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Prevalence of Primary Hyperaldosteronism in Moderate to Severe Hypertension in the Central Europe Region

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Prevalence of Primary Hyperaldosteronism in Moderate to Severe Hypertension in the Central Europe Region Journal of Human Hypertension (2003) 17, 349–352 & 2003 Nature Publishing Group All rights reserved 0950-9240/03 $25.00 www.nature.com/jhh ORIGINAL ARTICLE Prevalence of primary hyperaldosteronism in moderate to severe hypertension in the Central Europe region BSˇ trauch1, T Zelinka1, M Hampf2, R Bernhardt3 and J Widimsky Jr1 13rd Department of Medicine, First Faculty of Medicine, Charles University, General Faculty Hospital, Prague, Czech Republic; 2Max Delbruck Centrum fu¨r Molekula¨re Medizin, Berlin, Germany; 3Universita¨t des Saarlandes, Fachbereich Biochemie, Saarbru¨cken, Germany Recently published studies from different parts of the confirmed in 77 cases (89%); the total prevalence of PH world report significantly higher prevalence of primary was thus 19%. PH consisted of the following forms: hyperaldosteronism (PH) in hypertensives (ranging from idiopathic hyperaldosteronism 42%, unilateral aldoster- 5 to 25%) than the previously accepted figures. There one-producing adenoma 36%, unilateral hyperplasia 7%, have been no data so far about the prevalence of PH in nonclassifiable PH (refused operation/adrenal venous Central Europe. Therefore, we have undertaken this sampling) 13%, familial hyperaldosteronism type 1.2%. study to evaluate the prevalence of PH in patients with The prevalence of other types of secondary hyperten- moderate to severe hypertension referred to a hyperten- sion was as follows: pheochromocytoma 5%, renovas- sion unit in the Czech Republic, together with the cular 4.5%, hypercortisolism 2%, renal 0.75%. determination of the percentage of different subtypes In conclusion, we have noted that PH in the Central of PH including familial forms. In addition to that, we Europe region (Czech Republic) is the most frequent have evaluated the prevalence of other types of form of endocrine hypertension with a considerably secondary forms of hypertension. high prevalence in moderate to severe hypertension. A total of 402 consecutive patients (230 females and Application of more strict criteria raises the probability 172 males) with hypertension, referred to our hyperten- of correct diagnosis of PH including the early normoka- sion unit, were studied. Positive aldosterone/renin ratio laemic stages of PH. (ARR, (ng/100 ml)/(ng/ml/h)) X50 as a more strict marker Journal of Human Hypertension (2003) 17, 349–352. of PH was found in 87 patients (21.6%), 30% of them doi:10.1038/sj.jhh.1001554 were normokalaemic. The diagnosis of PH was later Keywords: primary aldosteronism; prevalence; aldosterone–renin ratio Introduction prevalence ranging from 5 to 25%.4–7 The apparent 1,2 differences in the described prevalences of PH in Conn, who first described the cure of a patient these studies may reflect different selection criteria/ with primary hyperaldosteronism (PH) in 1954, design and/or potential geographical differences in recognised that hypokalaemia was not present in the occurrence of PH. all cases of PH and suggested, that normokalaemic Another important finding is that normokalaemia PH may masquerade as essential hypertension and does not exclude the diagnosis of PH. In the case thus the prevalence could be higher. This idea was of the positive screening test, the diagnosis must at that time rejected and forgotten for nearly 40 years be confirmed by suppression tests (fludrocortisone and PH was considered to be rare. In the early 1980s 3 or salt loading test) and morphological methods Hiramatsu et al described the utility of aldosterone/ (CT or MRI scan). Adenomas/hyperplasias o1cm renin ratio (ARR) and reported a prevalence of 2.6%. could be possibly missed on CT scan and there- The utility of ARR has been further explored, and fore, if suppression tests confirm the diagnosis in the 1990s many studies were reported with of PH, adrenal venous sampling (AVS) is indi- cated.8 Furthermore, the use of ARR as the screen- Correspondence: Dr B Sˇ trauch, 3rd Department of Medicine, First ing test has important clinical implicationsF Faculty of Medicine, Charles University, General Faculty Hos- more patients would be diagnosed and possibly pital, U Nerocnice 1, Prague 2, 12808, Czech Republic. cured when surgically treated. However, the indi- E-mail: [email protected] Received 15 November 2002; revised 25 January 2003; accepted 3 cations for the use of the ARR in all hyper- February 2003 tensive patients still remain controversialFsome Prevalence of primary hyperaldosteronism BS˘trauch et al 350 authors dispute the validity of such an application.9 (3) the absence of or mild suppression of plasma Another problem is that different diagnostic aldosterone after saline infusion (plasma aldo- criteria are being usedFARR values ranging from sterone p85 ng/l) as previously described.10 The 20 to 50. suppression test was performed in the morning after So far there have been no data about the at least 8 h of recumbent position. In patients who prevalence of PH in Central Europe (Czech Repub- were treated by adrenalectomy, the diagnosis was lic). Therefore, we have undertaken this study to also confirmed by histology. The adrenal CT scan evaluate the prevalence of primary aldostero- was performed in all the patients screened positive nism in patients with moderate to severe hyper- for PH. In all, 20 patients also underwent adrenal tension referred to a hypertension unit in this area, venous sampling in order to further differentiate the together with the determination of the percentage subtypes of PH. of different subtypes of PH. We have used stric- Genetic screening for the exclusion of dexametha- ter screening criteria (ARR X50) for PH. Addition- sone-suppressible hyperaldosteronism was also per- ally, we have evaluated the prevalence of other formed in patients with PH. The molecular genetic types of endocrine-mediated and secondary test can be performed with a single PCR according to hypertension. our previously published procedure.11,12 Other potential secondary causes of hypertension were confirmed by means of the usual morphologi- Subjects and methods cal and laboratory methods. In case no secondary cause was elucidated, the patient was considered to We have studied 402 consecutive hypertensive have ‘essential’ hypertension. subjects from all regions of the Czech Republic in 1997–2001, most of them with moderate to severe hypertension who were examined in our Results hypertension unit. The group consisted of 172 men and 230 women of mean age 51 years. All ARRX50 was found in 87 patients (21.6%). In all, patients discontinued their usual antihypertensive 30% of them were normokalaemic. The diagnosis of therapy at least 14 days before admission to the PH was confirmed by the criteria described earlier in hospital and were given only alpha-blockers depen- this text in 77 cases of the 87 (89%); the total ding on the blood pressure (BP) (the medication prevalence is hence 19%. The prevalence of PH and was withdrawn and patients were followed up by other types of secondary hypertension is shown in the GPs). All subjects underwent diagnostic workup Figure 1 (PH 19%, pheochromocytoma 5%, renal during short hospitalisation (3–5 days), which artery stenosis (renovascular) 4%, hypercortisolism consisted of a variety of laboratory and morpho- 2%, renal hypertension 1%). Basic characteristics of logical methods to exclude potential secondary the patients with PH are shown in Table 1. forms of hypertension. Basic characteristics of all the hypertensive We measured office BP (by a mercury sphygmo- patients and hypertensive patients without PA are manometer in the sitting position according to ISH shown in Table 2. recommendations) and also performed 24-h ambu- The presence of the different forms of PH is shown latory blood pressure monitoring (ABPM) (Space- in Figure 2 (idiopathic hyperaldosteronism 42%, labs 90207, Redmont, CA, USA) in all subjects. aldosterone-producing adenoma 36%, unilateral Blood samples were taken for electrolytes as well hyperplasia 7%, nonclassifiable PA (refused opera- as for hormonal tests including PRA and aldosterone tion, adrenal venous sampling) 13%, familial hyper- in both recumbent and upright positions. All aldosteronism type I 2%). hormonal parameters were calculated by the usual commercial methods. Aldosterone and renin con- centrations were measured using commercial RIA methods (Immunotech, France). Our laboratory’s aldosterone normal reference values were 20– 150 ng/l and PRA 0.7–2.6 ng/ml/h. (The conversion between units used for aldosterone levels is as follows: to get aldosterone in pmol/l, multiply aldosterone in ng/100 ml by 27.7.) We have calcu- lated the ARR (ng/100 ml)/(ng/ml/h) in all 402 patients both in recumbent and upright positions. The criterion for provisional diagnosis of PH was the ARR X50 (PRA and aldosterone levels measured after 2 h upright position). The confirmation of the diagnosis of PH was based on (1) elevated ARR (X50 ng/l), (2) suppressed PRA (p0.7 ng/ml/h) and Figure 1 Prevalence of different forms of secondary hypertension elevated plasma aldosterone (X150 ng/l) levels, and in 402 patients with moderate to severe hypertension. Journal of Human Hypertension Prevalence of primary hyperaldosteronism BS˘trauch et al 351 Table 1 Basic characteristics of patients with confirmed primary studies,3–7 we have confirmed that PH is not as rare aldosteronism (values are means 7 s.d.) as was previously thought and appears to be the most frequent form of endocrine-mediated hyper- Total 77 Mean age (years) 50 7 11 tension. It thus appears that there are no major Sex M/W 37/40 geographical differences in the occurrence of PH. As Casual BP (SBP/DBP) (mmHg) 167 7 22/103 7 11 of the percentage of the subtypes of PH, the majority Plasma potassium levels (mmol/l) 3.51 7 0.55 of our patients had idiopathic hyperaldosteronism Plasma aldosterone levels (ng/l) 422 7 369 PRA (ng/ml/h) 0.22 7 0.19 with bilateral overproduction. One-third of our ARR (ng/100 ml)/(ng/ml/h) 459 7 733 patients had an aldosterone-producing adenoma BMI (kg/m2) 29.2 7 5.4 later confirmed by histology.
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