PRIMARY HYPERALDOSTERONISM – FACTORS OF EMERGENCE OF SECONDARY ARTERIAL HYPERTENSION
DOI:
https://doi.org/10.11603/2415-8798.2019.1.10010Keywords:
primary hyperaldosteronism, secondary arterial hypertensionAbstract
Primary hyperaldosteronism is now recognized as the most common factor of secondary hypertension. This disease is characterized by inadequately high and independent of the regulatory effects renin-angiotensin-aldosterone system by secretion of aldosterone. Among the causes of secondary arterial hypertension, primary hyperaldosteronism is from 4.6 to 13.0 %, and among patients with refractory to the medical treatment hypertension – about 20 %. It is believed that the main causes of such arterial hypertension are aldosterone-producing adenoma and bilateral hyperplasia of the adrenal glands, whose frequency is 35 and 60 % respectively. In recent years, there have been reports of genetically-identified family types of primary hyperaldosteronism, but they are not well-known to the broad public of doctors.
The aim of the study – to learn the current state of the problem about the causes of secondary hypertension with primary hyperaldosteronism.
Materials and Methods. The literature data for the last 5–10 years on the problem of primary hyperaldosteronism has been the material for this work to find out the current trends and views on the causative factors of the development of secondary arterial hypertension.
Results and Discussion. The analysis of literature data has made it possible to determine the level of knowledge about the causes of secondary hypertension on the basis of hyperaldosteronism. It has been established that, thanks to advances in genetic research, new types of family hyperaldosteronism and aldosterone clusters of producing cells that over-produce aldosterone has been discovered, even in the absence of structural alterations in the adrenal glands. However, the problem of the influence of the results of genetic research on the choice of treatment method and treatment of patients with primary hyperaldosteronism remain questions of discourse and unexplored problems.
References
Baudrand, R., & Vaidya, A. (2018). The. Low-Renin Hypertension Phenotype: Genetics and the Role of the Mineralocorticoid Receptor. Review Int. J. Mol. Sci., 19 (2), 546. doi:10.3390/ijms19020546.
Pinggera, A., Mackenroth, L., Rump, A., Schallner, J., Beleggia, F., Wollnik, B., & Striessnig, J. (2017). New gain-of-function mutation shows CACNA1D as recurrently mutated gene in autism spectrum disorders and epilepsy. Hum Mol Genet, 26, 2923-2932. doi: 10.1093/hmg/ddx175.
Williams, T.A., Lenders, J.W.M., Mulatero, P., Burrello, J., Rottenkolber, M., Adolf, C., … & Deinum, J. (2017). Outcomes after adrenalectomy for unilateral primary aldosteronism: An international consensus on outcome measures and analysis of remission rates in an international cohort. Lancet Diabetes Endocrinol, 5, 689-699.
Ntali, G., Asimakopoulou, A., Siamatras, T., Komninos, J., Vassiliadi, D., Tzanela, M., Tsagarakis, S., … & Karavitaki, N. (2013). Mortality in cushing’s syndrome: Systematic analysis of a large series with prolonged follow-up. Eur. J. Endocrinol., 169, 715-723.
Nieman, L.K., Biller, B.M., Findling, J.W., Murad, M.H., Newell-Price, J., Savage, M.O., Tabarin, A., & Endocrine, S. (2015). Treatment of cushing’s syndrome: An endocrine society clinical practice guideline. J. Clin. Endocrinol. Metab., 100, 2807-2831.
Lopez, D., Luque-Fernandez, M.A., Steele, A., Adler, G.K., Turchin, A., & Vaidya, A. (2016). “Nonfunctional” adrenal tumors and the risk for incident diabetes and cardiovascular outcomes: A cohort study. Ann. Intern. Med., 165, 533-542.
Isidori, A.M., Graziadio, C., Paragliola, R.M., Cozzolino, A., Ambrogio, A.G., Colao, A., … & Group, A.B.C.S. (2015). The hypertension of cushing’s syndrome: Controversies in the pathophysiology and focus on cardiovascular complications. J. Hypertens, 33, 44-60.
Baudrand, R., & Vaidya, A. (2015). Cortisol dysregulation in obesity-related metabolic disorders. Curr. Opin. Endocrinol. Diabetes Obes., 22, 143-149.
Albani, A., Theodoropoulou, M., & Reincke, M. (2017). Genetics of cushing’s disease. Clin. Endocrinol, 88, 3-12.
Funder, J.W. (2017). Apparent mineralocorticoid excess. J. Steroid Biochem. Mol. Biol., 165, 151-153.
Ozgur, M. & Kai, D. (2018). The Many Faces of Primary Aldosteronism and Cushing Syndrome: A Reflection of Adrenocortical Tumor Heterogeneity Review article. Front. Med. Retrieved from: https://doi.org/10.3389/fmed.2018.00054.
Mulatero, P., Tizzani, D., Viola, A., Bertello, C., Monticone, S., Mengozzi, G., … & Veglio, F. (2011). Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in TOrinoGENetic forms). Hypertension, 58, 797-803. doi:10.1161/ HYPERTENSIONAHA.111.175083.
Elke Tatjana Aristizabal, P., Jacopo, B., Martin, R., Tracy Ann, W. (2017). Old and New Concepts in the Molecular Pathogenesis of Primary Aldosteronism. Hypertension, 70, 5, 875-881.
Sutherland, D.J., Ruse, J.L., & Laidlaw, J.C. (1966). Hypertension, increased aldosterone secretion and low plasma renin activity relieved by dexamethasone. Can Med Assoc J, 95, 1109-1119.
Lifton, R.P., Dluhy, R.G., Powers, M., Rich, G.M., Cook, S., Ulick, S., & Lalouel, J.M. (1992). A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature, 355, 262-265.
Lifton, R.P., Dluhy, R.G., Powers, M., Rich, G.M., Cook, S., Ulick, S., & Lalouel, J.M. (1992). A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature, 355, 262-265.
Pascoe, L., Jeunemaitre, X., Lebrethon, M.C., Curnow, K.M., Gomez-Sanchez, C.E., Gasc, J.M., … & Corvol, P. (1995). Glucocorticoid-suppressible hyperaldosteronism and adrenal tumors occurring in a single French pedigree. J Clin Invest, 96, 2236-2246.
Rich, G.M., Ulick, S., Cook, S., Wang, J.Z., Lifton, R.P., & Dluhy, R.G. (1992). Glucocorticoid-remediable aldosteronism in a large kindred: clinical spectrum and diagnosis using a characteristic biochemical phenotype. Ann Intern Med, 116, 813-820.
Stowasser, M., Gartside, M.G., & Gordon, R.D. (1997). A PCR-based method of screening individuals of all ages, from neonates to the elderly, for familial hyperaldosteronism type I. Aust N Z J Med, 27, 685-690.
Stowasser, M., Bachmann, A.W., Huggard, P.R., Rossetti, T.R., & Gordon, R.D. (2000). Treatment of familial hyperaldosteronism type I: only partial suppression of adrenocorticotropin required to correct hypertension. J Clin Endocrinol Metab, 85, 3313-3318.
Pallauf, A., Schirpenbach, C., Zwermann, O., Fischer, E., Morak, M., & Holinski-Feder, E. (2012). The prevalence of familial hyperaldosteronism in apparently sporadic primary aldosteronism in Germany: a single center experience. Horm Metab Res., 44 (3), 215-220.
Stowasser, M., & Gordon, R.D. (2003). Primary aldosteronism: from genesis to genetics. Trends Endocrinol Metab, 14, 310-317.
Scholl, U.I., Nelson-Williams, C., Yue, P., Grekin, R., Wyatt, R.J., & Dillon, M.J. (2012). Hypertension with or without adrenal hyperplasia due to different inherited mutations in the potassium channel KCNJ5. Proc Natl Acad Sci U S A., 109 (7), 2533-2538.
Geller, D.S., Zhang, J., Wisgerhof, M.V., Shackleton, C., Kashgarian, M., & Lifton, R.P. (2008). A novel form of human mendelian hypertension featuring nonglucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab., 93, 3117-3123. doi: 10.1210/jc.2008-0594.
Choi, M., Scholl, U.I., Yue, P., Björklund, P., Zhao, B., Nelson-Williams, C. … & Richard P. (2011). Lifton K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Science, 331, 768-772. doi: 10.1126/science.1198785.
Oki, K., Plonczynski, M.W., Luis, L.M., Gomez-Sanchez, E.P., & GomezSanchez, C.E. (2012). Potassium channel mutant KCNJ5 T158A expression in HAC-15 cells increases aldosterone synthesis. Endocrinology, 153, 1774-1782. doi: 10.1210/en.2011-1733.
Scholl, U.I., Stölting, G., Nelson-Williams, C., Vichot, A.A., Choi, M., Loring, E., … & Lifton, R.P. (2015). Recurrent gain of function mutation in calcium channel CACNA1H causes early-onset hypertension with primary aldosteronism. Elife, 4, e06315. doi: 10.7554/ eLife.06315.
Eckle, V.S., Shcheglovitov, A., Vitko, I., Dey, D., Yap, C.C., Winckler, B., & Perez Reyes, E. (2014). Mechanisms by which a CACNA1H mutation in epilepsy patients increases seizure susceptibility. J Physiol, 592, 795-809. doi: 10.1113/jphysiol.2013.264176.
Korah, H.E., & Scholl, U.I. (2015). An update on familial hyperaldosteronism. Horm Metab Res., 47, 941-946. doi: 10.1055/s-0035-1564166.
Vaidya, A., & Dluhy, R. (2016). Hyperaldosteronism. Retrieved from: www.endotext.org.
Perez-Rivas, L.G., Williams, T.A., & Reincke, M. (2018). Inherited Forms of Primary Hyperaldosteronism: New Genes, New Phenotypes and Proposition of A New Classification. Exp Clin Endocrinol Diabetes, doi: 10.1055/a-0713-0629Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/30199917.
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