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)

The state of knowledge in the area of suggested biological markers that may delineate subpopulations of patients with borderline personality disorders (BPD) is reviewed. There is widespread disagreement as to the specificity of these markers. The clinical implications of Axis I--Axis II, state vs. trait, acute vs. chronic, and definite vs. probable diagnoses, all seem to contribute to the confusion in this area. Some patients with BPD and with schizotypal personality disorders (SPD) share neuroendocrine abnormalities with affective disorders (AD) and schizophrenic (SCH) patients respectively. This interface and/or potential overlap between personality disorders (PD) and the major mental disorders is discussed with special reference to the DST, TRH/TSH test, and REM latency which have already been established as valuable biological markers for certain subtypes of depression. In contrast, biologic abnormalities observed in chronic schizophrenia are also present in some SPD patients. Current data are supportive of the hypothesis that some PD patients are independent whereas others are genetically related to the major mental disorders.
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PMID:Biological markers in borderline personality disorders: an overview. 313 5

Flunarizine (FLU) treatment has proved effective for migraine but there have been reports--though controversial--of depression and/or extrapyramidal signs and symptoms in cases of chronic therapy. It has been suggested that FLU may interfere with the activity of central dopaminergic systems. In this study, prolactin (PRL) secretion was chosen as a parameter for functional exploration of central dopaminergic systems in normal and migraineous women before and after FLU treatment. Five healthy women were given FLU (20 mg) and placebo per os, each for one day. A significance increase of serum PRL levels was found after FLU administration, but not after placebo. Ten women with common migraine underwent TRH stimulation test (200 micrograms i.v.) before and after a 30-day FLU therapy (10 mg per os). Basal PRL levels were not modified by the treatment, but TRH stimulated PRL values were significantly enhanced after a 30-day FLU therapy. These results seem to confirm the hypothesis that FLU interferes with central dopaminergic activity.
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PMID:Flunarizine increases PRL secretion in normal and in migraineous women. 313 30

The relationship between age and TSH response to TRH was studied in 40 men with unipolar major depressive disorder (range 24-65 years, mean 44.7 years) and 36 healthy male volunteers of similar ages. Both groups were subdivided into younger and older than 40 years of age. "Blunted" TSH response to TRH was observed in 58% of depressed men and in 28% of controls, using a dTSH maximum of less than or equal to 6 microU/ml as a cut-off criterion. Older healthy men had a higher blunting rate (40%) than the younger group (19%). In depressed patients, by contrast, the blunting rate was 50% in the older group and 65% in the younger group. Higher mean maximum dTSH, higher basal TSH and lower mean circulating FT4 levels were also noted in older depressed men, suggestive of a subtle thyroid subsensitivity to TSH stimulation and subclinical primary hypothyroidism that may have contributed to the depression. Age is known to be a confounder of TRH test results. There may be a subset of depressed patients over 40 where the confounding effect of age is associated with an exaggerated, rather than decreased TSH response to TRH.
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PMID:Relationship of age to TSH response to TRH in depressed men. 314 25

1. The tripeptide TRH exerts a spectrum of biological activities in both animals and man. Some of these activities have been extensively studied, particularly in psychiatric patients. 2. Behaviorally, TRH appears to increase the sense of well-being, motivation, relaxation, and coping capacity in both normal subjects and patients with psychiatric and neurologic disease. These effects are not disease-specific; attempts to use TRH as a treatment tool have thus been disappointing. 3. Endocrinologically, administration of TRH stimulates the response of TSH; this response has been reported to be blunted in approximately 30% of patients with major depression. However, TSH blunting is not specific for depression, it has also been observed in a variety of other psychiatric conditions. 4. The relevance of these effects for psychiatry in general, and for psychoneuroendocrinology especially, is discussed in this review.
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PMID:TRH: behavioral and endocrine effects in man. 315 May 83

Blunted TSH response to TRH and elevation of reverse T3 (rT3) have been reported in depression, though the relationship between these two abnormalities has not been clear. The authors measured basal levels of T4, T3, rT3 and the TSH response to TRH in a group of 28 depressed men and women, unipolar and bipolar subtypes. No significant difference was found between these two subtypes of depression with respect to mean basal hormonal levels or magnitude of the TSH response to TRH. Two males had slight, but significant elevations of rT3 though only one of them had a blunted TSH response to TRH levels and the TSH response to TRH. Finally no significant correlation was found between rT3 levels and the TSH response to TRH.
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PMID:The TRH stimulation test and reverse T3 in depression. 316 Jul 37

Previous studies demonstrated alterations of thyroidal economy in untreated diabetes mellitus both in man and experimental animals. To test the role of beta-hydroxybutyric acid (BHB) and acidosis in generating such changes, we studied the pituitary-thyroid axis of streptozotocin-diabetic rats, BHB or ammonium chloride (NH4Cl)-treated normal rats. Serum TSH, pituitary content and pituitary concentration of TSH, serum T4, T3 and free T4 (FT4), were all measured by RIA. In short term (2 days) diabetic rats the pituitary content of TSH was normal whereas the concentration (per mg of protein) was elevated (p less than 0.05 versus control group). Serum TSH (p less than 0.05), serum T4 (p less than 0.05), serum T3 (p less than 0.01) and serum FT4 (p less than 0.05) were all significantly decreased. In long term (30 days) untreated diabetic rats serum changes were similar to the short term diabetic group, though the pituitary content of TSH was significantly decreased (p less than 0.05). Animals treated with NH4Cl had no variations from controls. However, rats treated with BHB displayed a significant decrease in pituitary content of TSH (p less than 0.05), pituitary concentration of TSH (p less than 0.05) and in plasma TSH (p less than 0.01), and normal thyroid hormones in serum. No significant changes were seen in the TSH response to TRH in 2 or 30 days untreated diabetic and in BHB - treated animals. The data suggest that BHB, although not NH4Cl acidosis, may be capable of inducing a moderate depression of pituitary and plasma TSH of a lesser magnitude of that accompanying the full, long term diabetic state in the rat.
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PMID:Effects of diabetes, beta-hydroxybutyric acid and metabolic acidosis on the pituitary-thyroid axis in the rat. 316 31

Different neurotransmitters (Dopamine, serotonin, GABA...) and hormones (TRH, oestrogenes...) are involved in the central regulation of prolactin synthesis and release. Under physiological conditions, prolactin levels are related to correlate with age, sex, sexual maturational changes (puberty, menopause...), menstrual cycling... In this review of literature there exists a great amount of data concerned with changes in prolactin in affective disorders illustrating the validity of the biochemical and neuroendocrinological approach specially in depression. Different research paradigms are presently reviewed: measurement of plasma levels of prolactin under basal conditions, in a circadian pattern or after pharmacological challenge with TRH and/or morphine (stimulation), L-dopa and/or dexamethasone (inhibition) and its response to antidepressant drugs. The authors emphasize the contradictory results reported in the literature and suggest the need for extreme caution before considering the validity of prolactin as a biochemical test in depression.
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PMID:[Prolactin, depression and antidepressive agents. Review of the literature]. 329 33

Hypercortisolism due to Cushing's syndrome or glucocorticoid therapy induces disturbances in several other endocrine systems and may also cause mental changes, predominantly depression of various degrees. On the other hand, it has repeatedly been shown that endogenous depression is often accompanied by hypercortisolemia, usually of a modest degree, and/or by changes in other hormonal systems similar to those observed in Cushing's syndrome and during treatment with glucocorticoids. Research performed at the MPIP on 327 psychiatric patients and 103 healthy subjects has demonstrated that, in contrast to Cushing's syndrome, the circadian rhythm in depression is usually well preserved, and that diurnal variation in mood is correlated with that rhythm. Furthermore, it was found that a modest hyperactivity of the HPA system, as indicated by enhanced UFC excretion and nonsuppression in the DST, is not specific for depression in general or its endogenous subtype. It can also be observed in many other psychiatric disorders and seems to mirror stress and the influence of other factors, such as weight loss due to anorexia, rather than a particular nosology. TSH blunting in the TRH test appears as a consequence of hypercortisolemia in psychiatric disorders as is the case in Cushing's syndrome and in the course of glucocorticoid therapy. Differences in the patterns of neuroendocrine abnormalities in depressives and other psychiatric patients probably reflect differences in the individual responsiveness of the various hormonal axes to stress rather than nosological subtypes of the disorder. A comparison of these results with the past and current literature reveals remarkable changes in the concepts of neuroendocrine dysfunctions in depression and leads to suggestions of new strategies for research on this subject.
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PMID:Neuroendocrinological studies on depression with special reference to research at the Max-Planck-Institute of Psychiatry. 354 21

The relationship between thyroid disorders and depression is well known. This type of endocrine disease is mainly observed in patients with depression resistant to appropriate antidepressor therapy. Three clinical forms of this association may be distinguished: hypothyroidism in a patient with depression but without a previous psychiatric history; a relapse of depression in a manico depressive patient who has developed hypothyroidism; the finding of slight thyroid dysfunction (increased TSH response after injection of TRH) in a patient with depression. The frequency of the association of hypothyroidism and resistant depression underlines the need to perform thyroid function tests in all depressed patients who do not respond normally to appropriate antidepressor therapy. The precise mechanism of the resistance of depressive symptoms to tricyclic antidepressors is unclear. Several arguments point to an effect of triiodothyronine on central noradrenergic receptors. In practice, significant hypothyroidism implies substitute therapy. Minor thyroid dysfunction (abnormal TRH test alone) may require the association of tricyclic antidepressors and thyroid hormone although the indications and precise dosages of this drug association have not been established.
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PMID:[Depressions resistant to tricyclic antidepressive treatment and hypothyroidism]. 357 93

The study reported here was undertaken to establish the degree to which a person in a preclinical state of hyperthyroidism, with (by definition) euthyroid T3 and T4 levels but suppressed TRH on testing, already exhibits psychological changes and clinical symptoms. Two groups of 20 patients each, with clear clinical and preclinical hyperthyroidism (as defined by laboratory parameters), were studied, as well as a group of 20 controls. The subjects' psychological state of mind was investigated using self-rating scales, including the state-trait-anxiety inventory (STAI), "Befindlichkeits"-Skala (Bf-S'), depression scale (D-S'), and a list of adjectives (EWL-K) with 14 different aspects of affective moods. Cognitive achievements were evaluated using the d2 test. Subjects were examined for somatic symptoms in accordance with Crooks' index of hyperthyroidism. The results clearly showed that typical psychological and somatic changes are already present in preclinical hyperthyroidism, these changes being partly identical with those of definite hyperthyroidism. In both patient groups, a significant increase in anxiety, a sense of not feeling well, and emotional irritability were found, as well as a tendency towards depressiveness, and an increased lack of vitality and activity. Attentiveness and concentration in both patient groups were lower than in the control group. Both patient groups showed the same prevalence of symptoms, such as palpitations, preference of cold over heat, excessive sweating, nervousness, fine digital tremor, and increased heart rate. With regard to the results, the diagnosis "preclinical hyperthyroidism" thus gains importance. Further prospective studies are required to answer the question whether antithyroidal treatment will influence the described psychological and somatic state of patients with preclinical hyperthyroidism.
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PMID:[Correlation of "latent hyperthyroidism" with psychological and somatic changes]. 358 69


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