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)

Depression is both a common and a greatly undertreated illness in the United States today. The focus of this review is a definition of the characteristics of four subtypes of depression which appear to be differentially sensitive to four different classes of medications. The tricyclic antidepressants should be used for patients with unipolar depression and vegetative symptoms. Lithium appears to be most effective for bipolar depressives. The monoamine oxidase (MAO) inhibitors are best used for patients with atypical depression. Antipsychotic medications appear to be useful for depressed patients with psychotic symptoms or agitation. Recent pharmacokinetic and biochemical data, including serum lithium levels, plasma tricyclic levels, and the predictive ability of pretreatment urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) levels are also reviewed.
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PMID:Subtypes of depression--diagnosis and medical management. 1 27

As requirements for tryptophan for synthesis of protein and 5-hydroxytryptamine were comparable in rat brain, during depletion of tryptophan there could be competition between the two pathways for the amino acid. This implied that tryptophan should be rate-limiting for protein synthesis and this was found in the short term when concentrations of the amino acid were reduced in rats. Multicompartmental studies of tryptophan and tyrosine in controls and patients subject to unipolar depression defined two main pools of the amino acid provisionally assigned to extracellular and intracellular spaces. For tyrosine, mean values for the extracellular space were comparable to those of controls. The concentration of tyrosine was low in the intracellular space in both depressed and recovered patients, but the raised fractional clearance rates for this compartment during depression had returned to normal on remission. Plasma tryptophan concentrations were significantly reduced in depression with intermediate values after recovery. This suggested that the procedure used may have been mildly stressful and that this had evoked an idiosyncratic response to the stress in the depressed patients, which was characterized by inability to maintain concentrations of this amino acid in plasma. The findings for both amino acids may have a bearing on the aetiology of unipolar affective disorder.
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PMID:Distribution of tryptophan and tyrosine in unipolar affective disorders as defined by multicompartmental analysis. 29 Jul 58

1. Central dopamine turnover may be lowered in patients with unipolar endogenous depression particularly when associated with retardation. 2. Nomifensine selectively activates the central dopaminergic system and may be of special therapeutic value in patients with motor inhibition. 3. A double-blind comparison of clomipramine and nomifensine was carried out in patients with recurrent unipolar depression. Biochemical and clinical assessments were carried out weekly for 4 weeks. 4. The mean homovanillic acid level in cisternal liquor of those patients who responded to nomifensine, was significantly lower than the mean level of the total group. 5. The factor "retardation" on the Hamilton Depression Scale was improved more with nomifensine than with clomipramine.
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PMID:Controlled study comparing nomifensine and clomipramine in unipolar depression, using the probenecid technique. 33 21

TRH and LHRH were simultaneously infused into a group of five male patients with primary unipolar depression and four male secondary depressed patients. Blood samples were measured for LH and TSH just before and two hours following infusion. Six healthy male subjects matched for age were similarly studied. Our results showed: 1) that basal levels of TSH and LH were not different in any of the three groups of subjects, 2) TSH responses in the three groups were not significantly different, and 3) the LH response was significantly greater in the secondary depressed patients than the primary unipolar depression and normal controls at all time intervals after infusion. Our results add to the existing evidence for an abnormality in the hypothalamo-pituitary regulation of pituitary hormones-in particular LH. Such an abnormalit has not been reported in the literature to our knowledge. Our results tend to suggest a biological difference in the two subtypes of depression studied. Neuroendocrine studies would appear to be a useful diagnostic procedure in the differentiation of these subtypes of depression.
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PMID:TSH and LH responses in subtypes of depression. 38 24

1. Association or linkage between a known genetic marker and an illness with a presumed genetic etiology supports two conclusions: a) The genetic etiology would be considered definite, and b) the illness should be considered a homogeneous disease. 2. After separating depressions on the basis of gross familial differences, a finding of linkage or association in any subgroup would indicate that the particular illness is autonomous. Data on association between bipolar and unipolar depression and subtypes of the ABO system are given. 3. Methodological problems in association studies are discussed. 4. Preliminary data suggest the possibility of linkage between the alpha-haptoglobin locus and third component of complement locus and depression spectrum disease, a depression which is familially defined by the presence of alcoholism in the first-degree family member.
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PMID:Genetic markers in depressive disorders. 40 56

SAdness and normal grief are distinguished from pathological grief and depression by intensity, duration, precipitating events, and the quality of psychopathological features. Depression is evaluated as a final common pathway of potential psychodynamic, genetic, psychosocial, physiological, and personality characteristics or events. The clinical entity of depression is diagnosed by describing some of each of the affective, behavioral, and cognitive changes concomitant with depression. The clinical entity of depression is further differentiated for purposes of treatment into the categories of bipolar depression (manic-depressive illness), unipolar depression (psychotic depressive reaction or involutional melancholia), neurotic depression, and secondary depression (secondary to somatic disease, drugs, or to other psychiatric disorders). The immediate treatment depends on the type of depression diagnosed. Unipolar and bipolar depressions respond to specific pharmacologic therapy and supportive care. Neurotic and characterologic depressions respond to supportive or insight psychotherapy with possible brief adjunctive anti-anxiety or hypnotic medication. All of the treatment modalities, with the possilbe exception of insight psychotherapy, can be effected very adequately by the primary care physician who is given clear diagnostic and assessment guidelines with specific treatment approaches.
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PMID:The depressed patient. 42 80

Depression spectrum disease is an unipolar depressive illness in which at least one member of the family has unipolar depression and at least one other first degree relative has alcoholism and/or antisocial personality; using this definition, 14 depression spectrum disease families are studied. Assuming, among other things, that variability in age of onset is environmentally caused and lognormally distributed, segregation analysis shows that the data are compatible with the dichotomy of 'affected' versus 'not affected' being due to an autosomal dominant gene. A simple environmental hypothesis in which the transmission of the illness does not depend upon the parents' type could be rejected (p less than 0.001). Linkage analysis is performed by the method of maximum likelihood, taking the best fitting Mendelian model found in the segregation analysis. The results show virtually no evidence of linkage between depression spectrum disease and C3, but suggestive evidence (lod score = 1.03) of linkage between depression spectrum disease and alpha-haptoglobin (both these linkages were previously suggested by significant results in sib-pair analyses).
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PMID:Possible linkage between alpha-haptoglobin (Hp) and depression spectrum disease. 43 98

Twelve acute depressed patients were studied in the course of antidepressant treatment. Three-day-24-hour urine samples for 3-methoxy-4-hydroxy-phenylglycol (MHPG) were collected both before and after a five week treatment schedule. MHPG were estimated by spectrophotometry. Initial MHPG excretion did not reflect the severity of pretreatment depression and final MHPG showed no specific correlation with post-treatment improvement. No specific or uniform influence of different anti-depressant treatments or changes in MHPG was evident. Depressed patients with bipolar affective disorder tend to have initially lower MHPG levels than patients with unipolar depression. Urinary MHPG excretion measurements may prove not to be a useful index in the diagnosis and choice of treatment in patients suffering from primary depression.
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PMID:Urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) excretion in depression. 48 Jun 80

Morning and evening plasma cortisol levels were checked in 123 consecutively newly admitted psychiatric patients with a variety of diagnoses. Questions asked were whether there were differences among groups with more severe illness, type of depression, alcohol abuse, or particular symptoms. Morning cortisol elevation was found in 33% of patients and was not associated with any particular diagnostic category. Evening cortisol elevation occurred in 85% of the subjects. It was significantly higher in those with unipolar depression and organic brain syndrome, also in those patients who abused alcohol regardless of diagnosis. Evening cortisol elevation was twice as common in patients with diagnoses of more severe psychiatric illness than in those with minor disorders. Further study is suggested to see if these patterns of cortisol elevation are sustained beyond the stress-of-admission period.
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PMID:Plasma cortisol levels in depression and other psychiatric disorders: a study of newly admitted psychiatric patients. 48 67

Depressive syndromes are a group of heterogenous mental disorders. On the basis of genetic studies, one distinguishes between bipolar and unipolar depression. Hereditary transmission varies according to the type of depressive syndrome, and is still the subject of controversies. The place of schizoaffective syndromes remains unclear in the nosology of depression.
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PMID:[Genetic aspects of depressive illness (author's transl)]. 57 87


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