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)

Eighteen male and female volunteers over the age of sixty who exhibited mild senile organic brain syndrome were administered ACTH 4-10 (Org OI 63) (30 mg, s.c.) or saline in a 2 X 2 Latin square design. Subjects experienced a reduction in depression and confusion and an increase in vigor. This evidence of an increase in vigor was supported behaviorally by a delay in the onset of increased latency in reaction time. Data also indicated that retrieval from memory may be enhanced by this compound. The electroencephalogram evinced a shift to lower frequencies under ACTH 4-10, but this effect was primarily noted in the females who received drug followed by placebo. These effects of ACTH 4-10 are intriguing and suggest that further work in this area should be encouraged.
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PMID:ACTH 4-10 in the amelioration of neuropsychological symptomatology associated with senile organic brain syndrome. 22 Jun 56

A 41-year-old man with hypothalamic hypopituitarism (CRF-ACTH type) that persisted for 2 years after discontinuation of exogenous dexamethasone was treated with bilateral ECT for severe chronic depression. The depression improved only evanescently after 17 ECT sessions but the hypothalamic-pituitary suppression cleared completely and permanently, based on responses to four metyrapone stress tests in a 2-year follow-up period. ECT may be an effective treatment for persistent hypothalamic-pituitary suppression, even in the absence of a psychiatric disorder.
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PMID:Electroconvulsive therapy for iatrogenic hypothalamic-hypopituitarism (CRF-ACTH type). 22 58

The acute in vitro action of ACTH and corticosterone individually and in combination were determined in the B-16 melanoma grown in vivo. ACTH elevated levels 10-fold while tyrosinase activity generally was depressed. Corticosterone depressed cAMP levels and tyrosinase activity. ACTH in the presence of corticosterone produced a coincident peak in tyrosinase activity and cAMP levels followed by a depression of enzymatic activity. The results demonstrate that cAMP is not the sole modulator of tyrosinase activity and that ACTH, corticosterone and cAMP interact in the regulation of B-16 melanoma tyrosinase activity.
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PMID:Effect of ACTH and corticosterone on melanogenesis and cyclic nucleotide levels in the B-16 melanoma. 22 4

The responses of serum concentrations of TSH, thyroxine (T4), triiodothyronine (T3) and of reverse triiodothyronine (rT3) to i. v. administration of 0.4 mg THR were examined prior to (and after) i. m. administration of ACTH (2 mg Synacthen Depot) in 7 euthyroid women using estrogen-containing oral contraceptives and in 8 controls, with the following results: (1) an increase in endogenous glucocorticoid secretion is associated with a depression of the TSH response to TRH; (2) TSH formed in decreased amounts is still capable of stimulating thyroid secretion; (3) the increased serum corticoid levels fail to affect the secretory response of the thyroid to TSH; (4) control of the pituitary-thyroid axis remains normal in the presence of increased serum thyroxine-binding globulin (TBG) levels. In a further series the serum levels of TBG, T4, T3, rT3 and cortisol under the effect of ACTH-induced endogenous glucocorticoid hypersecretion were studied in 6 normal untreated controls, in 6 normal women using oral contraceptives and in 10 untreated hyperthyroid patients. During four days subsequent to treatment the serum TBG levels decreased, maximum decrease being found in the users of oral contraceptives, minimum decrease in the controls. Serum T4 was found to decrease during 2 to 4 days, serum T3 parallel with an increase in serum rT3, for 1 to 2 days, subsequent for ACTH loading. In the euthyroid cases also the serum TSH levels showed a transitory decline. It is concluded that in case of endogenous hyperproduction of glucocorticoids (1) T4 leads to T3 monodeiodination decreases and T4 leads to rT3 conversion increases parallel with the changes in the serum cortisol levels; (2) TBG synthesis is inhibited by endogenous glucocorticoids; (3) the changes in serum TBG levels are accompanied by a decrease in the serum T4 concentrations.
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PMID:Effect of ACTH-stimulated glucocorticoid hypersecretion on the serum concentrations of thyroxine-binding globulin, thyroxine, triiodothyronine, reverse triiodothyronine and on the TSH-response to TRH. 23

Intramuscularly administered methylprednisolone sodium phosphate (Medrol Stabisol) in single doses of 40, 80, or 160 mg (methylprednisolone equivalents) had a similar effect as the same doses of methylprednisolone sodium succinate (Solu-Medrol) with regard to eosinophil suppression, elevation of glucose, white blood count differential shifts (lympholytic effect), urinary excretion of sodium and potassium, and localized (pain) and systemic side effects. The average plasma methylprednisolone concentration was approximately 20% higher after the intramuscular administration of methylprednisolone sodium phosphate than after methylprednisolone sodium succinate. The differences in plasma methylprednisolone levels produced by the two esters suggest that either hydrolysis of the succinate ester occurs more slowly or the succinate ester distributes more extensively. This difference in plasma level, however, is not reflected in any other pharmacologic evaluation of the two esters, e.g., both eosinophil depression and hyperglycemic response were identical. No clinically significant changes in the vital signs, standard hematology, and clinical chemistry parameters evaluated were noted after 21 successive doses (q.i.d. for five days with one dose in the morning of day 6) of 80 mg methylprednisolone sodium phosphate. An increase was noted in the systolic blood pressure from a pretreatment mean of 113 mm Hg to a posttreatment mean of 123 mm Hg and an increase in the body weight from a pretreatment mean of 177 pounds to a posttreatment mean of 183 pounds. No signs of adrenal suppression were found as judged by plasma cortisol and ACTH levels. Six (6/12) subjects of the methylprednisolone sodium phosphate group, one (1/12) subject of the vehicle group, and one (1/12) subject of the placebo (sterile saline) group reported the following systemic side effects: gas in stomach, headaches, anorectal itching, and dryness of itching of the skin. No trend was observed for any side effect reported. In these double-blind, randomized studies, single (40, 80, and 160 mg) and multiple (80 mg) intramuscular doses of methylprednisolone sodium phosphate were tolerated in healthy volunteers as well as the same doses of methylprednisolone sodium succinate and similar volumes of vehicle or placebo.
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PMID:The clinical pharmacology of methylprednisolone sodium phosphate. I. Intramuscular route of administration. 32 97

Steroid hormones, i.e., corticosteroids, estrogens, androgens and progestogens are formed in the adrenal cortex, male gonads, and the female placenta. Relatively little is known of their influence on behavior and their neuroendocrine function. On the cellular level, the rate of increase of RNA message to produce albumen and avidin is directly proportionate to the presence of steroids and their amount. Corticosteroid receptors are found in the thymus, liver, spleen and heart. The brain has receptors both for the corticosteroids and the sex hormones. These receptors are scattered throughout different regions of the brain, but the synthetic glucocorticoid dexamethasome is found only in the pituitary which accounts for its role in stopping the secretion of ACTH. Testosterone undergoes metabolic changes in the brain, affecting behavior. The A chain undergoes an enzyme reduction to 5aDHT and androstandiol. Following enzyme changes, the A chain of male testosterone can become female estradiol. Laboratory tests prove that sexual behavior in males is affected only by those androgens that can convert to estrogens, while in females it is dependent on the conversion of testosterone to estrogen. Lately psychiatrists have become very interested in the catechol estrogens, fairly new metabolites of estradiol which are produced in the hypothalamus and contain 2 hydroxyl groups (as compared with the 1 hydroxyl in estrogens). Catechol estrogens block estradiol receptors, behaving like antiestrogens. Researchers are investigating the possibility of signaling the desired neural messages without the concomitant effects that estrogen produces, through using catechol estrogens. They are examining this natural derivative of estradiol which may affect among others: sexual behavior, maturity, depression, migraines, and epileptic seizures.
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PMID:[Steroid hormones and the activity of the central nervous system]. 38 16

After exposure to a low and high dose dexamethasone regime, 11 of 34 acute psychiatric inpatients demonstrated abnormal dexamethasone suppression characterized by morning and/or mid-afternoon escape from suppression. This abnormality of suppression was found in primary depression, in mania, and in acute schizophrenia. In primary depression, the presence of abnormal dexamethasone suppression failed to discriminate "endogenous" depressed from "other depressed" subjects. Because nonsuppression to a high dose of dexamethasone is also found in patients with ectopic ACTH secretion and in patients with autonomous adrenal tumors, caution is necessary in the interpretation of nonsuppression which persists after recovery from psychiatric illness. As patients with Cushing's syndrome of uncertain etiology may be referred to a psychiatrist for a diagnostic evaluation, the psychological correlates of abnormal dexamethasone suppression need to be established with greater certainty.
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PMID:A two-dose dexamethasone suppression test in patients with psychiatric illness. 59 3

The endocrinometabolic effects of the aerosol administration of beclomethasone dipropionate (100 microng four times daily) were evaluated in 20 asthmatic patients (11 corticodependent and nine noncorticodependent) during one month. In the noncorticodependent group, aerosol administration of beclomethasone had no statistically significant effect on the results of the glucose tolerance test and the plasma levels of insulin; there was a slight decrease in basal levels of cortisol, but the response of the cortisol level to administration of ACTH remained quite normal. In corticodependent patients, after substitution of aerosol therapy with beclomethasone for the oral therapy with steroids, the depression of adrenal function disappeared, usually quickly (in less than one month), whereas the abnormalities in the results of the glucose tolerance test persisted. Thus, at the dosage used, beclomethasone dipropionate might have minor systemic endocrinometabolic effects.
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PMID:The endocrinometabolic effects of beclomethasone dipropionate in asthmatic patients. 86 40

To investigate the sites of the negative feedback of corticoids in the regulation of ACTH secretion, the effect of 10 mug of dexamethasone on adrenocortical responses to ether stress was studied in intact and fornix-sectioned rats. Dexamethasone pretreatment in both groups depressed significantly both the basal and stress plasma corticosterone levels. However, in rats with fornix section the amount of depression of the adrenocortical response was much smaller than in intact animals, when compared to the non-treated group. These data would inicate that extrahypothalamic regions play a role in the action of glucocorticoids in the feedback control of pituitary-adrenal function and that the hippocampus participates in this mechaism.
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PMID:Feedback effects of dexamethasone on adrenocortical responses in rats with fornix section. 100 17

In a patient with pituitary ACTH-dependent adrenal hyperplasia (AH), the standard oral metyrapone test resulted in a decrease in "apparent 11beta-hydroxylase activity" (-48%) accompanied by an increase in "apparent cholesterol cleavage activity" (+318%). When incubated adrenal mitochondria from this patient were studied, metyrapone inhibited both 11beta-hydroxylation of labeled 11-deoxycorticosterone and cleavage of labeled cholesterol, although at 0.1 and 1.0 mM metyrapone concentrations, depression of cholesterol cleavage (23 and 54%, respectively) was less than that of 11beta-hydroxylation (62 and 84%, respectively). The inhibition of cholesterol cleavage by metyrapone (26 and 62%, at 0.1 and 1.0 mM concentrations, respectively) was also demonstrable in adrenal mitochondria from a patient with hypercorticism resulting from an ACTH-independent adrenal adenoman (AA). Metyrapone administration to AA resulted in a significant depression of both 11beta-hydroxylase (-62%) and cholesterol cleavage (-36%) "apparent activities"; when metyrapone and ACTH were given together to this patient, however, only 11beta-hydroxylase "apparent activity" diminished (-26%), while cholesterol cleavage "apparent activity" was greatly augmented (+231%), thereby simulating the results of the standard metyrapone test in AH. These data demonstrate that metyrapone inhibits both mitochondrial reactions involved in cortisol synthesis--initial cholesterol cleavage and final 11beta-hydroxylation; these effects probably result from interference by this agent with the interaction between substrate and related cytochrome P - 450. Since ACTH has a major stimulatory effect on cholesterol cleavage but not on 11beta-hydroxylation, the outcome of metyrapone administration is thus determined by whether a change in ACTH level ensues: while 11beta-hydroxylation is inhibited by metyrapone under any circumstances, total steroid output rises when a compensatory ACTH increase overcomes metyrapone inhibition of cholesterol conversion into pregnenolone and falls when metyrapone inhibition of this reaction is unopposed.
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PMID:Dual sites of inhibition by metyrapone of human adrenal steroidogenesis: correlation of in vivo and in vitro studies. 126 43


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