Welcome to Francis Academic Press

Frontiers in Medical Science Research, 2022, 4(13); doi: 10.25236/FMSR.2022.041308.

Research progress on the correlation between primary aldosteronism and bone metabolism

Author(s)

Yueyue Chai1, Rui Ma1, Yuting Shao1, Fuguang He2, Fuqiang Liu1, Hong Lai1

Corresponding Author:
Hong Lai
Affiliation(s)

1Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, Shandong, China

2Department of Internal Medicine, Shandong Pingyuan County Hospital of Traditional Chinese Medicine, Dezhou, Shandong, China

Abstract

Primary aldosteronism is a clinical syndrome characterized by hypertension, with or without hypokalemia, low renin and hyperaldosteronism, which is a common endocrine hypertension due to adrenal cortical lesions and excessive autonomic aldosteronism, resulting in increased retention of sodium and potassium and volume load.  Studies have shown that aldosterone overdose increases the risk of cardiovascular disease, renal insufficiency, diabetes, metabolic syndrome and even death. In recent years, studies have pointed out that patients with primary aldosteronism have increased urinary calcium and elevated parathyroid hormone, and the prevalence of osteoporosis and fracture is higher than that of essential hypertension and healthy people. Primary aldosteronism may be a secondary cause of osteoporosis, but the specific pathogenesis remains unclear. This article reviews the correlation of bone metabolism and possible pathogenesis of primary aldosteronism.

Keywords

primary aldosteronism; parathyroid hormone; osteoporosis; fracture

Cite This Paper

Yueyue Chai, Rui Ma, Yuting Shao, Fuguang He, Fuqiang Liu, Hong Lai. Research progress on the correlation between primary aldosteronism and bone metabolism. Frontiers in Medical Science Research (2022) Vol. 4, Issue 13: 46-51. https://doi.org/10.25236/FMSR.2022.041308.

References

[1] Choy, K. W., Fuller, P. J., Russell, G., Li, Q., et al. Primary aldosteronism. BMJ. 2022, 377: e65250.

[2] Monticone, S., D'Ascenzo, F., Moretti, C., Williams, T. A., et al. Cardiovascular events and target organ damage in primary aldosteronism compared with essential hypertension: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 2018, 6(1): 41-50.

[3] Stavropoulos, K., Imprialos, K. P., Patoulias, D., Katsimardou, A., et al. Impact of Primary Aldosteronism in Resistant Hypertension. Curr Hypertens Rep. 2022.

[4] Hundemer, G. L. Primary Aldosteronism: Cardiovascular Outcomes Pre- and Post-treatment. Curr Cardiol Rep. 2019, 21(9): 93.

[5] Vaidya, A., Mulatero, P., Baudrand, R., Adler, G. K. The Expanding Spectrum of Primary Aldosteronism: Implications for Diagnosis, Pathogenesis, and Treatment. Endocr Rev. 2018, 39(6): 1057-1088.

[6] Shi, S., Lu, C., Tian, H., Ren, Y., et al. Primary Aldosteronism and Bone Metabolism: A Systematic Review and Meta-Analysis. Front Endocrinol (Lausanne). 2020, 11: 574151.

[7] Resnick, L. M., Laragh, J. H. Calcium metabolism and parathyroid function in primary aldosteronism. Am J Med. 1985, 78(3): 385-390.

[8] Salcuni, A. S., Carnevale, V., Battista, C., Palmieri, S., et al. Primary aldosteronism as a cause of secondary osteoporosis. Eur J Endocrinol. 2017, 177(5): 431-437.

[9] Rossi, E., Sani, C., Perazzoli, F., Casoli, M. C., et al. Alterations of calcium metabolism and of parathyroid function in primary aldosteronism, and their reversal by spironolactone or by surgical removal of aldosterone-producing adenomas. Am J Hypertens. 1995, 8(9): 884-893.

[10] Petramala, L., Zinnamosca, L., Settevendemmie, A., Marinelli, C., et al. Bone and mineral metabolism in patients with primary aldosteronism. Int J Endocrinol. 2014, 2014: 836529.

[11] Lv, X., Hu, H., Shen, C., Zhang, X., et al. Risk Factors Associated With Lower Bone Mineral Density in Primary Aldosteronism Patients. Front Endocrinol (Lausanne). 2022, 13: 884302.

[12] Pilz, S., Kienreich, K., Drechsler, C., Ritz, E., et al. Hyperparathyroidism in patients with primary aldosteronism: cross-sectional and interventional data from the GECOH study. J Clin Endocrinol Metab. 2012, 97(1): E75-E79.

[13] Maniero, C., Fassina, A., Seccia, T. M., Toniato, A., et al. Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism. J Hypertens. 2012, 30(2): 390-395.

[14] Salcuni, A. S., Palmieri, S., Carnevale, V., Morelli, V., et al. Bone involvement in aldosteronism. J Bone Miner Res. 2012, 27(10): 2217-2222.

[15] Gravvanis, C., Papanastasiou, L., Glycofridi, S., Voulgaris, N., et al. Hyperparathyroidism in patients with overt and mild primary aldosteronism. Hormones (Athens). 2021, 20(4): 793-802.

[16] Zavatta, G., Di Dalmazi, G., Altieri, P., Pelusi, C., et al. Association between Aldosterone and Parathyroid Hormone Levels in Patients With Adrenocortical Tumors. Endocr Pract. 2022, 28(1): 90-95.

[17] Ismail, N. A., Kamaruddin, N. A., Azhar, S. S., Sukor, N. The effect of vitamin D treatment on clinical and biochemical outcomes of primary aldosteronism. Clin Endocrinol (Oxf). 2020, 92(6): 509-517.

[18] Ceccoli, L., Ronconi, V., Giovannini, L., Marcheggiani, M., et al. Bone health and aldosterone excess. Osteoporos Int. 2013, 24(11): 2801-2807.

[19] Notsu, M., Yamauchi, M., Yamamoto, M., Nawata, K., et al. Primary Aldosteronism as a Risk Factor for Vertebral Fracture. J Clin Endocrinol Metab. 2017, 102(4): 1237-1243.

[20] Loh, H. H., Kamaruddin, N. A., Zakaria, R., Sukor, N. Improvement of bone turnover markers and bone mineral density following treatment of primary aldosteronism. Minerva Endocrinol. 2018, 43(2): 117-125.

[21] Adolf, C., Braun, L. T., Fuss, C. T., Hahner, S., et al. Spironolactone reduces biochemical markers of bone turnover in postmenopausal women with primary aldosteronism. Endocrine. 2020, 69(3): 625-633.

[22] Law, P. H., Sun, Y., Bhattacharya, S. K., Chhokar, V. S., et al. Diuretics and bone loss in rats with aldosteronism. J Am Coll Cardiol. 2005, 46(1): 142-146.

[23] Chhokar, V. S., Sun, Y., Bhattacharya, S. K., Ahokas, R. A., et al. Hyperparathyroidism and the calcium paradox of aldosteronism. Circulation. 2005, 111(7): 871-878.

[24] Chhokar, V. S., Sun, Y., Bhattacharya, S. K., Ahokas, R. A., et al. Loss of bone minerals and strength in rats with aldosteronism. Am J Physiol Heart Circ Physiol. 2004, 287(5): H2023-H2026.

[25] Kim, B. J., Kwak, M. K., Ahn, S. H., Kim, H., et al. Lower Trabecular Bone Score in Patients With Primary Aldosteronism: Human Skeletal Deterioration by Aldosterone Excess. J Clin Endocrinol Metab. 2018, 103(2): 615-621.

[26] Yokomoto-Umakoshi, M., Sakamoto, R., Umakoshi, H., Matsuda, Y., et al. Unilateral primary aldosteronism as an independent risk factor for vertebral fracture. Clin Endocrinol (Oxf). 2020, 92(3): 206-213.

[27] Genant, H. K., Wu, C. Y., van Kuijk, C., Nevitt, M. C. Vertebral fracture assessment using a semiquantitative technique. J Bone Miner Res. 1993, 8(9): 1137-1148.

[28] Athimulam, S., Bancos, I. Evaluation of bone health in patients with adrenal tumors. Curr Opin Endocrinol Diabetes Obes. 2019, 26(3): 125-132.

[29] Wu, V. C., Chang, C. H., Wang, C. Y., Lin, Y. H., et al. Risk of Fracture in Primary Aldosteronism: A Population-Based Cohort Study. J Bone Miner Res. 2017, 32(4): 743-752.

[30] Asbach, E., Bekeran, M., Reincke, M. Parathyroid Gland Function in Primary Aldosteronism. Horm Metab Res. 2015, 47(13): 994-999.

[31] Maniero, C., Fassina, A., Guzzardo, V., Lenzini, L., et al. Primary hyperparathyroidism with concurrent primary aldosteronism. Hypertension. 2011, 58(3): 341-346.

[32] Zheng, M. H., Li, F. X., Xu, F., Lin, X., et al. The Interplay Between the Renin-Angiotensin-Aldosterone System and Parathyroid Hormone. Front Endocrinol (Lausanne). 2020, 11: 539.

[33] Makras, P., Anastasilakis, A. D. Bone disease in primary hyperparathyroidism. Metabolism. 2018, 80: 57-65.

[34] Gao, X., Yamazaki, Y., Tezuka, Y., Onodera, Y., et al. The crosstalk between aldosterone and calcium metabolism in primary aldosteronism: A possible calcium metabolism-associated aberrant "neoplastic" steroidogenesis in adrenals. J Steroid Biochem Mol Biol. 2019, 193: 105434.

[35] Andrukhova, O., Slavic, S., Smorodchenko, A., Zeitz, U., et al. FGF23 regulates renal sodium handling and blood pressure. EMBO Mol Med. 2014, 6(6): 744-759.

[36] Zhang, B., Umbach, A. T., Chen, H., Yan, J., et al. Up-regulation of FGF23 release by aldosterone. Biochem Biophys Res Commun. 2016, 470(2): 384-390.

[37] Lin Y, Tang J, Zhang S, et al. Calcium and phosphorus metabolism in patients with primary aldosteronism and its correlation with fibroblast growth factor-23. Lingnan Modern Clinics in Surgery 2018; 18(02): 137-141(in Chinese)

[38] Gupta, M., Cheung, C. L., Hsu, Y. H., Demissie, S., et al. Identification of homogeneous genetic architecture of multiple genetically correlated traits by block clustering of genome-wide associations. J Bone Miner Res. 2011, 26(6): 1261-1271.

[39] Arlt, W., Lang, K., Sitch, A. J., Dietz, A. S., et al. Steroid metabolome analysis reveals prevalent glucocorticoid excess in primary aldosteronism. JCI Insight. 2017, 2(8).

[40] Wang Z, Sun D, Li T, et al. Advances in the pathogenesis of glucocorticoid-induced osteoporosis. . World Clinical Drugs 2022; 43(01): 5-10(in Chinese)

[41] Buckley, L., Humphrey, M. B. Glucocorticoid-Induced Osteoporosis. N Engl J Med. 2018, 379(26): 2547-2556.

[42] Atashi, F., Modarressi, A., Pepper, M. S. The role of reactive oxygen species in mesenchymal stem cell adipogenic and osteogenic differentiation: a review. Stem Cells Dev. 2015, 24(10): 1150-1163.

[43] Sun, Y., Ahokas, R. A., Bhattacharya, S. K., Gerling, I. C., et al. Oxidative stress in aldosteronism. Cardiovasc Res. 2006, 71(2): 300-309.

[44] Ahokas, R. A., Sun, Y., Bhattacharya, S. K., Gerling, I. C., et al. Aldosteronism and a proinflammatory vascular phenotype: role of Mg2+, Ca2+, and H2O2 in peripheral blood mononuclear cells. Circulation. 2005, 111(1): 51-57.

[45] Ahokas, R. A., Warrington, K. J., Gerling, I. C., Sun, Y., et al. Aldosteronism and peripheral blood mononuclear cell activation: a neuroendocrine-immune interface. Circ Res. 2003, 93(10): e124-e135.