Hipertensión arterial en entidades endocrinas
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Hipertensión arterial
entidades endocrinas

How to Cite

Orrego M, A. (2018). Hipertensión arterial en entidades endocrinas. Revista Colombiana De Endocrinología, Diabetes &Amp; Metabolismo, 5(3), 19–27. https://doi.org/10.53853/encr.5.3.430


La hipertensión arterial puede ser la primera presentación en al menos 15 entidades endocrinas. Un diagnóstico preciso temprano de una hipertensión endocrina brinda la posibilidad al internista o endocrinólogo de conseguir una cura por medio de cirugía o de obtener un control estricto de la entidad con una terapia farmacológica específica. La experiencia ha demostrado que los clínicos deben tener presente la presencia de hiperaldosteronismo primario en la mayoría de los casos de hipertensión arterial y de estar alerta sobre la presencia de un feocromocitoma o un paraganglioma o ciertos casos sospechosos de la entidad.
El estudio de los pacientes hipertensos con una entidad endocrina hace posible con frecuencia llegar a un diagnóstico de precisión en entidades en las cuales es difícil pensar, con base solamente el cuadro clínico solapado o inexistente o por su rareza, como el síndrome de aparente exceso de mineralo-corticoides, la hiperplasia adrenal congénita, o la apnea obstructiva; haciendo posible el control de las complicaciones a largo plazo de la hipertensión.

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1. Yoon SS, Ortega Y, Louis T. Recent trends in the prevalence of high blood pressure and its treatment and control, 1999-2008. NCH Data Brief. 2010; (48):1-8.
2. James PA, Oparil S, Cushman WC, et al. 2014 evidence-based for the manegment of high blood pressure in adults: report from the panel members appointed to Eight Join National Committel (JNC.8). JAMA 2014; 311 (5): 507- 520.
3. Fields LE, Burt VL, Cutler, et al. The burden of adult hypertension in the United States. 1999 to 2000: a rising tide. Hypertension Res. 2004;44(4): 398-404.
4. Rudnick KV, Sackett DL, Hirst S, et al. Hypertension in a family practice. Can Med Assoc J, 1977 17(5): 492-497.
5. Omura M, Saito J, Yamaguchi K, et al. Prospective study on the prevalence of secondary hypertension among hypertensive. Patents visiting a general clinic in Japan. Hypertension Res 2004; 27 (3): 193-202.
6. Gupta-Malhotra M, Banker A, Shetes, et al. Essential hypertension vs secondary hypertension among childrens. Am J Hipertension. 2015; 28 (1): 73-80.
7. Camelli S, Bobrie G, Postel-Viney E, et al. Prevalence of secondary hypertension in young hypertensive adults. J Hipertension. 2015; 33 (Suppl 1): c47.
8. O. Shea PM,Griffin TP, Fitzgibbon M, Hypertension: The role of biochemistry in the diagnosis and manegement.ClinChim Acta. 2017; 465:131-143.
9. Funder JW. Carey RM, Mantero F, et al.The manegement of primary aldosteronism: case detection, diagnosis and treatment in Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(5): 1889-1916.
10. Lender JW, Eisenhofer G,Monnelli M, et al. Phaechromocytoma. Lancet. 2005;366 (9486): 655-675.
11. Delellis R, Lloyd R, et al. Pathologic and genetics of tumours of endocrine organs. Lyon, France: IAAC Press. 2004.
12. Mansmann G, Lau J,Balk E, et al. The clinically inapparent adrenal mass: uptodate in diagnosis and management Endocr Rev.2004; 25 (2): 309-340.
13. Lo CY, Lam KY, Wat MS, et al. Adrenal pheocromocytoma remains frequently overlooked diagnosis . Am J Surg. 2000; 179 (3): 212-215.
14. Beard CM, Sheps SG, Kurland LT, et al. Ocurrence of preochromocytoma in Rochester, Minnesota, 1950 through 1979. Mayo Clin Proc. 1983;58 (12): 802-804.
15. Kimura N,Miura Y Nagatsu N, et al. Catecholamines synthesizing enzimes in 70 cases of functioning and no functioning and extradrenal paraganglioma. Virhows Arch A Pathol Anat Histopathol. 1992; 421(1): 25-32.
16. Eisenhofer G, Lenders JW, Golstein DS,et al. Pheochromocytoma catecholamines phenotypes and prediction of tumor size and localization by use of plasme metanephrines. Clin Chem. 2005;51(4): 735-744.
17. Eisenhofer G, Pack K, Huynh TT, et al. Catecholamic metabolic and and secretory phenotypes in phaeochromocytoma. Endocr Relat Cancer. 2010;18(1): 977-1111.
18. Eisenhofer G, Huynh TT, Elkahloun A, et al. Differential expression of the regulated catecholamines secretory pathway in different hereditary forms of pheochormocytoma. Am j Phisiol Endocrinol Metab. 2008; 295 (5): E1223-E1233.
19. Bravo EL, Tagle, R. Pheochomocytoma: of-the-art and future prospects. Endocr Rev. 2003; 24(4): 539-553.
20. Young F, Young Jr. Calhoun AD, et al- Screeming for endocrine hypertemsion: An Endocrine Society Scientific Statement. Endocr Rev. 2017; 38(2): 103- 122.
21. Young WF, Jr. Clinical practice. The incidentally discoverd adrenal mass. New Engl J Med. 2007; 356(6): 601-610.
22. Lender JW, Duh QY, Eisenhofer G, et al. Endocrine Society Clinical. Pheochromocytoma and paraglanglioma: Endocrine Clinical Society. Practice guideline. J Clin Endocrinol Metab. 2014: 99(6): 1915-1942.
23. Eisenhofer G, Lender JW, Siegert G, et al. Plasma methoxy tyramine a novel biomarker of metastasic pheochomocytoma and paraganglioma in relation to established size factor of tumor rize localization and SDHB mutation status. Eur J Cancer. 2012; 48(11): 1739-1749.
24. Algeciras-Schimmich A, Preissner CM, et al. Plasma chormogranin A or urine factioned metanephrines follow-up testing improves the diagnost accuracy of plasma fractioned metanephrines for pheocromocytoma, J Clin Endocrinol Metab. 2008: 93(1): 91-95.
25. Eisenhofer G, Golstein DS, Walther MM, et al. Biochemical diagnosis of pheocromocytoma: how to distinguish true-from false-positive test result. J Clin Endocrinol Metab. 2003; 88(6). 2656-2666.
26. Conn JW, Presidential address. I. Painting II. Primary aldosteronism, a new clinical-syndrome. J Lab Clin Med. 1995; 45(1): 3-17.
27. Rossi GP, Bernini G, Caliumi C, et al. Study Investigator. A prospective of the prevalence of primary aldosteronism in 1.125 hipertensive patients. J Am Coll Cardiol. 2006: 48(11): 2293- 2300.
28. Conn JW, Knopf RF, Nesbit RM. Clinical characteristics of primary aldosteronism from ananalysis of 145 cases. AM J Surg. 1964; 107: 159-172.
29. Mulatero P, Stowasser M, Loh KC, et al. Increased diagnosis of primary al- dosternonism, in cluding surgical correctable forms , in centers from five continents. J Clin Endocrinol Metab. 2004; 89(3): 1045-1050.
30. Young WF, Jr; Klee GG. Primary aldosteronism .Diagnostic evaluation. Endocrinol Metab Clin North Am. 1988; 17(2): 367-395.
31. Ono Y, Iwakura Y, Morimoto R, et al. Os 35-01 the prevalence of sleep apnea sindrome in primary aldosteronism. J Hypertens. 2016; 34 (Suppl 1- ISH2016 Abstrat Book: e399.
32. Cellen O,O`Brien MJ, Beazley RM, et al. Factors influencing outcome of surgery for primary aldosteronism. Arch Surg. 1996; 131(6): 646-650.
33. Rutherford JC, Tayor WL Stowasser M, et al. Success of surgery for primary aldosteronism judged by residual autonomous aldosterone production. World J Surg. 1998;22 (12): 1243-1245.
34. Stowasser M, Gordon. Primary aldosteronism- careful investigation is essential and rewarding. Moll Cell Endocrinol. 2004; 217(1-2): 33-39.
35. Speiser PW, Azziz R, Baskin LS, et al. Congesnital adrenal hiperplasia due to steroid 21- hyrdoxylase deficiency: an Endocrine Society clinical Practical Guideline. J Clin Encodrinol Metab. 2010; 95 (9): 4133-4160.
36. Kim YM, Kang M, Choi JM, et al. Areview of the literature on common YP17A1 mutations in adults with 17-hydroxilase/17,20, lyase deficiency, a case series of such mutations among koreans and functional characteristics of a novel mutation. Metabolism 2014; 63(1): 42-49.
37. Ishikawa SE, Saito T, Kaneko K, et al. Hipermineracorticism without elevation of plasma aldosterone; deoxicorticosterone-producing adrenal adenoma and hiperplasia. Clin Endocrinol (Oxford). 1988;29 (4): 367.
38. Chapman K, Holmes M, Seckl J. 11 beta- Hidroxiesteroid dehidrogenase; in tracellar gatekeepers of tissue glucorticoid action. Phisiol Rev. 2013; 93(3): 1139-1206.
39. Stewart PM, Krozowski ZS, Gupta A, et al. Hypertension in the sysdrome of apparent mineralocorticoid excess due to mutation of the 11beta hidroxiesteroid deshidrogenasa type 2 gene. Lancet 1996: 347(8994): 88-91.
40. Nieman L, Biller BM, Findling W, et al. The diagnosis of Cushing syndrome: an Endocrine Society Clinical Practice Guideline.J Clin Endocrinol Metab. 2008; 93 (5): 1526-1540.
41. Liddle G W. A familial renal disorder simulating primary aldosteronism but with negligible aldosterone secretion. Trans Assoc An Physicians. 1963; 76:199-213.

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