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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to ascertain the extent of hypothalamo--pituitary--thyroid (HPT) axis dysfunction in endogenous depression, we determined nocturnal serum thyrotropin (TSH) concentrations, TSH responses to thyrotropin releasing hormone (TRH) administration, and serum triiodothyronine (T3) and thyroxine (T4) concentrations in 40 Research Diagnostic Criteria primary, definite endogenous depressives and 40 individually matched normal control subjects. We also examined the relationships of the HPT measures to pre- and post-dexamethasone (DEX) serum and urine cortisol measures and, in the patients, to subject characteristics, the diagnosis of endogenous/melancholic depression by different systems, and the overall severity and specific dimensions of depressive symptomatology. Compared to their matched controls, the patients showed significant reductions in nocturnal serum TSH and serum T3 concentrations. Neither the TSH responses to TRH nor serum T4 concentrations were significantly different between the two groups of subjects. In the patients, none of the subject characteristics, diagnostic schemes for endogenous/melancholic depression or specific aspects of depressive symptomatology were significantly related to HPT activity. The measures of HPT activity were unrelated to measures of hypothalamo--pituitary--adrenal cortical (HPA) axis activity in both groups of subjects.
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PMID:Neuroendocrine aspects of primary endogenous depression--IV. Pituitary-thyroid axis activity in patients and matched control subjects. 312 56

The reports tries to show the intercorrelations between the TRH-test and the peripheric thyroid function during the course of affective disorders. The sample comprised 22 manic (15 follow-up) and 24 depressive (13 follow-up) patients. As parameters serum thyroxine, triiodothyronine, T3-uptake, FT4-index, T3/T4-ratio, TSH basal and 30 min after 200 micrograms TRH i.v. were determined. In a smaller group of patients reverse-T3 was measured, too. During acute mania and depression there is an increase of thyroxine. We observed a stronger conversion of T4 to rT3 with less inactivation of T4 to T3 in mania than in depression. Both groups show attenuated TSH response to TRH stimulation in florid psychoses. Comprehensing all results we come to the conclusion that the changes in the pituitary-thyroid axis accompanying affective psychoses start from the thyroidea and not from the anterior pituitary gland.
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PMID:Changes in the pituitary-thyroid axis accompanying major affective disorders. 312 5

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

Depression in children has signs and symptoms similar to those observed in depressed adults. Neuroendocrine abnormalities have been consistently observed in depressed adults. Now, neuroendocrine abnormalities are beginning to be studied in depressed children and adolescents. Results of these studies should help clarify the relationship between depression in adults and in children. Careful psychiatric diagnosis is required for studies of the neuroendocrine concomitants of depression. When establishing a diagnosis of depression in children and adolescents, one must pay attention to differences in such variables as cognitive development. Studies of neuroendocrine functioning in depressed children are at an earlier stage than those in depressed adults. To date, most studies have centered on cortisol secretion, the DST, and GH. In general, studies of cortisol secretion (most of which utilize the DST) indicate that a majority of depressed children and adolescents have positive DSTs (that is, dexamethasone fails to suppress their cortisol secretion) and cortisol secretion appears to be increased. These findings are similar to those observed in adults. Results of GH studies are more mixed. Some studies found hypersecretion of GH in depressed children, whereas others found hyposecretion of GH in depressed children. The few studies of TRH stimulation of TSH and melatonin secretion have involved a small number of subjects and results must be considered preliminary.
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PMID:Neuroendocrine changes in affectively ill children and adolescents. 313 65

Depression in children has signs and symptoms similar to those observed in depressed adults. Neuroendocrine abnormalities have been consistently observed in depressed adults. Now, neuroendocrine abnormalities are beginning to be studied in depressed children and adolescents. Results of these studies should help clarify the relationship between depression in adults and in children. Careful psychiatric diagnosis is required for studies of the neuroendocrine concomitants of depression. When establishing a diagnosis of depression in children and adolescents, one must pay attention to differences in such variables as cognitive development. Studies of neuroendocrine functioning in depressed children are at an earlier stage than those in depressed adults. To date, most studies have centered on cortisol secretion, the DST, and GH. In general, studies of cortisol secretion (most of which utilize the DST) indicate that a majority of depressed children and adolescents have positive DSTs (that is, dexamethasone fails to suppress their cortisol secretion) and cortisol secretion appears to be increased. These findings are similar to those observed in adults. Results of GH studies are more mixed. Some studies found hypersecretion of GH in depressed children, whereas others found hyposecretion of GH in depressed children. The few studies of TRH stimulation of TSH and melatonin secretion have involved a small number of subjects and results must be considered preliminary.
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PMID:Neuroendocrine changes in affectively ill children and adolescents. 313 1

Bilateral destruction of the hypothalamic paraventricular nuclei (PVN) produced a profound depression of plasma TSH and the median eminence TRH concentration in hypothyroid rats. Anterior pituitary type II iodothyronine 5'-deiodinase (5'-D) activity was consistently lower but not significantly different in sham- and PVN-lesioned rats. Treatment with suboptimal replacement doses of 0.15 and 0.75 micrograms T4/100 g BW.day produced a graded depression of plasma TSH in the PVN (P less than 0.02), but not in the sham (P greater than 0.8) groups. Adenohypophyseal 5'-D was depressed in both sham and PVN groups by the highest T4 dose. Plasma T4 was much lower in PVN than in sham rats given comparable doses of T4 (P less than 0.001), but plasma T3 was not significantly different. This suggests that an increase in peripheral T4 metabolism was produced by PVN lesions. Our data indicate that changes in adenohypophyseal 5'-D activity are not responsible for the decrease in plasma TSH in PVN-lesioned rats and that neither the PVN nor endogenous TRH plays a significant role in the regulation of anterior pituitary 5'-D activity.
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PMID:Anterior pituitary type II thyroxine 5'-deiodinase activity is not affected by lesions of the hypothalamic paraventricular nucleus which profoundly depress pituitary thyrotropin secretion. 313 10

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

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

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


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