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)

Circadian rhythms of body temperature, plasma cortisol, norepinephrine (NE), thyroid stimulating hormone (TSH), and melatonin were compared in 16 endogenously depressed, 15 recovered (after 3 weeks of anti-depressant treatment), and 16 normal subjects. The depressed patients showed clear circadian rhythm abnormalities, consisting mainly in amplitude reduction. This amplitude reduction was significantly correlated with the patients' Hamilton depression scores. Normal circadian profiles were restored after recovery when amplitude, in particular, was increased. Features of the circadian rhythms observed in remission may be associated with antidepressant drug effects, whereas those observed in depression resemble the circadian rhythms observed in normal subjects living under conditions of temporal isolation and those of blind subjects. Our findings suggest that depression may be related both to a weakening of the coupling processes between internal pacemakers and to an abnormal sensitivity to environmental information.
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PMID:Circadian rhythms in depression and recovery: evidence for blunted amplitude as the main chronobiological abnormality. 276 32

The experience of using thyroid hormones in affective disorders is summarized. This includes: 1) Using thyroid hormones alone in depression; 2) their combined use with tricyclic antidepressants; 3) addition of thyroid hormones to nontricyclic antidepressants; 4) the use of thyroid stimulating hormone; and 5) thyrotropin releasing hormone in depression. Suggested mechanisms of action are discussed. A special attention is paid to the place of thyroid hormones in the treatment of rapid cycling affective disorder.
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PMID:Thyroid hormones in the treatment of affective disorders. 304 8

A subgroup of individuals with major depressive disorder have an impaired thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH). The molecular relationship between the mechanism of this "blunted" TSH response and depression is unknown. Numerous recent studies have characterized similarities and interactions between the immune and neuroendocrine systems. As the immune system both produces and responds to TSH, we utilized a peripheral blood leukocyte system to compare immunoreactive (ir)-TSH responsiveness in 10 adult patients (1 man, 9 women) with Research Diagnostic Criteria for major depressive disorder to that of 9 control subjects. All subjects had normal baseline serum TSH and T4 concentrations. Isolated mononuclear leukocytes were treated in vitro with either 0.5 micrograms/ml staphylococcal enterotoxin A (SEA), 50 micrograms/ml TRH, or no stimulant. After incubation, the cells were monitored for ir-TSH production by indirect immunofluorescence and reverse hemolytic plaque assay using antisera to TSH-beta. The culture supernates were analyzed by TSH radioimmunoassay. SEA- and TRH-treated cell cultures from depressed individuals had significantly fewer immunofluorescent positive cells, as well as significantly fewer and smaller plaques, than did similarly treated leukocytes from control subjects. The increase in supernatant ir-TSH was significantly less in TRH-treated cultures from depressed patients as compared to normals (p less than 0.05). These results suggest that examination of mononuclear leukocyte TSH production may reflect an altered state of neuroendocrine function and may thus be a useful marker for major depressive disorder.
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PMID:Decreased mononuclear leukocyte TSH responsiveness in patients with major depression. 313 Jan 7

Ninety-five inpatient, RDC-diagnosed major depressives, 68 unipolar and 27 bipolar, underwent 72-hour urine collection for the measurement of 3-methoxy-4-hydroxyphenylglycol (MHPG). The average 24-hour urinary MHPG was compared by multivariate analysis of variance with the postdexamethasone cortisol (DST), the delta thyroid stimulating hormone (TRHST), six quantitative EEG (QEEG) measures of regional interhemispheric symmetry and six QEEG measures of focal frequency abnormalities. MHPG failed to discriminate between unipolar and bipolar II depression. It showed no significant correlations with postdexamethasone cortisol or delta TSH. It failed to correlate with QEEG regional coherence or with focal frequency abnormalities. MHPG covaries independently of other markers of depression.
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PMID:Limited clinical utility of urinary MHPG. 313 45

Plasma cortisol, prolactin (PRL), growth hormone (GH), and thyroid stimulating hormone (TSH) responses to intravenous morphine (0.1 mg/kg body weight) were investigated in five healthy women and 22 female psychiatric inpatients (eight with major depression, 12 with schizophrenia and two with personality disorders) during a 120 min period. The results were also related to a subsequent dexamethasone suppression test (DST). Morphine caused a strong and progressive decline in plasma cortisol which was uniform in controls, depressed, and nondepressed patients. DST nonsuppressors had significantly higher cortisol levels during the entire period, but the same response to morphine. Morphine strongly stimulated PRL secretion, which was found to be significantly smaller in patients than in controls, but no difference was seen between depressed and nondepressed subjects. GH and TSH showed only minor and variable changes after morphine, with no overall significant differences. The data in this study do not support the assumption of a major alteration in opiate receptor responsivity either in depression or in DST nonsuppressor patients insofar as the regulation of the adrenal, thyroid, GH and PRL hormone secretion is concerned.
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PMID:Multiple hormonal responses to morphine: relationship to diagnosis and dexamethasone suppression. 358 10

The effects of acute and chronic water restriction on the circadian rhythms of corticosterone, growth hormone (GH), and thyroid stimulating hormone (TSH) were studied in adult male rats. Water restricted rats were allowed to drink between 9:00 and 9:30 a.m. only. Chronic water restriction but not one day of such treatment altered the circadian pattern of corticosterone so that a peak of this hormone appeared before water presentation. In contrast, neither acute nor chronic water restriction altered the qualitative patterns of circadian GH and TSH rhythms although both treatments depressed the secretion of the two hormones, the depression being greater in chronic than in acute water restricted rats. These results indicate that water restriction did not resynchronize the GH and TSH circadian rhythms. It appears that reduced secretion of GH and TSH observed in water restricted rats would be due to the concomitant reduction in food intake.
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PMID:Effects of water restriction on circadian rhythms of corticosterone, growth hormone and thyroid stimulating hormone in adult male rats. 378 12

Baseline and TRH-induced changes of thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) were measured in 15 healthy control subjects and 63 psychiatric inpatients with DSM-III diagnoses of major depression (n = 19), schizophrenic disorder (n = 20), alcohol dependence (n = 10), and adjustment disorder (n = 14); baseline and postdexamethasone cortisol (CS) were also determined 3-6 days after the TRH-challenge. All patients and controls were women of similar mean age, weight, height, and they were free from interfering illness or drugs. Baseline TSH and PRL were lower in depression, TRH-induced TSH and PRL responses were lower in the whole patient group, but most markedly in depression and alcohol dependence. Postdexamethasone CS was significantly higher in depression, schizophrenia and alcohol dependence. Basal GH did not differentiate the subgroups; TRH-induced pathological GH responses were sometimes found in the patient groups. The differences were most marked quantitatively in major depression: a multivariate analysis of variance showed that delta TSH, postdexamethasone CS and delta PRL were the most important variables in separating patients from controls. A discriminant function derived from these variables classified all controls and 18 of 19 depressed patients correctly; however, 25 of the 44 other patients were also classified with depression. It was confirmed that psychiatric patients show significantly more endocrine disturbances than controls, and this was seen not only in major depression but also in at least three other conditions. Further work is needed to identify other neuroendocrine patterns more specific to depressive disorder.
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PMID:Dexamethasone suppression and multiple hormonal responses (TSH, prolactin and growth hormone) to TRH in some psychiatric disorders. 393 Feb 50

Peptides regulate neuroendocrine and limbic system functioning in animals. Both systems show major disturbances in the affective disorders. Only thyrotropin releasing hormone (TRH), luteinizing hormone releasing hormone (LHRH), melanocyte stimulating hormone inhibiting factor (MIF-I), and 1-desamino-8-D-arginine vasopressin (DDAVP) have been administered to affectively ill patients. The thyroid stimulating hormone (TSH) response to TRH is blunted (less than or equal to 5 microU/ml) in some patients during depression and mania and in alcoholics. The blunted response may be an important tool in the diagnosis of depression and mania. Together with other demonstrated endocrine abnormalities, the blunted TSH response suggests a profound alteration in the physiological relationship between the central nervous system and the anterior pituitary in affective illness. Behaviorally, TRH, LHRH, DDAVP, and MIF-I have general activating effects in human that have not yet been demonstrated to be restricted to or specific to affective illness. The interpretation of peptide challenges, however, in the study of affective illness is obfuscated by the small number of patients used and the multiple sites that peptides at pharmacological doses may affect.
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PMID:Peptide challenges in affective illness. 611 86

Serum thyroid stimulating hormone (TSH) levels were measured in 127 patients with varying grade of chronic renal failure (CRF). Sensitive immunoradiometricassays (IRMA) were used so that small changes in TSH levels if any, could be appreciated, and to see if such alterations exhibit some relationship with those in thyroid hormone levels. Mean serum TSH levels in the patient group of 2.33 microU/ml (0.07-7.3) was significantly higher in comparison to 1.73 microU/ml (0.25-4.6) in normal subjects (p < 0.001). However, they were not significantly different when measured by radioimmunoassay (RIA) as compared to normals. Serum triiodothyronine (T3), thyroxine (T4) and free triiodothyronine (FT3) levels of 72 +/- 32 ng/dl, 7.4 +/- 2.6 micrograms/dl and 2.9 +/- 0.9 pg/ml were significantly lower than in normal subjects, whereas serum free thyroxine (FT4) showed a slight though not significant elevation. When patients were divided in three subgroups according to the degree of renal insufficiency, TSH levels showed a gradual rise with corresponding depression in their T3, FT3 and T4 levels. In 19 patients who were on hemodialysis (HD) and subsequently received successful renal transplantation, most of the thyroid function parameters returned towards the normals with TSH undergoing significant depression from their pretransplant levels as well as from normal levels. The results indicated that a slight but significant elevation in TSH levels could be revealed by sensitive IRMA in patients with CRF. Rising TSH levels with increasing renal insufficiency and its inverse relationship with T3 and T4 levels suggest maintenance of pituitary thyroid axis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Measurement of serum thyrotropin levels using sensitive immunoradiometricassays in patients with chronic renal failure: alterations suggesting an intact pituitary thyroid axis. 752 29

Changes in the circadian rhythmicity in vital signs, catecholamines, thyroid hormones, and cortisol have been observed in psychiatric disorders, most notably in depression. With respect to schizophrenia, the literature is scanty. We report here on the circadian parameter estimates of the vital signs, epinephrine, norepinephrine, triiodothyronine, thyroxine, thyroid stimulating hormone, and cortisol in the blood of 34 healthy subjects, 89 drug-free schizophrenic patients, and 25 neuroleptic-treated schizophrenic patients. The analyses are based on the cosine model to fit the experimental data. The circadian profiles of heart rate, blood pressure, and oral temperature are similar among schizophrenic patients and healthy subjects. Neuroleptic-treated patients have significantly higher MESORs (the daily mean) of serum norepinephrine and epinephrine than healthy subjects. The TSH MESOR is significantly lower in schizophrenic patients; the MESOR of triiodothyronine also shows a tendency to be nonsignificantly lower in schizophrenic patients compared with control subjects. The circadian serum thyroxine and cortisol profiles are similar in the three groups. The data show that the circadian profiles of vital signs in drug-free chronic schizophrenic patients who are not chronically hospitalized are similar to those of healthy subjects and that the increase in serum catecholamines and the apparent lowering in some thyroid indices might induce a down-regulation in the noradrenergic receptor system that could contribute to the pathophysiology of schizophrenia.
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PMID:Circadian rhythm of vital signs, norepinephrine, epinephrine, thyroid hormones, and cortisol in schizophrenia. 756 56


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