonate because of his likelihood of possessing a bipolar genotype. The prophylactic use of this drug has been shown effective in reducing the frequency, duration, and intensity of both manic and depressive mood swings.
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PMID:Genetic aspects of manic-depressive disease in family practice. 84 63

The basic strategy for the pharmacological treatment of depression, with special regard to its continuance following the start of remission, is outlined. The problem of the prevention of recurrences of dysthymic symptomatology is discussed and emphasis laid on the importance of lithium about whose use a fair literature is already available. The results obtained to date demonstrate the undoubted advantages of lithium salts (particularly of carbonate) in the maintenance of good affective balance, above all in the case of those subjects in whom the frequency or gravity of dysthymia seriously handicaps working or social life.
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PMID:[Duration of antidepressive treatment. Recurrences and their prevention]. 86 8

The effects of carbon monoxide on ventilation were studied in unanesthetized goats. Responses to single breaths of 10-25% CO in O2, which rapidly raised carboxyhemoglobin (COHb) from 5 to 60%, were considered to reflect peripheral chemoreceptor-mediated reflexes whereas responses to continuous inhalation of 1% CO in O2, which slowly raised COHb from 0 to 60%, were considered to reflect both peripheral chemoreceptor and nonperipheral chemoreceptor mechanisms. In each of six goats, single breaths of CO failed to elicit any immediate ventilatory response. However, slow buildup of carboxyhemoglobinemia in the same animals always elicited ventilatory stimulation (from a mean of 7.43 to 16.02 liter/min, P less than 0.001) beginning 5-6 min after onset of 1% CO in O2 inhalation when COHb saturation reached 50-60%. In eight studies of six animals HCO3- concentration fell (from 21.3 to 15.8 meq/liter; P less than 0.001) and lactate concentration rose (from 2.5 to 4.2 meq/liter; P less than 0.05) in the cisternal cerebrospinal fluid during the CO-induced hyperpnea. Additional studies ruled out ventilatory stimulation from left heart failure or enhanced chemo-sensitivity to carbon dioxide. Although the delayed hyperpnea was associated with a hyperdynamic cardiovascular response to CO, blockade of these circulatory effects with propranolol (2 mg/kg) failed to abolish the delayed hyperpnea; however, the propranolol did unmask an element of ventilatory depression which preceded the hyperpnea. Conclusions were: (a) hyperventilation in response to CO inhalation is not mediated by the carotid bodies; (b) the delayed hyperpnea in response to CO inhalation is primarily due to brain-cerebrospinal fluid acidosis; (c) mobilization of body CO2 stores due to the circulatory response to CO may obscure an initial depression of ventilation by CO.
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PMID:Mechanism of the ventilatory response to carbon monoxide. 94 62

The authors analyze a series of 20 patients seen over the past 4 years who have shown a dramatic improvement following the introduction of lithium carbonate to their therapy. The results indicate that these patients showed a consistent syndrome with the following features: a) anergic endogenous depression; b) positive family history in first degree probands; c) obsessional personality traits and symptoms; d) hypochondriasis and somatic symptoms; e) failure to respond to previous antidepressant therapy with tricyclic and MAOI compounds as well as ECT. A previous study by Gittleson showed that one third of a series of psychotic depressives admitted to the Maudsley Hospital, London, also displayed obsessional symptoms and hypochondriasis. These patients, however, seemed to do as well with standard antidepressant treatment as a control group of psychotic depressives without obsessional features. However, in this series, there was a 7 per cent residue whose obsessional symptoms worsened, even after recovery from their depression. The authors' group of patients represented approximately 3 per cent of all psychotic depressives seen over the 4-year period and could, therefore, coincide with Gittleson's residue. The mean age of onset of illness in the authors' depressive group was 45.5 years, and this finding, coupled with the high incidence of psychotic depression in first degree relatives, indicates that these patients were suffering from a psychotic depression modified by personality traits, rather than an atypical obsessional neurosis. The consistency of clinical features and specificity of response to lithium therapy appear to indicate that this is a clearly definable clinical syndrome worthy of further investigation.
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PMID:A depressive syndrome responsive to lithium. An analysis of 20 cases. 97 30

Multiple indices of depression were used to evaluate the prophylactic efficacy of lithium carbonate versus placebo in a 4-year, double-blind study of unipolar, bipolar I, and bipolar II patients diagnosed according to strict criteria. Our data indicate lithium prophylaxis of depression on several indices in all three subtypes of affective illness. Additional studies are needed, comparing tricyclic antidepressants alone, monoamine oxidase inhibitors alone, or either drug combination with lithium carbonate for prophylaxis in clearly defined depressive subtypes.
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PMID:Lithium carbonate prophylaxis of depression in three subtypes in primary affective disorder. 98 26

A fatal pancytopenia occurred in a patient with an history of depression with hypomanic rebounds, admitted for a manic episode and treated with levomepromazine, diazepam and lithium carbonate.
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PMID:A fatal case of pancytopenia due to levomepromazine. 99 Jun 58

The effect of lithium carbonate therapy on patients with depression is still unconfirmed. Our past studies have shown a favorable response to the drug in patients with depression of mild or moderate severity. Therefore, we performed a controlled double-blind study of lithium carbonate and imipramine hydrochloride in 64 patients with depression. No significant differences were noted in the overall therapeutic response, depression scale scores, or clinical effects between the two drug groups.
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PMID:Double-blind comparison of lithium carbonate and imipramine in treatment of depression. 109 85

The prophylactic efficacy of lithium carbonate vs placebo was examined in a double-blind study in a carefully delineated group of 28 unipolar recurrent depressed patients followed up from three months to four years. Indexes of prophylactic efficacy revealed a statistically significant decrease in episode frequency, depth of global depression scores, and increased clinic attendance rate in the lithium carbonate group compared with the placebo group. Planned studies are now needed to determine which unipolar patients do best on a maintenance regimen of lithium carbonate alone, lithium carbonate plus tricyclic drugs, or tricyclic drugs alone.
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PMID:Lithium carbonate in affective disorders. IV. A double-blind study of prophylaxis in unipolar recurrent depression. 110 50

The efficacy of lithium carbonate as a prophylactic drug against depression in bipolar manic depressive patients was assessed through a double-blind, placebo-controlled study of patients who had histories of recurrent depressions and hypomanias ("bipolar II"). The results revealed that treatment with lithium carbonate resulted in a reduction in the frequency of depressive attacks was observed with lithium carbonate treatment during the study (mean length of study, approximately 16 months), although there was a suggestion that the depressive attacks that occurred during treatment with lithium carbonate might be less severe than with placebo treatment.
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PMID:Lithium carbonate and affective disorders. V: A double-blind study of prophylaxis of depression in bipolar illness. 110 32

In a fatal case of self-poisoning with lithium carbonate there was a progressive increase in serum lithium concentration for 48 hours after ingestion of the overdose. It is suggested that the continuous increase in serum lithium concentration reflects prolonged absorption of lithium from relatively insoluble aggregates of lithium carbonate in the gastrointestinal tract. In this case there was an interval of 45 hours between ingestion of the overdose and the onset of central nervous system depression. Simultaneous peritoneal dialysis and hemodialysis were effective in rapidly reducing the serum lithium concentration but there was little concomitant change in the patient's level of consciousness. The terminal event was a respiratory complication of the comatose state.
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PMID:Fatal self-poisoning with lithium carbonate. 112 60


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