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)

Hypothalamo-pituitary-adrenal [HPA] activation and abnormal HPA regulatory mechanisms have been observed in depressed patients. Depressed and schizophrenic patients were studied to determine whether the HPA disturbances in depression are specific to this psychiatric illness or are mediated by nonspecific breakdown of psychological defense mechanisms. Despite the presence of severe ego defense breakdown and considerable secondary depressive symptomatology, the schizophrenic patients had normal HPA function. The depressed patients had elevated urine free cortisol excretion, high CSF cortisol levels, and did not show normal HPA suppression in response to dexamethasone. Within the depressed group significant correlations of HPA parameters were obtained with somatic features but not with ego breakdown features. After recovery depressed patients had more normal HPA function. The results indicate that HPA dysfunction can occur in association with primary depressive illness, that a psychoendocrine distinction can be made between primary depressive illness and secondary depressive symptomatology, and that psychological defense breakdown is not related to these neuroendocrine observations. Attention is drawn to the utility of urinary free cortisol measurement as a valuable index of HPA activation in psychoendocrine studies.
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PMID:Limbic system-adrenal cortex regulation in depression and schizophrenia. 127 36

Graded doses arginine-vasopressin (AVP) were administered to depressed patients and control subjects to compare the sensitivity of the pituitary-adrenal system of these subjects for this compound. The plasma levels of cortisol, adrenocorticotropic hormone (ACTH) and beta-endorphin were measured before and after intravenous AVP injection. The hormonal output was taken as a measure of pituitary-adrenal function. In control subjects 3 doses AVP and placebo were used, whereas in patients two doses AVP, a low and a high dose, and placebo were tested. All tests were carried out in the afternoon when the pituitary-adrenal system is stable and more susceptible for stimulation. Patients were subdivided into dexamethasone suppressors and nonsuppressors based on their DST status before testing to look for differences among these groups. Control subjects showed no response of the hormones to the lowest dose AVP and a moderate response to the higher doses. Interestingly, depressed patients as compared to controls responded more to the lowest dose AVP in particular with respect to ACTH. DST status did not influence the results. These findings suggest an enhanced sensitivity of the pituitary to low doses AVP in depressed patients. Thus, AVP might play a role in HPA dysfunction in depression.
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PMID:Stimulation of the pituitary-adrenal axis with a low dose [Arg8]-vasopressin in depressed patients and healthy subjects. 133 98

This study defines the pituitary B-endorphin (BE) secretory response to a low dosage (0.3 ug/kg) of human corticotropin releasing hormone (CRH) in depressed patients and normal controls pretreated with metyrapone. We find no difference in the B-endorphin response to CRH in depressed subjects without evidence of HPA overactivity, compared with controls. This finding is contrasted with other data demonstrating a blunted B-endorphin response to CRH in depressives. The influence of metyrapone pretreatment on the pituitary B-endorphin response to CRH through a mechanism that minimizes the impact of cortisol negative feedback is discussed. Future studies which include low dose CRH infusion both in the presence and in the absence of metyrapone pretreatment will help investigate alterations in the regulation of pituitary B-endorphin secretion in depression including the possibility of increased pituitary sensitivity to the negative fast feedback of cortisol.
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PMID:B-endorphin response to a low dosage of human corticotropin releasing hormone during metyrapone administration in depression. 147 19

Considerable evidence exists that the limbic system and the hypothalamus play an important role in the HPA axis disturbances found in depressive disorders. Evidence also exists that the limbic system plays a role in the modulation of aggressive behavior. Yet the HPA function of individuals with a disordered regulation of aggression has received little scrutiny. Because aggressive behavior has been observed to be extensively correlated with heavy alcohol use, we explored the HPA function of alcoholics who had had a life-long history of violence. Basal 0700h cortisol was measured in 4 consecutive wk following cessation of drinking in 19 alcoholics with a history of depression, and 17 alcoholics with a history of violent behavior, eight of whom had been incarcerated because of the severity of their violent acts. When compared with alcoholics with no problem in mood or aggression regulation, significant cortisol increases were found in the group of patients who had been incarcerated for violent acts and not in any other group. This increase persisted for 4 wk after cessation of drinking. A variety of variables, including several measures of alcohol consumption, amounts of benzodiazepines used for detoxification, and liver function tests, failed to show significant associations with cortisol. Data are interpreted as indicating that individuals displaying severe forms of violence could have a dysregulated HPA function revealed by exposure to excessive amounts of alcohol.
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PMID:Cortisol in alcoholics with a disordered aggression control. 160 16

Two doses of dexamethasone (DEX) (0.5 and 1.0 mg) were administered in a randomized crossover design to 31 patients with major depression, 9 healthy controls, and 14 nondepressed psychiatric patients. Using this modified Dexamethasone Suppression Test (DST), minimum DEX levels of 6 nmol/liter at 8:00 AM and 2.0 nmol/liter at 4:00 PM were required to achieve reliable suppression of cortisol in healthy controls and nondepressed psychiatric patients. Failure to achieve these minimum plasma DEX levels was associated with similar rates of nonsuppression in both depressed and nondepressed patients, thereby reducing the specificity of the DST. Conversely, high DEX levels greater than 13 nmol/liter at 8:00 AM or 4.0 nmol/liter at 4:00 PM were associated with abnormal "suppressibility" in depressed patients, thereby reducing the sensitivity of the test. Controlling for plasma DEX concentrations by selecting a test result that fell within a plasma DEX window at 8:00 AM and 4:00 PM increased the sensitivity and specificity of the DST. Significant differences in plasma DEX between suppressors and nonsuppressors were no longer evident when comparing patients with adequate DEX levels, thus ensuring that cortisol escape reflected HPA axis changes associated with depression and not peripheral mechanisms responsible for the availability of DEX. These results suggest that the clinical utility of the DST would be significantly enhanced by extending the standard 1.0-mg DST and retesting those patients with levels outside the DEX window with a higher or lower dose. The data also indicate that the measurement of plasma DEX is essential to validly interpret DST status and highlight the need to standardize DEX assays to compare DST results between research centers.
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PMID:The plasma dexamethasone window: evidence supporting its usefulness to validate dexamethasone suppression test results. 292 36

The present study evaluates the relationship between cognitive impairment and the Dexamethasone Suppression Test (DST) in elderly persons suffering from depression. Twenty-nine subjects meeting DSM-III criteria for major depressive disorder (MDD) were assessed using the Global Deterioration Scale (GDS) and the DST. Plasma cortisol levels before and after receiving 0.5 mg dexamethasone were compared, and correlations were determined between GDS and postdexamethasone plasma cortisol levels. The results show that there is a positive correlation between the GDS scores and post-DEX cortisol levels (r = 0.57, p less than 0.005). It is suggested that increased activity of the HPA axis, seen in depression, could contribute to the cognitive impairments observed in this disorder.
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PMID:Cognitive impairment and cortisol resistance to dexamethasone suppression in elderly depression. 293 Aug 4

Morning plasma cortisol response to the 1 mg dexamethasone suppression test along with cortisol levels in blood, cerebrospinal fluid (CSF), and urine were measured in hospitalized male and female patients with primary major depressive disorder who reported hypersomnia (n = 23), or increase in appetite (n = 22). Comparisons were drawn to cortisol levels in patients with primary major depressive disorder who did not report hypersomnia or appetite increase (n = 23) and to normal controls (n = 23), all age- and sex-matched. Depressives with hypersomnia or increased appetite showed higher than normal 24-h urinary free cortisol concentrations. Depressed patients without hypersomnia or appetite increase had in addition to elevated free urinary cortisol concentrations higher than normal morning plasma cortisol levels before and after dexamethasone administration and a higher incidence of cortisol non-suppression after dexamethasone compared to normal subjects. The findings provide preliminary evidence that HPA activation in depression is diminished in the presence of hypersomnia and/or an increased appetite. Studies of the hypothalamic-pituitary-adrenal axis may be useful for differentiating subtypes of depression characterized by hypersomnia or enhanced appetite.
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PMID:Cortisol measures in primary major depressive disorder with hypersomnia or appetite increase. 297 83

Psychologic stressors are less potent stimuli of the HPA axis in humans than physical stressors, but they can cause mild changes in acute ACTH and cortisol production. These changes, however, are generally not of sufficient magnitude or duration to cause measurable changes in UFC excretion. Furthermore, chronic stress leads to an attenuation of the HPA axis response. This basic knowledge concerning psychologic stress helps explain the reason why patients with uncomplicated anxiety/panic disorder, a condition involving similar symptoms, do not demonstrate UFC abnormalities. Panic disorder, when accompanied by depression, however, is associated with an increase in UFC excretion which is probably more related to the depression than the panic state. Interestingly, panic disorder, when accompanied by agoraphobia, also shows an elevation in UFC levels which makes it endocrinologically distinct from uncomplicated panic disorder. The reason for this is unclear. Treatment of the panic disorder with benzodiazepines does not further lower the UFC levels in patients with uncomplicated panic disorder despite clinical improvement, but it does lower UFC levels into the normal range in those with concurrent depression and agoraphobia. Alteration in the UFC level with treatment is only partially related to clinical improvement.
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PMID:Similarities in hypothalamic-pituitary-adrenal axis activity between patients with panic disorder and those experiencing external stress. 304 3

Hypercortisolism in depression has been extensively studied during the last three decades. The main hypothesis regarding origin and clinical relevance of this phenomenon, however, has changed significantly. Up to the mid-seventies hypercortisolism was conceived as consequence of stress modified by the degree of unconscious defense mechanisms in different forms of depressive or non-depressive psychiatric disorders. At the end of the seventies this point of view changed considerably. Hypercortisolism was regarded as a biological statemarker of the endogenous subtype of depression with clinical differential-diagnostic relevance. An abnormal dexamethasone suppression test (DST) was assumed to be the best indication of increased activation of the cortisol system. These conclusions turned out to be wrong. DST results are not specific for melancholia and the test seems to be of limited value for measuring the function of the HPA-axis. Intervening variables, such as weight loss, drug and alcohol withdrawal or situational stress, influence the test results significantly, independent of the nosological classification. Additionally, interindividual differences in the susceptibility of the HPA-axis may decisively influence the the activation of the HPA-axis as well in healthy subjects under stress as in psychiatric patients.
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PMID:Past and present strategies of research on the HPA-axis in psychiatry. 304 48

The dexamethasone suppression test (DST) was performed on 30 patients fulfilling RDC or Kendell criteria for schizo-affective depression. Symptoms characteristic of depression or schizophrenia were noted, and the severity of psychosis and the severity and endogenicity of depression were assessed. Ratings of severity were repeated at 2-month follow-up. Ten of the 30 subjects were DST non-suppressors, but no clear differences in symptoms, severity of illness or outcome between suppressors and non-suppressors emerged. Thus, although schizo-affective depression is associated with an increased frequency of HPA axis abnormality as assessed by the DST, this test does not clarify the status of schizo-affective depression in the classification of psychiatric illness.
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PMID:The dexamethasone suppression test in schizo-affective depression. 315 18


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