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)

A prospective study of male in-patients over 55 years old who met Feighner criteria for non-bipolar depression was performed to determine if a previous history of alcoholism significantly influenced treatment or response to treatment. Among 58 subjects with complete follow-up information, the 16 who had a history of alcoholism had a presentation at index which differed from that of the non-alcoholics, and on follow-up they clearly had more chronic illness. This elderly sample with alcoholism resembles 'neurotic-reactive' depressives described in younger samples, and supports a past history of alcoholism as being a risk factor for chronicity of depression on follow-up in the elderly population.
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PMID:Depression and previous alcoholism in the elderly. 201 53

Among 100 consecutive suicide victims with primary major depression at the time of their suicide, 46% were found to have had bipolar II depression, 1% bipolar I disorder and 53% non-bipolar major depression. Since the lifetime prevalence rates of bipolar II and bipolar I depressions are relatively low compared to primary major non-bipolar depression, the present findings suggest that bipolar II disorder gives a particularly high risk of suicide among the different subtypes of primary major affective illness. Fifty-nine percent of the patients had medical contact during the depressive episode, but the depression was frequently undiagnosed, untreated or undertreated. The implications of these findings for suicide prevention are discussed briefly.
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PMID:Suicide in subtypes of primary major depression. 213 67

The familial aggregation of depressive disorders is a major cue for the etiology of depression. The review of family, twin, adoption and linkage studies demonstrates that genetic transmission is involved in the manifestation of bipolar affective disorders but it explains only part of the variance; the evidence of a genetic basis of unipolar depression is less clear; this is the case for endogenous depression, too. It ist recommended to examine if personality features may contribute to an improvement in the identification of the phenotype in genetic studies in unipolar and bipolar depression.
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PMID:[Contribution of genetics to research in the etiology of depressive diseases]. 219 4

Platelet MAO activity has been reported by several investigators to differentiate schizophrenia, schizophrenia related depressive disorders, alcoholism, unipolar and bipolar depression from normal controls. Evoked potentials likewise have differentiated schizophrenic and affective patients. However, the precise relationship between MAO activity, evoked potentials (EP), and psychiatric illness has not been clarified. A possible association between psychopathology and high MAO activity/EP reducing and low MAO activity/EP augmenting has been reported. Such a bidirectionality further confounds results. This study was undertaken to determine the association of psychopathological dimensions found in a group of subjects whose platelet MAO activity and evoked responses were obtained two years earlier. Utilizing the Gottschalk-Gleser verbal behavior scales of Anxiety, Depression, Social Alienation-Personal Disorganization and Cognitive Impairment a significant correlation was revealed between low platelet MAO activity and high Total Anxiety scale and Shame Anxiety subscale scores. Additionally, a significant correlation was demonstrated between reducing evoked potentials and elevated Death Anxiety, Somatic Concerns, and Total Death and Mutilation Depression subscales scores, combined and separately. Furthermore, a significant positive correlation was found between augmenting evoked potentials and Overt Hostility Outward scores. No significant correlations were demonstrated between platelet MAO activity or evoked potentials and Social Alienation-Personal Disorganization or Cognitive Impairment scores. These findings lend support to the position that biological markers may predict predispositions to anxiety and depression.
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PMID:Platelet monoamine oxidase activity and evoked response as predictors of anxiety and depression derived from the content analysis of speech. 221 39

Plasma levels of gamma-aminobutyric acid (GABA) were determined in 68 healthy controls and in 133 patients with mood disorder. Plasma GABA levels were significantly lower in the patients with mood disorder compared to controls. Levels of plasma GABA were similar among diagnostic groups (primary unipolar depression, bipolar depression, mania, and secondary depression). No differences in plasma GABA were found in patients classified according to family history, nor were any correlations found between plasma GABA levels and severity of depression as determined by the 17-item Hamilton Rating Scale for Depression. These findings support the notion that low plasma GABA may represent a biological marker for mood disorder.
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PMID:Plasma GABA in mood disorders. 223 51

The severity of the depressive and apathy syndrome, which are factoranalytically derived from the AMDP-system is reported for 428 patients with a monopolar depression. The data are compared with the results from 79 patients with a bipolar depression, 192 with a neurotic depression and 89 with a depressive reaction. The percentile scores can be used for the evaluation of the severity of a depressive and apathy syndrome in comparison to a reference sample.
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PMID:[Percentile distribution of depression scales of the AMDP system]. 232 91

Because the clinical actions of psychotherapeutic agents can be influenced by their pharmacokinetics, we investigated plasma tranylcypromine in relation to treatment outcome in 26 patients with bipolar depression. After oral administration of a tranylcypromine dose, plasma drug levels were measured hourly from 5-8 hours (N = 16) or 0-8 hours (N = 10) postdose, and pharmacokinetic parameters were calculated. Depressive symptoms were rated using the Hamilton Rating Scale for Depression (HAM-D), and subjects were categorized as responders, partial responders, or nonresponders, based on end-pair ratings. Twelve subjects were responders, seven were partial responders, and seven were nonresponders (mean scores = 3.2, 13.1, and 24.9, respectively); pretreatment HAM-D scores did not differ among the three groups. Tranylcypromine elimination (t1/2) was unrelated to clinical outcome. However, plasma tranylcypromine measured 5 hours postdose (5hTCP) was correlated with the end-pair HAM-D scores (r = 0.48, p less than 0.015) and was significantly higher in nonresponders than in responders (ANOVA, F = 4.7, p less than 0.02; Newman-Keuls test, p less than 0.05). For subjects who were studied from 0-8 hours postdose, the time to peak absorption (Tpeak), the area under the plasma tranylcypromine-versus-time curve, and the volume of distribution (Vd) were determined. Two subjects having delayed (3-4 hours) Tpeak also manifested elevated mean 5hTCP (63.9 vs. 34.1 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma tranylcypromine: relationship to pharmacokinetic variables and clinical antidepressant actions. 237 18

The authors report morbid risks found for depression, alcoholism, and bipolar disorder in first-degree relatives of 179 probands with recurrent depression. Comparisons were made for relatives' gender, probands' gender, and probands' age at onset. Results showed overall morbid risks of 20.7% for non-bipolar depression, 15.4% for alcoholism, and 1.1% for bipolar disorder. Female relatives were found to be at greater risk for depression than males, while the reverse was true for alcoholism. Sex of proband had no effect. Risk to relatives of early-onset probands was significantly elevated compared to late-onset probands. Various cutoffs for ages at onset were examined, and the effect became more marked as the cutoff age was decreased to 20.
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PMID:Family history in recurrent depression. 252 86

The question of the previously reported changes in the density of high-affinity binding sites for [3H]-imipramine (IMI) in platelets from depressed patients was reexamined among the different diagnostic subtypes of depression according to the DSM-III classification and taking into account the possible influence of the low-affinity binding site. Using a least-square computer-assisted analysis, a precise determination of the [3H]-IMI binding parameters exclusively in relationship to the high-affinity site was performed in 46 untreated depressed patients and compared to 35 healthy controls. The results revealed a clear and highly significant 22% decrease in the maximal density (Bmax) of [3H]-IMI binding in all of the depressed patients compared to controls with no change in affinity values. Considering the diagnostic subgroups, we found that all the bipolar patients, the depressed as well as the euthymic or manic ones, had very low Bmax values and that some of them also exhibited an unusual low-affinity binding. Mean Bmax of the unipolar and dysthymic patients significantly decreased when compared to controls, although the Bmax values showed a large variability. Only dysthymic patients presented Bmax values which were significantly associated to symptom severity as assessed by the Hamilton Depression Rating Scale scores. Our results confirm the lower density of platelet [3H]-IMI binding in affective disorders, particularly in bipolar patients, and also suggest that this biological parameter is a trait marker in bipolar depression and a state marker in dysthmic disorder.
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PMID:Platelet [3H]-imipramine binding according to DSM-III subtypes of depression. 256 83

The effects of amitriptyline (AMI) or imipramine (IMI) on levels of 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA) (the major brain metabolites of the neurotransmitters norepinephrine [NE], serotonin [5-HT], and dopamine [DA]) in cerebrospinal fluid were determined in 66 subjects with unipolar and bipolar depression. There were significant reductions in MHPG and 5-HIAA levels for the depressed group taken as a whole, but levels of HVA did not change significantly. The changes were similar when subjects were grouped as treated with AMI and IMI and with unipolar and bipolar depression. Reductions in MHPG and 5-HIAA levels were greater in women than in men. In all subjects with depression and in those treated with AMI and IMI, amine metabolite changes did not differ significantly between those who had a positive clinical response to drug therapy and those who did not. Responders with bipolar depression had smaller reductions in MHPG levels than did responders with unipolar depression. The similar effects of AMI and IMI on MHPG and 5-HIAA differ from the dissimilar effects of the two drugs on NE and 5-HT amine uptake systems reported in animal and in in vitro studies. Results provide conclusive evidence of the effects of AMI and IMI on noradrenergic and serotonergic (but not dopaminergic) systems in patients with depression.
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PMID:Effects of amitriptyline and imipramine on brain amine neurotransmitter metabolites in cerebrospinal fluid. 257 12


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