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 illness may be a relatively common missed diagnosis in the elderly. Inaccurate historical data, atypical course of illness and atypical clinical presentation are all sources of diagnostic error. Lithium and tricyclic antidepressants are effective agents in this age group but require close monitoring, with particular attention to their interaction with illness and other medications. A high index of suspicion for bipolar illness is suggested when elderly patients present with depression.
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PMID:Bipolar affective disorder in aged patients. 50 May 73

Platelet serotonin (5-HT) was higher at 8 a.m. in untreated bipolar depressives than in controls. This high 5-HT was different from unipolar depressives where 5-HT levels were similar to controls but showed altered diurnal rhythmicity. Further differences between unipolar and bipolar patients were found. 5-HT levels and 5-HT uptake into platelets were not correlated in bipolar depressives as found in both unipolar depressives and controls; and 5-HT levels and platelet monoamineoxidase activity tended to be negatively correlated in bipolar but not in unipolar depressives and controls. A longitudinal study of a bipolar II patient throughout three hospitalizations for depression followed by the switch into hypomania, indicated that 5-HT was state independent, remaining constantly high in all clinical conditions and upon remission, reduced only during and after treatment with clomipramine, a 5-HT uptakt dysfunction of indoleamines underlying bipolar illness.
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PMID:Increased platelet serotonin in bipolar depression and hypomania. 56 91

The effect of allopurinol on the kynurenine formation in three manic depressive patients, two in remission and on in depression, has been studied during long-term treatment with L-tryptophan. The patients were loaded with 100 mg L-tryptophan per Kg body weight prior to and after one week on allopurinol, 300 to 500 mg per day. The area under curve (AUC) of plasma total and free tryptophan increased slightly in the patients in remission but not in the depressive. The former showed no change in the AUC of plasma kynurenine whereas an increase was seen in the depressive. The results suggest that allopurinol does not inhibit the human tryptophan pyrrolase definitely during loadings with L-tryptophan.
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PMID:The effect of allopurinol on the kynurenine formation in humans following a tryptophan load. 58 96

The paper describes a two-month period of study in four bipolar manic-depressive patients in a metabolic ward. Plasma renin activity, packed cell volume, plasma sodium and potassium were determined at intervals. Twenty-four-hour urinary sodium, potassium and creatinine were also estimated daily. Aldosterone production rate was measured on two occasions for each patient. Three of the patients showed at least one episode each of mania and depression during the study, while the fourth patient, who was receiving prophylactic lithium throughout, had one ten-day depressive episode but was otherwise normal. No obvious relationship between mood and plasma renin activity was observed, but the group showed a high resting renin activity, a blunted renin response to posture, and inappropriate aldosterone production rates for the renin activity found. It is postulated that a primary defect in the aldosterone-renin system may be present in bipolar manic-depressive psychosis.
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PMID:Renin and aldosterone relationships in manic depressive psychosis. 59 84

Differences between bipolar and unipolar patients and the natural history of bipolar illness are discussed. Reviewing recent studies, the paper then outlines the treatment of mania, the treatment of depression, and the prophylactic treatment of bipolar illness.
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PMID:Bipolar affective disorder--techniques and results of treatment. 65 8

The relationship between the degree of depression and the circadian variation of serum TSH, T3 and T4 was investigated in 19 endogenously depressed patients. The difference between the hormone concentrations at 2 p.m. and at 12 p.m. was taken as an estimate of the magnitude of circadian variation. It was found that the circadian variation in serum TSH was inversely related to the degree of endogenous depression. This was mainly due to a diminution or absence of the night increase of TSH in severely depressed patients. A circadian variation of serum free T3 was found in the less depressed patients whereas no diurnal change was found in serum free T4. In severely depressed patients there were no significant diurnal changes in free thyroid hormone concentrations. The results indicate a hypothalamic dysfunction in manic-depressive psychosis.
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PMID:Disturbed circadian variation of serum thyrotropin in patients with endogenous depression. 66 84

All patients suffering from affective psychoses (ICD 296) who were admitted to the Psychiatric University Clinic of Zurich between 1959 and 1963 were studied in a follow-up investigation until 1975. Of 254 affective psychoses, 95 were bipolar patients (37.4%) and 159 were monopolar (62.6%). The sample of bipolar patients was complemented with all patients who had been admitted in the period 1959--1963 because of manic or mixed manic-depressive syndromes. This paper describes the change of diagnosis in the two diagnostic groups. In 10% (N = 20) of monopolar depression cases there was a change of diagnosis to bipolar affective illness. An analysis shows that the diagnosis of patients with three or more depressive episodes (unipolar depressives) was especially prone to change. A mathematical correction of some diagnostic errors leads to the conclusion that the ratio of unipolar depression to bipolar illness may be about 1:1. A major source of diagnostic error lies in the change of affective to schizo-affective illness. Up to now, no clinical criterion exists that would exclude this error, which was found in 6% (n=12) of the monopolar but also in 7.5% (n = 3) of the bipolar index patients. It is recommended that studies of affective disorders should be based on truly representative samples of the illness, including patients with one or two episodes, and that the term 'unipolar depression' be used synonymously with the term 'monopolar depression,' originally created by Kleist (1947) and Leonhard (1957).
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PMID:The course of affective disorders. I. Change of diagnosis of monopolar, unipolar, and bipolar illness. 70 27

The International Calassification of Diseases and other contemporary classifications of depression are discussed, together with some general and practical classification problems. Unambiguous operational criteria need to be used for establishing diagnostic validity and comparability. There is widespread agreement on the distinction between Type A and Type B depressions and between unipolar and bipolar illness.
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PMID:The diagnosis and classification of depressions. 75 66

Several recent data indicate the blood-brain transport of amino acids as a critical factor in the synthesis of monoamines. The complex, peripheral and central regulation of TP transport plays an essential role sine TP-hydroxylase is not a saturated enzyme. The hydroxylated derivatives 5-HTP and dopa are probably transported into the brain by similar mechanisms as their precursors TP and tyrosine, respectively. The maic-depressive patients show an increased uptake of administered L-5-HTP in the depressive phase, whereas L-dopa uptake is enhanced in the manic phase. Heuristically, we propose a biochemical model of manic-depressive psychosis in which an increased TP uptake causes alternation in the balance of monoaminergic system activity. Depression is possibly characterized by a hyperserotonergic and a relative hypocatecholaminergic activity. In contrast, mania is possibly determined by a hypercatecholaminergic (NA and DA) and a relative hyposerotonergic activity. The data offered by the physiology of monoamines, the semeiology and the biological alterations of the manic-depressive psychosis, as well as the monoaminergic and the electrolyte theory of manic-depressive psychosis. A diminution of the transport of TP with consequent increase of that of tyrosine represents a possible biochemical model of schizophrenia which may be well explained by a hyposerotonergic-hyperdopaminergic activity, with or without noradrenergic insufficiency. This model is compatible with our knowledge on the monoamine physiology, the biological alterations of schizophrenia, the therapeutical results as well as with the classical clinical notions (typology, intermediate syndromes and crossed heritance).
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PMID:The common pathophysiology of monaminergic psychoses: a new hypothesis. 77 59

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


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