Importancia de la reducción del metabolismo del cortisol | 29 ABR 13

Hipercortisolemia en los pacientes críticamente enfermos

La reducción de la degradación del cortisol debida a la supresión de la expresión y activación de las enzimas que lo metabolizan contribuye a la hipercortisolemia y por lo tanto a la supresión de la corticotrofina.
Autor/a: Dres. Eva Boonen, Hilke Vervenne, Philippe Meersseman, Ruth Andrew, Leen Mortier, Peter E. Declercq, Yoo-Mee Vanwijngaerden N Engl J Med 2013.
INDICE:  1. Artículo | 2. Referencias

1. Mesotten D, Vanhorebeek I, Van den Berghe G. The altered adrenal axis and treatment with glucocorticoids during critical illness. Nat Clin Pract Endocrinol Metab 2008;4:496-505.
2. Widmer IE, Puder JJ, Konig C, et al. Cortisol response in relation to the severity of stress and illness. J Clin Endocrinol Metab 2005;90:4579-86.
3. Vermes I, Beishuizen A. The hypothalamic- pituitary-adrenal response to critical illness. Best Pract Res Clin Endocrinol Metab 2001;15:495-511.
4. Annane D, Sebille V, Troche G, Raphael JC, Gajdos P, Bellissant E. A 3-level prognostic classification in septic shock based on cortisol levels and cortisol response to corticotropin. JAMA 2000;283:1038-45.
5. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002;288:862-71. [Erratum, JAMA 2008;300:1652.]
6. Selye H. The general adaptation syndrome and the diseases of adaptation. J Clin Endocrinol Metab 1946;6:117-230.
7. Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008;358:111-24.
8. Vermes I, Beishuizen A, Hampsink RM, Haanen C. Dissociation of plasma adrenocorticotropin and cortisol levels in critically ill patients: possible role of endothelin and atrial natriuretic hormone. J Clin Endocrinol Metab 1995;80:1238-42.
9. Bornstein SR, Engeland WC, Ehrhart- Bornstein M, Herman JP. Dissociation of ACTH and glucocorticoids. Trends Endocrinol Metab 2008;19:175-80.
10. Bornstein SR, Chrousos GP. Adrenocorticotropin (ACTH)- and non-ACTHmediated regulation of the adrenal cortex: neural and immune inputs. J Clin Endocrinol Metab 1999;84:1729-36.
11. Stimson RH, Andersson J, Andrew R, et al. Cortisol release from adipose tissue by 11beta-hydroxysteroid dehydrogenase type 1 in humans. Diabetes 2009;58:46-53.
12. Tomlinson JW, Walker EA, Bujalska IJ, et al. 11Beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response. Endocr Rev 2004;25:831-66.
13. Langlois VS, Zhang D, Cooke GM, Trudeau VL. Evolution of steroid-5alphareductases and comparison of their function with 5beta-reductase. Gen Comp Endocrinol 2010;166:489-97.
14. Ackermann D, Vogt B, Escher G, et al. Inhibition of 11beta-hydroxysteroid dehydrogenase by bile acids in rats with cirrhosis. Hepatology 1999;30:623-9.
15. McNeilly AD, Macfarlane DP, O’Flaherty E, et al. Bile acids modulate glucocorticoid metabolism and the hypothalamic- pituitary-adrenal axis in obstructive jaundice. J Hepatol 2010;52:705-11.
16. Stauffer AT, Rochat MK, Dick B, Frey FJ, Odermatt A. Chenodeoxycholic acid and deoxycholic acid inhibit 11 betahydroxysteroid dehydrogenase type 2 and cause cortisol-induced transcriptional activation of the mineralocorticoid receptor. J Biol Chem 2002;277:26286-92.
17. Vanwijngaerden YM, Wauters J, Langouche L, et al. Critical illness evokes elevated circulating bile acids related to altered hepatic transporter and nuclear receptor expression. Hepatology 2011;54:1741-52.
18. Knaus WA, Draper EA, Wagner DP,
Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med 1985;13:818-29.
19. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 1992;101:1644-55.
20. Coolens JL, Van Baelen H, Heyns W. Clinical use of unbound plasma cortisol as calculated from total cortisol and corticosteroid- binding globulin. J Steroid Biochem 1987;26:197-202.
21. Vanhorebeek I, Peeters RP, Vander Perre S, et al. Cortisol response to critical illness: effect of intensive insulin therapy. J Clin Endocrinol Metab 2006;91:3803-13.
22. Andrew R, Smith K, Jones GC, Walker BR. Distinguishing the activities of 11beta-hydroxysteroid dehydrogenases in vivo using isotopically labeled cortisol. J Clin Endocrinol Metab 2002;87:277-85.
23. Andrew R, Westerbacka J, Wahren J, Yki-Jarvinen H, Walker BR. The contribution of visceral adipose tissue to splanchnic cortisol production in healthy humans. Diabetes 2005;54:1364-70.
24. Basu R, Basu A, Grudzien M, et al. Liver is the site of splanchnic cortisol production in obese nondiabetic humans. Diabetes 2009;58:39-45. [Errata, Diabetes 2009;58:1936, 2010;59:1283.]
25. Hughes KA, Manolopoulos KN, Iqbal J, et al. Recycling between cortisol and cortisone in human splanchnic, subcutaneous adipose, and skeletal muscle tissues in vivo. Diabetes 2012;61:1357-64.
26. Best R, Walker BR. Additional value of measurement of urinary cortisone and unconjugated cortisol metabolites in assessing the activity of 11 beta-hydroxysteroid dehydrogenase in vivo. Clin Endocrinol (Oxf) 1997;47:231-6.
27. Andrew R, Phillips DI, Walker BR. Obesity and gender influence cortisol secretion and metabolism in man. J Clin Endocrinol Metab 1998;83:1806-9.
28. Ulick S, Tedde R, Wang JZ. Defective ring A reduction of cortisol as the major metabolic error in the syndrome of apparent mineralocorticoid excess. J Clin Endocrinol Metab 1992;74:593-9.
29. Palermo M, Shackleton CH, Mantero F, Stewart PM. Urinary free cortisone and the assessment of 11 beta-hydroxysteroid dehydrogenase activity in man. Clin Endocrinol (Oxf) 1996;45:605-11.
30. Walker BR. How will we know if 11beta-hydroxysteroid dehydrogenases are important in common diseases. Clin Endocrinol (Oxf) 2000;52:401-2.
31. Drake AJ, Livingstone DE, Andrew R, Seckl JR, Morton NM, Walker BR. Reduced adipose glucocorticoid reactivation and increased hepatic glucocorticoid clearance as an early adaptation to high-fat feeding in Wistar rats. Endocrinology 2005;146:913-9.
 32. Trainer PJ, Besser M. The Bart’s endocrine protocols. New York: Churchill Livingstone, 1995:52.
33. Fenske M. Urinary free cortisol and cortisone excretion in healthy individuals: influence of water loading. Steroids 2006; 71:1014-8.
34. Mericq MV, Cutler GB Jr. High fluid intake increases urine free cortisol excretion in normal subjects. J Clin Endocrinol Metab 1998;83:682-4.
35. Melby JC, Spink WW. Comparative studies on adrenal cortical function and cortisol metabolism in healthy adults and in patients with shock due to infection. J Clin Invest 1958;37:1791-8.
36. Sandberg AA, Eik-Nes K, Migeon CJ, Samuels LT. Metabolism of adrenal steroids in dying patients. J Clin Endocrinol Metab 1956;16:1001-16.
37. White PC, Mune T, Agarwal AK. 11 Beta-hydroxysteroid dehydrogenase and the syndrome of apparent mineralocorticoid excess. Endocr Rev 1997;18:135-56.
38. Barquist E, Kirton O. Adrenal insufficiency in the surgical intensive care unit patient. J Trauma 1997;42:27-31.
39. Stewart PM, Walker BR, Holder G, O’Halloran D, Shackleton CH. 11 Betahydroxysteroid dehydrogenase activity in Cushing’s syndrome: explaining the mineralocorticoid excess state of the ectopic adrenocorticotropin syndrome. J Clin Endocrinol Metab 1995;80:3617-20.
40. Quattropani C, Vogt B, Odermatt A, Dick B, Frey BM, Frey FJ. Reduced activity of 11 beta-hydroxysteroid dehydrogenase in patients with cholestasis. J Clin Invest 2001;108:1299-305.



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