Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study compared three measures of depression in schizophrenia and their correlation with the Dexamethasone Suppression Test (DST). The degree of overlap of these three measures with negative symptoms was also examined. The Hamilton Depression Rating Scale (HDRS), the depressive syndrome score of the Present State Examination (PSE), and the Scale for the Assessment of Negative Symptoms (SANS) were administered to 50 acutely ill, hospitalized schizophrenics. Patients were diagnosed using DSM-III criteria for schizophrenia. DSM-III criteria were also used to assess the presence of a major depressive episode. Results were that DST nonsuppression was significantly associated with the presence of a major depressive episode, but not with depressive rating scale scores or with negative symptoms. It is concluded that the DST may be of value in differentiating a depressive syndrome from a negative symptom syndrome in schizophrenia.
 ...
PMID:Depression dexamethasone nonsuppression and negative symptoms in schizophrenia. 237 54

In a double-blind clinical trial comprising 29 depressed patients citalopram, a highly selective 5-HT re-uptake inhibitor and maprotiline, a specific NA re-uptake inhibitor, were compared. Allowing for the small sample and taking into consideration that both groups consisted of severely ill, hospitalized patients, it is notable that half of them appeared to respond to treatment. Comparison of the clinical efficacy of the two drugs showed no significant difference, but the profiles of the side-effects appeared to be different. The patients treated with citalopram showed increased sweating, drowsiness, restlessness and headache. These side-effects were almost entirely reported by the non-responders. The maprotiline patients had anticholinergic symptoms, such as dryness of mouth and constipation, side-effects which were also reported by the responders. No correlation was found between plasma steady-state levels of either drug and clinical outcome. The Dexamethasone Suppression Test (DST) appeared to show some predictive value as regards treatment response. There was a tendency towards better overall treatment results in the non-suppressor group. Determination of post-probenecid 5-HIAA, HVA and MHPG concentrations in lumbar-CSF was made in 22 patients. There was a significant negative correlation between HVA and the severity of depression, as well as a significant negative correlation of MHPG with the Newcastle score. The 5-HIAA concentration was found to be correlated with HVA, but not with MHPG. Rather surprisingly significant negative correlation between 5-HIAA and treatment results with maprotiline was found, but no correlation with MHPG. The lumbar-CSF MHPG and HVA values did not appear to have any predictive value as regards treatment response to citalopram or maprotiline. As expected the serotonin (5-HT) concentration in blood and thrombocytes in patients treated with citalopram showed a highly significant reduction after 2 and 4 weeks of treatment.
 ...
PMID:A double-blind comparative clinical trial of citalopram vs maprotiline in hospitalized depressed patients. 244 51

The use of biologic markers in the evaluation of borderline personality disorder (BPD) patients is reviewed. Many patients with Axis II BPD have coexisting Axis I diagnoses of which depression is the most commonly reported. Biologic markers have not aided in the diagnosis of BPD, but some markers, particularly EEG sleep, are not only abnormal in BPD, but also appear to discriminate Axis I depression from other Axis I codiagnoses. Monoamine oxidase, in vitro red blood cell lithium ratio, and P300 auditory evoked potential when used alone or in a combined diagnostic approach, show promise in identifying these codiagnoses as well. Dexamethasone suppression and thyrotropin-releasing hormone tests appear nonspecific in this population. Pharmacologic trials have demonstrated that some BPD patients have good therapeutic response to antipsychotics and tranylcypromine and poor response to alprazolam.
 ...
PMID:Biologic markers in borderline personality disorder: a review. 249 95

The neuroendocrinology of bulimia nervosa has only recently been investigated, with initial research suggesting some biological overlap with both anorexia nervosa (AN) and depression. Similarities among AN, depression, and bulimia include a nonsuppressed Dexamethasone Suppression Test and an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH). Bulimics and anorectics both tend to have a delayed thyrotropin (TSH) response to TRH and elevated basal GH levels. Bulimics, however, have a normal GH response to clonidine, a nonblunted TSH response to TRH, low basal prolactin (PRL) levels, and may have an exaggerated PRL response to TRH. Unpublished data suggest bulimics may have a gonadotropin profile distinct from either AN or depression, as well as a variety of other endocrinopathies. Although many of these abnormalities may reflect malnutrition despite normal weight, other factors that are as yet unidentified are likely to be contributing to the neuroendocrine abnormalities seen in bulimia.
 ...
PMID:Neuroendocrine profile in bulimia nervosa. 252 54

In order to evaluate the possible effect of glucocorticoids as neuromodulators of the hypothalamic-pituitary-somatotropic system in depression, cortisol, growth hormone (GH), and insulin-like growth factor I (IGF-I) concentrations were studied before and after oral administration of 1 mg dexamethasone at 11 p.m. in 16 patients during depression and after recovery and in 28 healthy controls. While there were no significant differences in GH and IGF-I levels between depressed, recovered and control subjects, GH and IGF-I concentrations of cortisol non-suppressors were significantly elevated compared to suppressors. Moreover, post-dexamethasone cortisol, GH, and IGF-I levels were positively correlated. Dexamethasone had a stimulating effect on GH and IGF-I values in patients during depression and in cortisol non-suppressors only; this effect was absent in recovered and in control subjects and in cortisol suppressors. Thus, hypercortisolemia may be of great importance for the dysregulation of the hypothalamic-pituitary-somatotropic system reported in depression.
 ...
PMID:Effects of glucocorticoids on the regulation of the hypothalamic-pituitary-somatotropic system in depression. 252 80

Platelet 3H-clonidine (alpha 2-adrenergic agonist) binding and 3H-imipramine binding were measured and the Dexamethasone Suppression Test performed in 17 normal controls and 14 unmedicated depressed patients in order to clarify the relationship among these three biological markers. Increases in the Bmax and the Kd for 3H-clonidine binding and decreases in the Bmax for 3H-imipramine binding of the platelets from depressed patients were observed when compared with controls. There was a significant positive correlation among 3H-clonidine Bmax, the basal (predexamethasone) plasma cortisol levels, and the severity of depression, as indicated by the Hamilton Depression Rating Scale. On the other hand, no significant correlation was observed in 3H-imipramine binding between the Bmax and the severity of depression or between the Bmax and the basal plasma cortisol levels. There was no statistically significant correlation between the Bmax of 3H-clonidine binding and that of 3H-imipramine binding in depression, but there was a trend toward correlation in normal controls.
 ...
PMID:Platelet 3H-clonidine and 3H-imipramine binding and plasma cortisol level in depression. 254 8

A 45 year old female with Cushing's syndrome due to non-ACTH dependent bilateral adrenal macronodular hyperplasia (AMH) is reported. The diagnosis of Cushing's syndrome was based on the typical clinical features and on the demonstration of high urinary levels of free cortisol (microF) (630 micrograms/24 h) and 17 hydroxysteroids (17-OHS) which failed to suppress during the Liddle test (17-OHS, (mg/g creat), Basal: 68.5, post Dexamethasone 2 mg: 59.6 and post Dexamethasone 8 mg: 69.9). The adrenal CT scan showed bilateral multinodular enlargement while the pituitary CT scan was normal. Due to the presence of severe hypertension (240/150) and depression, the patient was treated with ketoconazole (800 mg/d) during 8 months achieving eucortisolism (microF 14-39 micrograms/24 h); however, plasma ACTH was not detectable at the end of this period. A bilateral adrenalectomy was performed, and both adrenals showed multiple nodules (0.3-4.5 cm in diameter) and weighed 136 and 31 g respectively. The lack of suppression of the 17-OHS with 8 mg of Dexamethasone, the persistence of an adequate inhibition of cortisol biosynthesis with ketoconazole, and the absence of plasma ACTH suggest that the patient had a non-ACTH dependent AMH. The possible pathogenic factors involved in this case are discussed.
 ...
PMID:[Cushing syndrome caused by macronodular adrenal hyperplasia, independent of ACTH: report of a case]. 256 12

Current theories of affective disorders do not account for many of the biological markers replicated in patient studies. We link many biological findings in a reasonable physiological relationship, compatible with mechanisms of action of pharmacological and electroshock therapies for depression. We propose that excessive phospholipase-A2 (PLA2) activity disrupts membrane fluidity, composition, and therefore, the activity, of membrane-dependent proteins. Similar disruptions in these proteins are documented in depressed patients and can be accounted for by excessive PLA2 activity. This paradigm accounts for disturbances in the activity of Na-K-ATPase, beta2- and alpha2-adrenergic receptors, MAO, norepinephrine and serotonin uptake, and imipramine binding. Disturbances in other membrane-dependent proteins, tyrosine and tryptophan hydroxylase, can explain the biogenic amine hypothesis. Inhibition of glucocorticoid receptor and TRH receptor binding to their respective ligands by PLA2 may explain patient nonsuppression in the Dexamethasone Suppression Test and poor response in the TRH stimulation test. Physiological regulators of PLA2 activity; calcium, cortisol, estrogen, progesterone, and PGE2 are documented abnormalities in some patients with affective disorders and consistent with excessive PLA2 activity. Thus, postpartum depression and premenstrual tension syndrome may be described in the paradigm. The mechanisms of action of tricyclic antidepressants, lithium, electroconvulsive shock, and some novel antimanic agents can be described in terms of alterations of PLA2 activity. Interestingly, ethanol perturbs membrane fluidity and membrane-bound enzymes in a manner similar to excessive PLA2 activity. A hereditary factor predisposing patients to affective disorders may be a gene defect at either PLA2 or in its regulation.
 ...
PMID:Are disturbances in lipid-protein interactions by phospholipase-A2 a predisposing factor in affective illness? 256 35

The present study reports the feedback suppression of basal and stimulated corticosterone secretion in rats by low doses of dexamethasone (DEX). DEX suppression of basal secretion 6 hr after administration was observed with doses as low as 0.005 mg/kg. The lowest dose capable of suppressing basal corticosterone levels for 24 hr with a return to normal values by 36 hr was established to be 0.025 mg/kg. The ability of DEX to decrease corticosterone responses to physostigmine, morphine, immobilization, and ether stress was determined. Although the magnitude of the rise in corticosterone did not differ significantly among these evocative stimuli, the degree to which DEX attenuated these responses varied. The response to morphine was completely prevented by 0.025 mg/kg and the rises following ether or immobilization were decreased significantly. In contrast, the response to physostigmine was not affected by DEX. With a higher dose of DEX (0.25 mg/kg), responses to morphine, ether, and immobilization were completely eliminated, but the response to physostigmine was only attenuated partway. The time course of the suppression in basal levels, the attenuation of several stimuli for corticosterone secretion, and the "escape" of physostigmine-induced corticosterone secretion resemble the clinical Dexamethasone Suppression Test of endogenous depression and suggest that this test might be useful in the study of animal models of depression.
 ...
PMID:Differential sensitivity to dexamethasone suppression in an animal model of the DST. 272 21

To explore corticosteroid-catecholamine interactions in depression, plasma dopamine, norepinephrine, and epinephrine concentrations were studied both before and after dexamethasone in 16 patients during depression and after recovery, and in 28 healthy controls. Dexamethasone had a significant suppressive effect on plasma epinephrine levels in depressed patients and controls, while dopamine and norepinephrine levels were not significantly affected following dexamethasone administration. Levels of norepinephrine, epinephrine, and cortisol were positively correlated, while dopamine showed no correlation with cortisol values. These findings point to differentiated interrelations between certain catecholamines and glucocorticoids which possibly are affected during depressive illness.
 ...
PMID:Effects of glucocorticoids on plasma catecholamines in depression. 279 97


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>