Primary hyperaldosteronism epidemiology and demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Prevalence of primary hyperaldosteronism is from 1,400-32,000 (median, 8,800) per 100,000 individuals around the world. Primary hyperaldosteronism incidence among patients with newly diagnosed hypertension is 11,200 of per 100,000 individuals. The case-fatality rate of primary hyperaldosteronism is approximately 23.4 per 1,000 individual-years. Patients of all age groups may develop primary hyperaldosteronism. There is no racial predilection for primary hyperaldosteronism.

Epidemiology and Demographics

Prevalence

Prevalence of primary hyperaldosteronism varies from 1,400 to 32,000 (median, 8,800) per 100,000 individuals around the world.^[1]^[2]
In patients with resistant hypertension, the prevalence of primary hyperaldosteronism is reported to be even higher, ranging from a low of 17,000 per 100,000 patients to a high of 23,000 per 100,000 patients.^[3]
The prevalence of familial hyperaldosteronism type II ranges from 1.2 to 6% in adult populations of primary hyperaldosteronism.^[4]

Incidence

Primary hyperaldosteronism incidence among patients with newly diagnosed hypertension is 11,200 of per 100,000 individuals.^[5]

Case-Fatality rate

The case-fatality rate of primary hyperaldosteronism is approximately 23.4 per 1,000 individual-years.^[6]

Age

Patients of all age groups may develop primary hyperaldosteronism.

Gender

Familial hyperaldosteronism type I accounts for 0.5 to 1.0% of primary hyperaldosteronism and occurs equally among women and men.^[7]
Males are more commonly affected by unilateral adrenal hyperplasia than females. The male to female ratio is approximately 4 to 1.
Females are more commonly affected by adrenal adenomas.
Bilateral adrenal hyperplasia affects men and women equally.^[8]

Race

There is no racial predilection for primary hyperaldosteronism.^[9]
Blacks have been found to have lower plasma renin activity than other populations.^[10]

References

↑ Rossi GP, Pessina AC, Heagerty AM (2008). “Primary aldosteronism: an update on screening, diagnosis and treatment”. J. Hypertens. 26 (4): 613–21. doi:10.1097/HJH.0b013e3282f4b3e6. PMID 18327065.
↑ Rossi GP, Seccia TM, Pessina AC (2007). “Clinical use of laboratory tests for the identification of secondary forms of arterial hypertension”. Crit Rev Clin Lab Sci. 44 (1): 1–85. doi:10.1080/10408360600931831. PMID 17175520.
↑ Stowasser M, Taylor PJ, Pimenta E, Ahmed AH, Gordon RD (2010). “Laboratory investigation of primary aldosteronism”. Clin Biochem Rev. 31 (2): 39–56. PMC 2874431. PMID 20498828.
↑ Stowasser M, Gordon RD (2000). “Primary aldosteronism: learning from the study of familial varieties”. J. Hypertens. 18 (9): 1165–76. PMID 10994747.
↑ Rossi GP (2010). “Prevalence and diagnosis of primary aldosteronism”. Curr. Hypertens. Rep. 12 (5): 342–8. doi:10.1007/s11906-010-0134-2. PMID 20665130.
↑ Wu, Vin-Cent; Wang, Shuo-Meng; Chang, Chia-Hui; Hu, Ya-Hui; Lin, Lian-Yu; Lin, Yen-Hung; Chueh, Shih-Chieh Jeff; Chen, Likwang; Wu, Kwan-Dun (2016). “Long term outcome of Aldosteronism after target treatments”. Scientific Reports. 6 (1). doi:10.1038/srep32103. ISSN 2045-2322.
↑ “Evidence for Abnormal Left Ventricular Structure and Function in Normotensive Individuals with Familial Hyperaldosteronism Type I | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic”.
↑ Woo K, Waisman J, Melamed J, Lepor H (2000). “Primary aldosteronism caused by unilateral adrenal hyperplasia”. Rev Urol. 2 (2): 100–4. PMC 1476104. PMID 16985748.
↑ Calhoun DA, Nishizaka MK, Zaman MA, Thakkar RB, Weissmann P (2002). “Hyperaldosteronism among black and white subjects with resistant hypertension”. Hypertension. 40 (6): 892–6. PMID 12468575.
↑ Lee MR, Critchley JA, Gordon CJ, Makarananda K, Sriwatanakul K, Balali-Mood M, Boye GL (1990). “Ethnic differences in the renal sodium dopamine relationship. A possible explanation for regional variations in the prevalence of hypertension?”. Am. J. Hypertens. 3 (6 Pt 2): 100S–103S. PMID 2383374.

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[pmid18327065-1] Rossi GP, Pessina AC, Heagerty AM (2008). “Primary aldosteronism: an update on screening, diagnosis and treatment”. J. Hypertens. 26 (4): 613–21. doi:10.1097/HJH.0b013e3282f4b3e6. PMID 18327065.

[pmid17175520-2] Rossi GP, Seccia TM, Pessina AC (2007). “Clinical use of laboratory tests for the identification of secondary forms of arterial hypertension”. Crit Rev Clin Lab Sci. 44 (1): 1–85. doi:10.1080/10408360600931831. PMID 17175520.

[pmid20498828-3] Stowasser M, Taylor PJ, Pimenta E, Ahmed AH, Gordon RD (2010). “Laboratory investigation of primary aldosteronism”. Clin Biochem Rev. 31 (2): 39–56. PMC 2874431. PMID 20498828.

[pmid10994747-4] Stowasser M, Gordon RD (2000). “Primary aldosteronism: learning from the study of familial varieties”. J. Hypertens. 18 (9): 1165–76. PMID 10994747.

[pmid20665130-5] Rossi GP (2010). “Prevalence and diagnosis of primary aldosteronism”. Curr. Hypertens. Rep. 12 (5): 342–8. doi:10.1007/s11906-010-0134-2. PMID 20665130.

[WuWang2016-6] Wu, Vin-Cent; Wang, Shuo-Meng; Chang, Chia-Hui; Hu, Ya-Hui; Lin, Lian-Yu; Lin, Yen-Hung; Chueh, Shih-Chieh Jeff; Chen, Likwang; Wu, Kwan-Dun (2016). “Long term outcome of Aldosteronism after target treatments”. Scientific Reports. 6 (1). doi:10.1038/srep32103. ISSN 2045-2322.

[urlEvidence_for_Abnormal_Left_Ventricular_Structure_and_Function_in_Normotensive_Individuals_with_Familial_Hyperaldosteronism_Type_I_|_The_Journal_of_Clinical_Endocrinology_&_Metabolism_|_Oxford_Academic-7] “Evidence for Abnormal Left Ventricular Structure and Function in Normotensive Individuals with Familial Hyperaldosteronism Type I | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic”.

[pmid16985748-8] Woo K, Waisman J, Melamed J, Lepor H (2000). “Primary aldosteronism caused by unilateral adrenal hyperplasia”. Rev Urol. 2 (2): 100–4. PMC 1476104. PMID 16985748.

[pmid12468575-9] Calhoun DA, Nishizaka MK, Zaman MA, Thakkar RB, Weissmann P (2002). “Hyperaldosteronism among black and white subjects with resistant hypertension”. Hypertension. 40 (6): 892–6. PMID 12468575.

[pmid2383374-10] Lee MR, Critchley JA, Gordon CJ, Makarananda K, Sriwatanakul K, Balali-Mood M, Boye GL (1990). “Ethnic differences in the renal sodium dopamine relationship. A possible explanation for regional variations in the prevalence of hypertension?”. Am. J. Hypertens. 3 (6 Pt 2): 100S–103S. PMID 2383374.

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