Plasma ACTH Levels (plasma + acth_level)

Distribution by Scientific Domains


Selected Abstracts


Preclinical Cushing's syndrome: Report of seven cases and a review of the literature

INTERNATIONAL JOURNAL OF UROLOGY, Issue 4 2000
Masaaki Morioka
Abstract Background: Adrenal adenomas showing autonomous cortisol secretion without specific endocrine symptoms are sometimes discovered in patients with adrenal incidentalomas. This entity has been described as subclinical or preclinical Cushing's syndrome (PCS), but the endocrine data of reported cases have varied and the diagnostic criteria of PCS have been uncertain. Methods: We report seven Japanese cases of PCS due to a unilateral, solitary adrenal adenoma with examination of the endocrine data of these patients. The diagnostic parameters of subtle hypercortisolism and the risk of postoperative adrenal insufficiency and surgical indications are discussed and reviewed. Results: In the present cases, the most frequently found biochemical parameters of autonomous cortisol secretion were a low adrenocorticotropic hormone (ACTH) level (100%) and insufficient suppression of cortisol by low-dose dexamethasone (85.7%). Unilateral accumulation of radiopharmaceuticals in tumors was also frequently observed (100%). A postoperative hydrocortisone supplement was given to six of the seven patients for 5,122 days. It was not given to case 4, because a moderate response of 11-deoxycortisol to metyrapone was identified. Plasma ACTH levels and the diurnal rhythm of plasma cortisol rapidly recovered within 3 weeks postoperatively in six of the seven cases. Conclusion: This entity is heterogeneous and various degrees of cortisol excess have been observed. It should be diagnosed in the wide spectrum and the risk of adrenal insufficiency after surgery should be evaluated by dynamic tests such as the corticotropin-releasing hormone (CRH) test. Based on the results of the present study and a review of the literature, PCS patients may not require hydrocortisone supplement therapy for a long period. [source]


CDP-choline increases plasma ACTH and potentiates the stimulated release of GH, TSH and LH: the cholinergic involvement

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 5 2004
Sinan Cavun
Abstract In the present study, we investigated the effect of intracerebroventricular (i.c.v.) administration of cytidine-5,-diphosphate (CDP) choline on plasma adrenocorticotropin (ACTH), serum growth hormone (GH), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels in conscious rats. The involvement of cholinergic mechanisms in these effects was also determined. In basal conditions, CDP-choline (0.5, 1.0 and 2.0 ,mol, i.c.v.) increased plasma ACTH levels dose- and time-dependently, but it did not affect the TSH, GH, FSH and LH levels. In stimulated conditions, i.c.v. administration of CDP-choline (1 ,mol, i.c.v.) produced an increase in clonidine-stimulated GH, thyrotyropin-releasing hormone (TRH)-stimulated TSH, LH-releasing hormone (LHRH)-stimulated LH, but not FSH levels. Injection of equimolar dose of choline (1 ,mol, i.c.v.) produced similar effects on hormone levels, but cytidine (1 ,mol, i.c.v.) failed to alter plasma levels of these hormones. Pretreatment with hemicholinium-3, a neuronal high affinity choline uptake inhibitor, (20 ,g, i.c.v.) completely blocked the observed hormone responses to CDP-choline. The increase in plasma ACTH levels induced by CDP-choline (1 ,mol, i.c.v.) was abolished by pretreatment with mecamylamine, a nicotinic receptor antagonist, (50 ,g, i.c.v.) but not atropine, a muscarinic receptor antagonist, (10 ,g, i.c.v.). The increase in stimulated levels of serum TSH by CDP-choline (1 ,mol, i.c.v.) was blocked by atropine but not by mecamylamine pretreatment. However, CDP-choline induced increases in serum GH and LH levels were greatly attenuated by both atropine and mecamylamine pretreatments. The results show that CDP-choline can increase plasma ACTH and produce additional increases in serum levels of TSH, GH and LH stimulated by TRH, clonidine and LHRH, respectively. The activation of central cholinergic system, mainly through the presynaptic mechanisms, was involved in these effects. Central nicotinic receptors solely mediated the increase in plasma ACTH levels while the activation of central muscarinic receptors was involved in the increase in TSH levels. Both muscarinic and nicotinic receptor activations, separately, mediated the increases in serum GH and LH levels after CDP-choline. [source]


Stress Hormone Dysregulation at Rest and After Serotonergic Stimulation Among Alcohol-Dependent Men With Extended Abstinence and Controls

ALCOHOLISM, Issue 5 2001
Robert M. Anthenelli
Background: Alcohol dependence has been associated with long-lasting alterations in limbic-hypothalamic-pituitary-adrenal (LHPA) axis and serotonin (5-hydroxytryptamine [5-HT]) function. Other conditions that are associated with alcoholism (cigarette smoking and antisocial personality disorder [ASPD]) have been linked with disturbances in these interrelated systems. We evaluated the stress hormone response to 5-HTergic stimulation in alcohol-dependent men with extended abstinence (average abstinence duration, 4.3 months) and controls to determine the relative contributions of alcoholism, cigarette smoking, and ASPD on baseline and provoked plasma cortisol and adrenocorticotropin hormone (ACTH) concentrations. Methods: One hundred nine alcohol-abstinent men with alcohol dependence (62%), habitual smoking (70%), and ASPD (43%) received d,l-fenfluramine (100 mg po) in a randomized, double-blind, placebo-controlled, crossover trial. The group of recovering alcohol-dependent individuals included abstinent primary alcohol-dependent men and alcohol-dependent men with ASPD, whereas the group of non-alcohol-dependent men comprised healthy controls and non-alcohol-dependent men with ASPD. Plasma cortisol and ACTH levels were obtained at AM baseline and at half-hour intervals after drug administration. Subjective ratings of drug response and physiological measures were also obtained at baseline and every 30 min. Results: Abstinent alcohol-dependent men had significantly lower (approximately 20%) AM baseline plasma cortisol concentrations than non-alcohol-dependent men on both challenge days; however, no differences between the groups were observed with regard to resting AM plasma ACTH levels. After adjusting for these baseline differences, recovering alcohol-dependent men (area under curve = 35.6 ± 37.4 [,g/dl] × min) had a twofold greater cortisol response to fenfluramine than non-alcohol-dependent men (area under curve = 17.5 ± 32.5 [,g/dl] × min) (F= 5.1;df= 1,105;p < 0.03). The elevated cortisol response, which occurred primarily along the descending limb of the response curve, was paralleled by a nonsignificant statistical trend for alcohol-dependent men to also exhibit a greater ACTH response to fenfluramine at the 210-min (p < 0.07) and 240-min (p < 0.09) time points as compared with non-alcohol-dependent men. Cigarette smoking and ASPD did not affect hormonal responses, nor could the groups' subjective ratings and physiological measures be distinguished. Conclusions: Alcohol-dependent men with extended abstinence differed from age- and race-matched non-alcohol-dependent men in resting AM and fenfluramine-induced plasma cortisol levels. This dysfunction in glucocorticoid homeostatic mechanisms was associated with alcoholism and not with smoking or ASPD. We also observed a nonsignificant statistical trend for plasma ACTH levels to be elevated among alcohol-dependent men along the descending limb of the response curve. Alcohol-dependent men seemed to have inherited or acquired damage to 5-HT-regulated LHPA axis function, the precise mechanisms and sites of which remain to be determined. [source]