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)

When 500 micrograms of TRH is given intravenously, an increase in TSH, blood pressure, plasma catecholamines and positive emotions follows. Four groups of patients with major, minor or bipolar depression or schizoaffective disorder increased their TSH levels by similar amounts after TRH. The neurohormone also significantly increased diastolic blood pressure by 5.5 +/- 1.6 mm Hg, and decreased heart rate by 7.6 +/- 1.3 beats/min. There was a weak trend for bipolar depressives to have less cardiovascular response to TRH than the other groups. Plasma norepinephrine (NE) was higher after TRH than after placebo. The NE response differed between patient groups (P = .0023) because of a smaller response by major depressives. TRH decreased anger, tension and depression, and increased friendliness. Positive emotional responses were significantly greater in the bipolar depressives than in other groups. Forty-one other studies have found a subnormal TSH response does not distinguish between subtypes of the affective disorders, but cardiovascular, catecholamine and mood responses may do so.
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PMID:Cardiovascular, catecholamine and psychological responses to TRH in four types of affective disorder patients. 310 31

To evaluate the diagnostic utility of TSH blunting, the TRH-induced TSH response was measured in 168 normal subjects and 176 psychiatric patients. It was blunted in some acutely depressed, alcoholic, and borderline patients, but not in schizophrenic patients. In both depression and alcoholism the fault also occurred during symptomatic recovery, though with reduced frequency. Although TSH blunting was useful in distinguishing between borderline and schizophrenic patients, its diagnostic utility in identifying or confirming an existing psychiatric disorder appears to be limited. TSH blunting is not specific for any particular psychiatric diagnosis, and its sensitivity generally is low. However, the fault has promising research utility, particularly for study of the biologic interface between depression, alcoholism and borderline personality disorder. Beyond this, further study of the possible trait nature of TSH blunting in both depression and alcoholism appears warranted.
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PMID:Evaluation of the diagnostic utility of the TRH-induced TSH response in psychiatric disorders. 311 Aug

Three biological markers of affective disorders and response to desipramine were used to study the relationship of posttraumatic stress disorder (PTSD) to affective illness. Blunted TRH response and decreased REM latency in eight patients with PTSD occurred at frequencies similar to those that have been found in patients with major affective disorder. Pretreatment Hamilton Rating Scale for Depression and Beck Depression Inventory scale scores were elevated; scores after 4 weeks' treatment with desipramine revealed significant (p less than .05 and p less than .005, respectively) improvement. These findings support a link between PTSD and affective illness.
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PMID:Biological markers of affective disorders and posttraumatic stress disorder: a pilot study with desipramine. 311 42

A group of 27 patients with definite (n = 20) or probable (n = 7) RDC major depressive disorder underwent 2 sleep EEGs and 1 TRH test while in a drug-free depressive phase. A short mean REM latency (less than 60 min) identified 55.5% of major depressives while added use of blunted TSH responses (delta max. less than 5 microU/ml) increased that percentage by 11%. When patients were subdivided into RDC endogenous and nonendogenous, mean REM latency and global depression scores distinguished the 2 groups, while delta TSH did not. A short mean REM latency identified endogenous depression with 80% specificity and 76% sensitivity. The combination of REM latency and delta TSH reduced the specificity to 60%, and therefore cannot be recommended for differentiating endogenous from nonendogenous depression.
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PMID:Biological heterogeneity of major depressive disorder: indications by sleep EEG and TRH stimulation test findings. 312 30

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

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

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


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