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Cortisol levels

Interference with corticosteroid function and the stress response has been shown for a variety of chemicals, including the pharmaceutical salicylate (Gravel and Vijayan 2006) and the PAH, phenanthrene (Monteiro et al. 2000a, 2000b). Other classes of chemicals shown to have significant effects on cortisol levels include PCBs and PAHs (Hontela et al. 1992,1997). The precise mechanisms for these effects are poorly understood, but for PCBs, are believed to be via their actions through the Ah receptor (Aluru and Vijayan 2006). [Pg.268]

Check a pre-ACTH stimulation test cortisol level at 30, 60, and possibly 90 min post-ACTH administration... [Pg.69]

Some clinicians advocate a baseline cortisol level <15 mcg/dlV or <25 mcg/dL in critically ill patients as the diagnostic threshold for relative (or functional) adrenal insufficiency... [Pg.69]

Adrenal hormone production is controlled by the hypothalamus and pituitary gland. Corticotropin-releasing hormone (CRH) is secreted by the hypothalamus and stimulates secretion of adrenocorticotropic hormone (ACTH), also known as corticotropin from the anterior pituitary. ACTH, in turn, stimulates the adrenal cortex to produce cortisol. When sufficient or excessive cortisol levels are reached, a negative feedback is exerted on the secretion of CRH and ACTH, thereby decreasing overall cortisol production. The control of adrenal androgen synthesis also follows a similar negative-feedback mechanism. [Pg.687]

Decreased basal and stress-induced cortisol levels... [Pg.688]

Stress-induced adrenal insufficiency complicates 9% to 24% of septic patients and is associated with increased mortality. Adrenal-insuffident patients are identified by a adrenocorticotropic hormone (ACTH) stimulation test. Patients are given 250 meg ACTH and a cortisol level is checked within 30 to 60 minutes. Responders are defined as a greater than 9-mcg/dL increase in cortisol and non-responders as a less than 9-mcg/dL increase in cortisol. Septic shock patients refractory to resuscitation and vasopressors, and with adrenal insufifidency (non-responders to the ACTH test) should be administered intravenous hydrocortisone 200 to 300 mg per day in three divided doses for 7 days.24,44... [Pg.1195]

V4. Vermes, I., Beishuizen, A., Hampsink, R. M and Haanen, C., Dissociation of plasma adreno-corticotropin and cortisol levels in critically ill patients Possible role of endothelin and atrial natriuretic hormone. J. Clin. Endocrinol. Metab. 80, 1238-1242 (1995). [Pg.129]

In sum, Wilkinson focuses his explanatory hypothesis on social anxiety. He links social anxiety to shame, depression and violence, and emphasizes that social anxiety has its roots in perceptions of inferiority, unattractiveness, failure or rejection. This helps explain why health is so closely related to lack of friends, low social status, violence and poor early emotional attachment, all of which are associated with similar patterns of raised basal cortisol levels and attenuated responses to experimental stressors. He concludes, therefore, that social anxiety is a very plausible central source of the chronic anxiety that depresses health standards and feeds into the socioeconomic gradient in health. As he puts it, the most important psychosocial determinant of population health is the levels of the various forms of social anxiety in the population, and these in turn are determined by income distribution, early childhood and social networks (Wilkinson, 1999, p. 60). Thus, social anxiety is suggested as an explanation for the links between health and friendship, health and early emotional development, health and the direct psychosocial effects of low social status, the patterning of violence and health in relation to inequality, and health and social cohesion (Wilkinson, 1999, p. 61). [Pg.74]

The observed Li+-induced stimulation of corticotropin (ACTH) secretion from cells in culture, requiring extracellular Ca2+, involves a corresponding and apparently associated increase in the concentration of Ins(l)P, indicating some interaction with phosphoinositide metabolism [176], Pretreatment with Li+ desensitizes the cells, reducing this Li+-induced stimulation of ACTH secretion. Li+ initially raises plasma cortisol levels in manic-depressives however the levels are subsequently reduced with chronic Li+ treatment in both patients and controls [177]. This effect is probably secondary to the stimulation and subsequent desensitization of ACTH secretion by Li+, as observed in cultured cells. [Pg.31]

Rapid and sustained elevation of plasma cortisol levels altered plasma cholesterol and sodium levels... [Pg.191]

Close monitoring of 24-hour urinary free cortisol levels and serum cortisol levels are essential to identify adrenal insufficiency in patients with Cushing s syndrome. Steroid secretion should be monitored with all drug therapy and corticosteroid replacement given if needed. [Pg.220]

The short cosyntropin-stimulation test can be used to assess patients with suspected hypocortisolism. An increase to a cortisol level >18 mcg/dL (500 mmol/L) rules out adrenal insufficiency. [Pg.221]

Most importantly, the determination of cortisol levels is considered useful in the diagnosis and treatment of various ailments, namely Addison s Disease i.e., pernicious anaemia—a condition whereby the maturation of the red cells may not proceed beyond the stage of megaloblasts Cushing s Syndrome. [Pg.64]

Neuroendocrine Tobacco smoking is acutely related to elevations in plasma arginine vasopressin, neurophs I, j8-endorphin, and j8-lipotropin (Pomerleau et al. 1983). Cigarette smoking elevates plasma cortisol levels via a central mechanism in the hypothalamus or brain stem... [Pg.111]

Chronic elevation of corticosteroids has been shown to impair cognitive processes and have neurotoxic effects (Sheline et al. 1996 de Kloet et al. 1999). The cumulative effects of elevated cortisol levels are associated with cognitive impairments in human aging (Lupien et al. 1999). Thus, the cognitive and neuroprotective effects of ginkgo may be partly mediated through its neuroendocrine effects. [Pg.172]

Lupien SJ, Nair NP, Briere S, Maheu F, Tu MT, Lemay M, McEwen BS, Meaney MJ. (1999). Increased cortisol levels and impaired cognition in human aging implication for depression and dementia in later life. Rev Neurosci. 10(2) 117-39. [Pg.481]

O Brien, J.T., Lloyd, A., McKeith, 1., Gholkar, A., Ferrier, N. (2004) A longitudinal study of hippocampal volume, cortisol levels, and cognition in older depressed subjects. Am. J. Psychiatry, 161, 2081-2090. [Pg.356]

Plasma cortisol levels are increased and the normal diurnal variation is lost. [Pg.361]

The first example shows the circadian rhythm of the cortisol level. As an activator of gluconeogenesis (see p. 158), cortisol is mainly released in the early morning, when the liver s glycogen stores are declining. During the day, the plasma cortisol level declines. [Pg.372]

The administration of spironolactone (Aldactone) interferes in the determination of 11-hydroxy corticosteroid by methods that depend on formation of fluorescence in strong sulfuric acid (W15). In 5 patients, the administration of the drug produced as much as a 5-fold increase in the apparent plasma cortisol levels. Aspirin interferes in the determinations of homovanillic acid (HVA) by a fluorometric method. The HVA fluorophore occurs at 320 nm and 420 nm, and acetylsalicylic acid produces fluorescence at 305 to 405 nm (H12). [Pg.31]


See other pages where Cortisol levels is mentioned: [Pg.222]    [Pg.454]    [Pg.687]    [Pg.689]    [Pg.693]    [Pg.698]    [Pg.65]    [Pg.89]    [Pg.90]    [Pg.91]    [Pg.99]    [Pg.127]    [Pg.144]    [Pg.71]    [Pg.250]    [Pg.892]    [Pg.899]    [Pg.502]    [Pg.512]    [Pg.516]    [Pg.66]    [Pg.151]    [Pg.200]    [Pg.73]    [Pg.290]    [Pg.281]    [Pg.16]    [Pg.250]    [Pg.741]   
See also in sourсe #XX -- [ Pg.144 , Pg.175 ]




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