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)

Dexamethasone suppression test (DST), imipramine platelet binding and sleep EEG in depressed patients were studied by the network of WHO Collaborating Centers. DST and sleep EEG indicated abnormalities characteristic to depression, but imipramine platelet binding failed to show difference between depressed and normal subjects. 20 papers related to markers of depression were presented at the 17th Congress of CINP, Kyoto, 1990. They were introduced under 5 headings: 1) DST and its modifications, 2) serotonergic functions, 3) platelet studies, 4) ocular potentials and melatonin, and 5) brain imaging. There are reviewed here.
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PMID:Biological markers of depression: WHO multi-center studies and future perspective. 151 28

The perioperative courses of 10 patients with obstructive sleep apnea syndrome who underwent uvulopalatopharyngoplasty were reported. No hypnotic was administered at night before operation. Premedication consisted of atropine 0.5 mg, meperidine 35 mg, given i.m. 1 hr prior to surgery. No patients developed respiratory depression after premedication. General anesthesia was induced with iv thiopental, and succinylcholine was given to facilitate tracheal intubation. Airway management was technically difficult in all patients. Anesthesia was maintained with N2O-O2-enflurane under controlled ventilation. At the end of the surgery the insertion of a nasopharyngeal airway was performed for the prevention of airway obstruction. In 8 patients it was possible to remove the airway in the next morning. Dexamethasone was administered 3 times to reduce pharyngeal edema during perioperative period. Trachea was extubated when the patient was fully awake and alert. Perioperatively the following points are important in the management of uvulopalatopharyngoplasty. 1. Assessment of airway and the method of airway control. 2. Reduction of pharyngeal edema. 3. Using caution against the postoperative hemorrhage. 4. Avoidance of sedation. 5. Close observation extending into the postoperative period.
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PMID:[Perioperative management of uvulopalatopharyngoplasty for the obstructive sleep apnea patient]. 154 94

Ten depressed patients and eight control subjects received 1 mg of dexamethasone intravenously at two different time points. Depressed patients were studied when they were depressed and following an improvement in their depression. In control subjects the first and second studies were performed approximately 1 month apart. Dexamethasone and cortisol were determined at 0, 5, 15, and 30 minutes, then at 1, 1.2, 2, 3, 4, 5, 6, 7, 9, 12, 17, and 24 hours following dexamethasone administration. Data from each patient was fit using a computer to a two compartment pharmacokinetic model and area under the time versus plasma concentration curve, elimination half-life, and clearance were also determined. Depressed patients exhibited a slower dexamethasone clearance and a larger area under the curve than control subjects at the first time point, but not at the second time point. The groups did not differ significantly in any of the other pharmacokinetic parameters (including distribution half-life, elimination half-life, or volume of distribution) at either time point. The possible causes and implications of these findings are discussed.
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PMID:A longitudinal evaluation of dexamethasone pharmacokinetics in depressed patients and normal controls. 162 86

Plasma beta-endorphin-like immunoreactivity (BEP-ir) and cortisol levels were measured by radioimmunoassay (RIA) in nine patients who were at least 12 months status post spinal cord injury (SCI). Plasma levels were obtained at 8:00 am and 4:00 pm to determine circadian rhythm, and on the day following administration of 1 mg dexamethasone, levels were again obtained at 8:00 am and 4:00 pm. The mean morning levels of plasma BEP-ir were significantly lower than control values for this laboratory (6.2 +/- 1.2 v 12.0 +/- 2.3 pg/mL). The morning BEP-ir values were lowest in patients who were closer to the time of injury (described by a second-order polynomial regression, R = .89; P less than .01). Mean morning cortisol levels were not significantly different from controls, but showed greater variability (mean, 15.1; range, 0.7 to 22.7 micrograms/dL v control, 15.5; range, 7 to 35). Dexamethasone suppressed cortisol secretion in all patients and BEP-ir levels in six of nine patients. Failure to detect BEP-ir suppression occurred in patients whose BEP-ir levels were less than 4.5 pg/mL and close to the minimum detection limit of the assay. Depression was present in five of nine patients as measured by the Beck Depression Inventory (BDI) and in three of nine patients as measured by the Hamilton Depression Scale (HSRD). However, the depression indices did not correlate with the neuroendocrine measures.
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PMID:beta-Endorphin and cortisol abnormalities in spinal cord-injured individuals. 164 Aug 43

In order to investigate pituitary alpha-melanocyte-stimulating hormone (alpha-MSH), intact (1-39 structure) adrenocorticotropic hormone (ACTH), and adrenal cortisol secretion, we measured 8 a.m. plasma levels of those hormones before and after administration of 1 mg dexamethasone in 39 depressed inpatients and 10 healthy controls. We found a significantly lower baseline alpha-MSH secretion in melancholic patients as opposed to healthy controls. There were no significant relations between alpha-MSH secretion on the one hand and ACTH or cortisol secretion on the other. Dexamethasone did not affect the 8 a.m. alpha-MSH circulating levels. The post-dexamethasone intact ACTH and cortisol values were significantly higher in melancholics as compared with healthy, minor and simple major depressed subjects. ACTH non-suppression was defined as post-dexamethasone intact ACTH greater than or equal to 12 pg/ml. ACTH non-suppression was found to be more sensitive (70%) and specific (100%) for melancholia than cortisol non-suppression. By means of pathway analysis we have established that cortisol non-suppression during a severe depression is completely determined by an augmented ACTH escape from suppression by dexamethasone. It is concluded that the assay of post-dexamethasone intact ACTH could, in the future, replace post-dexamethasone cortisol determination.
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PMID:Abnormal pituitary function during melancholia: reduced alpha-melanocyte-stimulating hormone secretion and increased intact ACTH non-suppression. 165 52

Dysthymic disorder (DD) is a chronic subsyndromal depressive condition that has generated increasing interest since its formal introduction into the psychiatric nomenclature in 1980. Although DD was included among the affective disorders in DSM-III, this classification was controversial. Some clinical and family studies support an association between DD and major depression disorder (MDD), but there has been little additional research firmly establishing the diagnostic validity of DD or clarifying its relation to MDD and to personality disorders. In this article, the literature on the biology of DD is reviewed. Studies of rapid eye movement (REM) latency, electrodermal activity, and the thyroid axis show similarities between DD and MDD, but the findings are mixed. Other investigations, including the Dexamethasone Suppression Test (DST), catecholamines, and several other electroencephalogram (EEG) sleep variables, show more consistent differences between DD and MDD. These findings suggest that DD manifests primarily trait characteristics of depression, thus differentiating it from the state characteristics of MDD. The methodological problems and implications of these studies, and suggestions for future research, are discussed.
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PMID:Biological studies of dysthymia. 168 Apr 72

There is an international consensus on the indications of electroconvulsive treatment (ECT): they result in particular from the limitations of antidepressant drug treatment. Even though the global effect of ECT is considered as satisfactory, 10 to 20% of depressed patients eligible for ECT are treatment refractory. This warrants a search for factors predicting efficacy or lack of efficacy of ECT. Predicting factors prior to ECT: Usual clinical criteria, such as the presence of delusional thoughts, are generally classified with endogenous signs of depression. Among biological criteria, EEG data, tests assessing reactivity of autonomous nervous system, plasma measures of catecholamines, calcium and cortisol do not seem relevant parameters. Dexamethasone suppression test and stimulation of TSH by TRH have no more predictive value. Predictive indices during treatment: Empirically clinicians identified a sequence in the response of depressive symptoms, although no conclusion can be drawn from these clinical impressions. Among biological factors some authors stress the importance of the epileptogenic threshold and of measuring plasma levels of peptides released by the posterior lobe of hypophysis. Such data have to be confirmed and their physiopathological value better understood. Actually some parameters representing good therapeutic practices are valued by physicians using ECT: sufficient duration of electrical crisis, total seizure time during the series of electroshocks. Those conceptions are close to the classical emphasis on the adequate number of ECTs and to the discussion on the comparative efficacy of unilateral and bilateral ECT. After ECT most authors shift to antidepressants, although data about medium and long term outcome prediction with this approach are also lacking.
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PMID:[Predictive factors of response to electronarcosis]. 180 65

Even though the DST has not proved successful as a marker for depression, it has stimulated a considerable amount of research into the interaction between neuroendocrine function and mood states. With the objective of perfecting the DST methodology, investigators have explored the interaction between dexamethasone plasma concentrations and cortisol response, and have found that there is a significant inverse correlation between dexamethasone concentrations and cortisol concentrations. Although this relationship is one of the factors that affects cortisol response in depressed patients, it usually explains less than 20 percent of the variance of cortisol response. One can only conclude that the affective state explains a certain amount of the remaining variance. Dexamethasone plasma concentrations may be altered by a variety of drug and disease interactions. Many enzyme inducers, including phenytoin, carbamazepine, and phenobarbital, increase dexamethasone CL, but some drugs that might be expected to alter dexamethasone CL, such as cimetidine and tobacco smoke, do not affect it. Any disease that causes hepatic dysfunction could be expected to decrease dexamethasone CL, whereas renal failure may increase dexamethasone CL. Neither Cushing's syndrome nor congenital adrenal hyperplasia appear to alter dexamethasone CL. Alcoholism has a dual effect on the DST. Chronic alcohol abuse may cause a cushingoid state, which could interfere with the DST interpretation. Also, chronic alcohol use may result in hepatic dysfunction, or an induction of P-450 enzymes. As a result of these different actions, alcohol could result in either an increase or decrease in dexamethasone CL. Studies of dexamethasone pharmacokinetics conducted in depressed patients are few, but they generally agree that DST nonsuppressors exhibit an increased dexamethasone CL when compared with suppressors. The only two studies to investigate this population longitudinally report somewhat contradictory results; one study reports an increase in dexamethasone CL following recovery from depression, and the other a decrease. Since only one of the studies was conducted using intravenous dexamethasone, differences in bioavailability might explain some of the differences in results between the two studies. In spite of the unresolved questions, these studies have stimulated research into an entirely new area: the possibility that affective diseases may alter the pharmacokinetics of some drugs.
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PMID:The impact of dexamethasone pharmacokinetics on the DST: a review. 181 2

Naturally-occurring neosporosis with multiple organ involvement was identified in a 10-year-old neutered male Basset hound dog. Clinical signs were first noticed 3 weeks prior to referral and consisted of crouched stance and mild pelvic limb ataxia. Dexamethasone administration had provided transient improvement. On presentation to the teaching hospital, clinical signs included depression, pelvic limb ataxia, inability to stand without assistance, and pain on deep palpation of the cervical and lumbar vertebral column. Lesions were found in the myocardium, liver, spleen, adrenal glands, brain, and spinal cord. Tachyzoites of Neospora caninum were found in the myocardium and adrenal glands. Organisms stained with anti-Neospora caninum, but not to anti-Toxoplasma gondii serum in an immunohistochemical test.
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PMID:Disseminated infection with Neospora caninum in a ten-year-old dog. 187 45

In order to delineate putatively coexisting dysregulations between sympathoadrenal system and hypothalamic-pituitary-adrenal (HPA)-axis during depression, the authors measured the following: the pre and postdexamethasone (1 mg) 24 hr urine excretion of noradrenaline, dopamine, adrenaline, 3-methoxy-4-hydroxyphenylglycol (MHPG), free cortisol (UFC), and plasma cortisol. Melancholic patients were characterized by a significantly higher excretion of noradrenaline, dopamine and adrenaline, combined with significantly increased UFC, postdexamethasone plasma cortisol, and UFC values. We found significant and positive correlations between UFC on the one hand, and the 24hr urine excretion of noradrenaline, dopamine, and adrenaline, on the other. By the same token, we established significant relationships between the 24 hr urine excretion of those catecholamines and the postdexamethasone UFC and plasma cortisol values. Cortisol nonsuppressors exhibited a significantly higher excretion of noradrenaline, dopamine and adrenaline, as compared with cortisol suppressors. Dexamethasone administration did not have a significant effect on the urinary output of noradrenaline, dopamine, adrenaline or MHPG.
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PMID:Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia. 193 Aug 81


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