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)

The mechanisms and pathophysiology of sleep disturbances in patients with endocrine diseases are reviewed. Abnormalities in sleep regulations were demonstrated in patients with thyrotoxicosis and hypothyroidism in a use of electroencephalogram during sleep. Mental disorders are one of the causes of sleep disturbance, for example insomnia due to depression in Cushing's syndrome. Metabolic abnormalities such as hyponatremia and hypoglycemia due to adrenal insufficiency could also contribute to sleep disturbance. Obstructive, central and mixed types of sleep apnea syndrome are known to occur in hypothyroidism, acromegaly and diabetic neuropathy with autonomic dysfunction. Thus, multiple factors are involved in sleep disturbance in patients with endocrine disorders.
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PMID:[Sleep disorders in several pathologic states--endocrine diseases]. 950 51

The present study was designed to elucidate the effect of depressive symptomatology on the cortisol response to strenuous exercise. Thirteen healthy, post-menopausal women participated in this study. The results show that acute bicycle exercise activates the hypothalamic-pituitary-adrenal (HPA) axis resulting in rapid increases in plasma cortisol. Concerning the effect of depressive symptomatology on cortisol release during physical performance, we found a trend toward a negative relation between the level of depression and the change in cortisol measured after termination of the exercise, but it failed to reach statistical significance, probably due to the small sample size. Interestingly, we found a significant negative correlation between basal cortisol levels and cortisol release to the exercise protocol. Although this finding is preliminary, it seems to suggest that a sustained activation of the HPA axis may coincide with an adrenal insufficiency in response to physical performance of post-menopausal women.
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PMID:The effect of depressive symptomatology on plasma cortisol responses to acute bicycle exercise among post-menopausal women. 1019 22

Corticotropin-releasing factor 1 (CRF(1)) receptor antagonists may represent a novel group of drugs for the pharmacotherapy of depression and/or anxiety disorders. We have investigated the behavioral, endocrine, and neurochemical effects of chronic administration of a selective CRF(1) receptor antagonist, CP-154,526. After 9 to 10 days of treatment with CP-154,526 (3.2 mg/kg/day), defensive withdrawal behavior was significantly decreased suggesting anxiolytic activity. In animals treated for 14 days with the low dose of CP-154,526, serum corticosterone concentrations returned to baseline levels faster after application of an airpuff startle. Using in situ hybridization, no changes in CRF(1) receptor mRNA expression were detected in parietal cortex, basolateral amygdala, or cerebellum after chronic treatment with CP-154,526. A dose-dependent decrease in CRF mRNA expression was observed in the hypothalamic paraventricular nucleus (PVN) and the Barrington's nucleus, an effect that was significant at the high but not the low dose of CP-154,526. CP-154,526 did not alter central CRF(2A) receptor binding or mRNA expression, or urocortin mRNA expression. The present findings suggest that chronic administration of CP-154, 526 produces anxiolytic-like effects but no evidence of adrenal insufficiency. Previous postmortem studies revealed increased CRF peptide and mRNA levels in the PVN of depressed patients, which may mediate the hyperactivity of the hypothalamic-pituitary-adrenal axis observed in such patients. In view of a possible use for CRF(1) receptor antagonists in the treatment of depression, the present finding that CP-154,526 decreases CRF synthesis in the PVN is of considerable interest.
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PMID:Chronic administration of the selective corticotropin-releasing factor 1 receptor antagonist CP-154,526: behavioral, endocrine and neurochemical effects in the rat. 1090 Feb 36

Standard replacement for adrenal insufficiency (AI) consists of glucocorticoids and mineralocorticoids while DHEA deficiency is routinely ignored. Thus, AI represents the ideal pathophysiological model of isolated DHEA deficiency. We investigated the effects of DHEA replacement in 24 women with primary and secondary AI employing a double blind, placebo-controlled, randomized crossover design. A DHEA dose of 50 mg/d was chosen based on preceding single-dose pharmacokinetics and bioconversion studies. Each patient received four months of treatment with DHEA and four months placebo, with a one-month washout period. Measurements included serum steroid hormones, somatotropic parameters and psychometric assessment of well-being, mood, cognition and sexuality. Treatment with DHEA raised the initially low serum concentrations of DHEA, DHEAS, androstenedione, and testosterone into the normal range. DHEA induced a slight increase in serum IGF-I, but only in patients with primary AI, suggesting a growth hormone-mediated effect. DHEA treatment significantly improved overall wellbeing as well as scores for depression, anxiety, and their physical correlates. Furthermore, DHEA significantly increased both sexual interest and the level of satisfaction with sex. DHEA replacement had no influence on the cognitive performance, which was already on a high level at baseline. In conclusion, DHEA replacement improves well-being and sexuality in women with adrenal insufficiency. If this is due to a direct effect of DHEA on the brain, an indirect effect via increased androgen synthesis, or both, remains to be elucidated. Long-term studies in patients of both sexes are needed to further define the role of DHEA in standard replacement for adrenal insufficiency.
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PMID:DHEA replacement in women with adrenal insufficiency--pharmacokinetics, bioconversion and clinical effects on well-being, sexuality and cognition. 1119 20

The metabolic response to critical illness promotes catabolism, which mobilizes substrates for energy. Initially the hypothalamic-pituitary-adrenal axis is stimulated, but later there appears to be anterior pituitary depression. Despite this, the early increase in plasma cortisol levels is usually maintained by means independent of (falling) corticotropin levels. Some patients, however, develop acute adrenal insufficiency and appear to benefit from replacement exogenous glucocorticoid. However, identifying such patients is often difficult. The replacement of other deficiencies may not be in the patients' interests. For example, leptin, a stress-related hormone, has multiple effects, some seemingly advantageous and others detrimental in critical illness. Its overall influence and significance remains unclear.The health of gut mucosa and the inflammatory response might be improved or influenced to the (presumed) benefit of the patient by agents such as glutamine, arginine, some eicosanoids, and exogenous nucleic acids. Such "immunonutrition" appears to improve mortality and other measures of outcome in surgical intensive care unit patients and those with sepsis.
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PMID:The metabolic and nutritional response to critical illness. 1132 6

Lisa Capaldini, a physician who treats patients with HIV-related fatigue, discusses symptoms, diagnosis techniques, and treatments of depression, anemia, and various other roots of fatigue in HIV-positive patients. Biochemical depression, caused by abnormal levels of serotonin and norepinephrine in the brain, is easily misdiagnosed or overlooked. Physical and emotional symptoms of depression mirror common effects of HIV such as exhaustion, anger, and irritability. Knowing the history of depression prior to HIV infection, including previous drug abuse and family history of depression, will help to diagnose fatigue. Dr. Capaldini recommends antidepressants provided the condition is properly diagnosed and the side effects are not harmful to the patient. Selective serotonin reuptake inhibitors (SSRI), the most frequently prescribed antidepressants, can cause short term sexual dysfunction. Bupropion and Wellbutrin can be prescribed to avoid this side effect. Psychotherapy can be effective if therapists are familiar with HIV disease and can distinguish between symptoms brought on by behavior, addictive habits, or pre-existing depression. Consideration also must be given to drug interactions, particularly with the antiretrovirals ritonavir and delavirdine, which can cause seizures or disturb cardiac rhythm. Anemia is most noticeable after physical exertion, and symptoms are more evident based on the increased rate that red blood cells move out of the normal range. To determine the course of treatment, physicians need to clarify the cause of anemia. Anemia can be caused by drugs, vitamin deficiencies, or other nutritional problems. Adrenal insufficiency, methemoglobinemia, and malnutrition are also causes of fatigue. Diagnosing fatigue due to hepatitis B or C, rather than HIV, can be achieved by measuring hepatitis levels and observing T cell counts and viral load. Dr. Capaldini suggests that proper diet and exercise prevent fatigue from getting worse.
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PMID:Fatigue and HIV: interview with Lisa Capaldini, M.D. Part II. Interview by John S. James. 1136 84

The exact physiological role of DHEA remains unknown but DHEA supplementation has recently been proven beneficial in typical deficient states like adrenal insufficiency or major depressive illlnesses. The putative favorable effects of DHEA in other conditions remain controversial. However, recent studies confirmed positive effects of DHEA administration in healthy elderly people, mostly more than 70 years old women, on skin, bone density, muscle strength and several neuropsychological symptoms. Positive effects on sexual interest and satisfaction and sense of well-being are more consistent in elderly women than in men. The recommended administered dose is 25 mg to 50 mg once a day in women and 100 mg in men. Androgenic side effects (greasy skin, acne, increased growth of body hair) are frequent but reversible side effects. Dose adaptation is recommended in these conditions. It is justifiable to prescribe DHEA in patients with adrenal insufficiency. Other possible indications are depression and prolonged glucocorticoid therapy. In elderly people, DHEA administration might be considered in DHEA depleted-patients with skin dryness or atrophy, muscle weakness, low bone density or neuropsychological symptoms. The treatment should be taken under close medical supervision in order to detect a possible hormone-dependent cancer such as breast cancer in women and prostatic cancer in men. The patients should be informed on the potential risks of DHEA administration and on the lack of definitive proven beneficial effects of DHEA, waiting the results of well-conducted controlled double blind prospective studies.
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PMID:[DHEA: orthodox or alternative medicine?]. 1168 Feb 5

A 9-year-old, spayed female domestic shorthair cat presented for polyphagia, polydipsia, and polyuria following chronic methylprednisolone acetate therapy for pruritus. Initial diagnostics were consistent with uncomplicated diabetes mellitus. Serum calcium was within reference range. Within 12 hours the cat developed depression, anorexia, vomiting, and severe dehydration. Laboratory analysis indicated marked hypercalcemia as measured by both ionized and total calcium concentration. No underlying neoplastic or inflammatory process was identified. An adrenocorticotropic hormone stimulation test was indicative of adrenocortical insufficiency. The hypercalcemia resolved with glucocorticoid supplementation and correction of the dehydration. The diabetes mellitus and adrenal insufficiency both resolved within 9 weeks.
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PMID:Hypercalcemia due to latrogenic secondary hypoadrenocorticism and diabetes mellitus in a cat. 1180 13

Congenital adrenal hyperplasia describes a group of inherited autosomal recessive disorders characterized by an enzymatic defect in cortisol biosynthesis, compensatory increases in corticotropin secretion, and adrenocortical hyperplasia. 21-Hydroxylase deficiency is responsible for more than 95% of cases and is one of the most common known autosomal recessive disorders. The classic or severe type presents in the newborn period or early childhood with virilization and adrenal insufficiency, with or without salt loss; the mild or nonclassic form presents in late childhood or early adulthood with mild hyperandrogenism and is an important cause of masculinization and infertility in women. This wide range of phenotypic expression is mostly explained by genetic variation, although genotype-phenotype discrepancies have been described. Reproductive, metabolic, and other comorbid conditions, including risk for tumors, are currently under investigation in both forms of the disease. A high proportion of patients with adrenal incidentalomas may be homozygous or heterozygous for 21-hydroxylase deficiency. Women with congenital adrenal hyperplasia often develop the polycystic ovary syndrome. Ectopic adrenal rest tissue is often found in the testes of men with congenital adrenal hyperplasia; characteristic clinical and radiologic findings help differentiate this tissue from other tumors. Levels of corticotropin-releasing hormone are elevated in patients with depression and anxiety and are expected to be elevated in patients with congenital adrenal hyperplasia; it is unknown whether patients with 21-hydroxylase deficiency have an increased incidence of these psychiatric disorders. Abnormalities in both the structure and function of the adrenal medulla have been shown in patients with classic congenital adrenal hyperplasia, and the degree of adrenomedullary impairment may be a biomarker of disease severity. The 21-hydroxylase-deficient mouse has provided a useful model with which to examine disease mechanisms and test new therapeutic interventions in classic disease, including gene therapy. Treatment of this condition is intended to reduce excessive corticotropin secretion and replace both glucocorticoids and mineralocorticoids. However, clinical management is often complicated by inadequately treated hyperandrogenism, iatrogenic hypercortisolism, or both. New treatment approaches currently under investigation include combination therapy to block androgen action and inhibit estrogen production, and bilateral adrenalectomy in the most severely affected patients. Other approaches, which are in a preclinical stage of investigation, include treatment with a corticotropin-releasing hormone antagonist and gene therapy.
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PMID:NIH conference. Future directions in the study and management of congenital adrenal hyperplasia due to 21-hydroxylase deficiency. 1184 30

Korsakoff's syndrome of obscure etiology was observed in a 34-year-old single woman with an 11-year history of hirsutism and mood swings, and previous hospitalizations for mania three years ago and depression 11 years ago.Recently the virilism had intensified with increased muscularity and coarsening of facial features. The 24-hour urinary 17-ketosteroids ranged between 14.4 mg. and 21.5 mg. and were suppressed by dexamethasone. The 17-hydroxycorticosteroid excretion was normal. These and other findings suggested a diagnosis of adrenal virilism due to adrenocortical hyperplasia. In the absence of other discernible causes it appeared that the adrenal pathology was responsible for the Korsakoff's syndrome. Both conditions responded well to glucocorticoid therapy although low doses were necessary to avoid mania.It is speculated that the encephalopathy was due to an associated adrenal insufficiency. Although hypoadrenalism is accepted as a complication of only the infant form of adrenal virilism, it is noteworthy that this patient had pathological pigmentation of her skin.
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PMID:KORSAKOFF'S SYNDROME ASSOCIATED WITH ADRENAL VIRILISM. 1415 54


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