Predictive factors of left ventricular mass changes after treatment of primary aldosteronism

A variety of abnormalities that occur in patients with primary aldosteronism indicate the capability of elevated aldosterone to induce cardiac damage over that induced by hypertension itself. This study investigates factors that can predict structural and functional changes of the heart after treatment of primary aldosteronism in a post-hoc analysis of 54 patients who were enrolled in a long-term follow-up study that was conducted after either adrenalectomy or treatment with spironolactone. Cardiac ultrasound assessment was performed before treatment and after with an average follow-up of 6.4 years. During follow-up, blood pressure decreased significantly and comparably in both treatment groups. In both treatment groups, left ventricular mass decreased significantly with a trend to improved diastolic filling profile and no changes in ventricular geometry. At univariate analysis, changes in left ventricular mass induced by treatment of primary aldosteronism were directly related with changes in systolic blood pressure and pretreatment plasma aldosterone levels measured both at baseline and after an intravenous saline load. This relationship was maintained when patients treated with adrenalectomy and spironolactone were analyzed separately. Multivariate regression analysis showed that changes in systolic blood pressure and pretreatment aldosterone levels were independent predictors of left ventricular mass changes after treatment. This study strongly supports a role of aldosterone in promoting left ventricular hypertrophy that is independent of the hypertension-related hemodynamic load and suggests a practical way to predict left ventricular mass changes following surgical and medical treatment of primary aldosteronism.     

Leptin levels are suppressed in primary aldosteronism.

Primary aldosteronism is associated with hypertension secondary to salt and water retention, hypokalemia and impaired insulin secretion with glucose intolerance in some patients. The secretion of leptin, a hormone produced by adipocytes, may be altered by reduced insulin secretion in primary aldosteronism. We measured plasma leptin approximately 3 months before and 3 months after curing of primary aldosteronism in 18 patients (12 male, 6 female, body mass index 29.1+/-4.4, mean +/- SD). Patients were treated by unilateral laparoscopic adrenalectomy to remove an aldosterone-producing adenoma. There was a 46% postoperative increase in plasma leptin concentrations from 6.65+/-0.81 to 9.68+/-1.50 ng/ml (P=0.004), despite a non-significant fall in body mass index. Plasma leptin was noted to increase after adrenalectomy in 16 of the 18 patients. The patients also had improved blood pressure and a significant increase in plasma potassium post-operatively. It is proposed that increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism. Further studies are indicated to identify the mechanism of plasma leptin suppression in primary aldosteronism.     

New aspects on primary aldosteronism

The adrenal cortex synthesizes and releases steroid hormones, mainly mineralocorticoids and glucocorticoids. There is a functional zonation of the adrenal cortex and steroid synthesis is thoroughly regulated. Overproduction of aldosterone, primary aldosteronism, may be much more common than previously known and may be responsible for 10% of essential hypertension. Primary aldosteronism is characterized by autonomous production of aldosterone, suppressed renin activity, hypokalemia, and hypertension. The two most common forms are unilateral adenoma and bilateral hyperplasia. In spite of thorough clinical workup and careful histopathology it is often difficult to differentiate between adenoma and hyperplasia. The gene CYP11B2 encodes the steroid synthesizing enzymes for aldosterone production, while the genes CYP17 and CYP11B1 are needed for cortisol production. Most normal controls show expression of CYP11B2 in zona glomerulosa. Expression of CYP11B1 and CYP17 is seen in zona fasciculata and reticularis, whereas the expression of CYP21 is present in all three cortical layers. Adenomas from patients with primary aldosteronism show considerable variation in the expression of CYP11B2. Adenomas from patients with Cushing's syndrome have a strong expression of CYP11B1 and CYP17. In a patient material of 29 cases of primary aldosteronism, 4 patients had small nodules detected with expression of CYP11B2 gene. These nodules were not visualized on CT, whereas adrenal masses seen on CT in these patients showed CYP11B1 and CYP17 gene expression. This suggests that these small nodules are responsible for the aldosterone production and this is characteristic of nodular hyperplasia in patients with primary aldosteronism. In conclusion, this method to visualize mRNA gene expression of steroidogenic enzymes, and especially expression of CYP11B2, has increased the knowledge of adrenal pathophysiology. The results emphasize the value to include functional studies (venous sampling and/or scintigraphy) in the preoperative work up of patients with primary aldosteronism.     

两种腹腔镜肾上腺切除术式治疗原发性醛固酮增多症效果评价

目的：比较腹腔镜肾上腺全切术与部分切除术治疗原发性醛固酮增多症的效果。方法：对152例原发性醛固酮增多症分别采用肾上腺全切术（A组82例）和肾上腺部分切除术（B组70例）进行治疗,测量并比较两组患者手术时间、手术失血量、住院时间以及术后一月内血压恢复者比例。结果：两组患者性别、年龄、高血压和低血钾在组间情况无统计差异,具备可比性（P〉0．05）。A组患者手术时间、术后一月内血压恢复比例高于B组（P〈0．05）,而失血量和住院时间无组间差异（P〉0．05）。结论：在腹腔镜肾上腺切除手术中,肾上腺全切取得了较好的效果,具有较高的临床应用价值。     

An easy diagnostic approach to primary aldosteronism.

The infusion of 40 mEq potassium (aspartate) in 250 ml isotonic 1-fructose at a rate of 20 mEq/h into 5 patients (34-56 years old) with aldosteronoma and 2 patients with bilateral primary aldosteronism consistently raised their mean arterial pressure by 15-20 mmHg. Their pressure values returned to the baseline levels 4-5 h after the infusion. In contrast, in controls (10 patients with idiopathic arterial hypertension, matched for age, sex, and magnitude of the untreated hypertension, and 7 patients with inactive adrenal nodules as incidental findings on upper abdomen ultrasound or computerized tomography) the same procedure caused negligible arterial pressure changes. The cause of the rise in blood pressure observed uniquely in patients with primary aldosteronism after infusion of potassium (aspartate) cannot be accounted for by an increase in plasma aldosterone, blood volume, or plasma angiotensin II. The cause of this response thus remains obscure; nonetheless, this simple procedure may prove useful in differentiating primary aldosteronism from idiopathic hypertension, in excluding the adrenal disorder, and in revealing even its mildest forms.     

Diabetes related knowledge among residents and nurses: a multicenter study in Karachi,Pakistan

The existence of unilateral adrenal hyperplasia (AH) has been considered a rare cause of primary hyperaldosteronism (PA). In a prospective study we screened for PA in a non-selected (NSP) and selected hypertensive population (SP), to define the cause of PA. We included 353 consecutive patients with hypertension; age 20 to 88 years, 165 women and 188 men, from a university-based Hypertension and Nephrology Outpatient clinics (123 SP) and two primary care centres, (230 NSP) from the same catch-up area. Serum aldosterone and plasma renin activity (PRA) were measured and the ARR calculated. Verifying diagnostic procedure was performed in patients with both elevated aldosterone and ARR. Patients diagnosed with PA were invited for adrenal venous sampling (AVS) and offered laparoscopic adrenalectomy when AVS found the disease to be unilateral. After screening, 46 patients, 13% of the whole population (22.8% SP and 7.8% NSP) had aldosterone and ARR above the locally defined cut-off limits (0.43 nmol/l and 1.28 respectively). After diagnostic verification, 20 patients (6%) had PA, (14.5% SP and 1.4% NSP). Imaging diagnostic procedures with CT-scans and scintigraphy were inconclusive. AVS, performed in 15 patients verified bilateral disease in 4 and unilateral in 10 patients. One AVS failed. After laparoscopic adrenalectomy, 4 patients were found to have adenoma and 5 unilateral AH. One patient denied operation. The prevalence of PA was in agreement with previous studies. The study finds unilateral PA common and unilateral AH as half of those cases. As may be suspected PA is found in much higher frequency in specialised hypertensive units compared to primary care centers. AVS was mandatory in diagnosis of unilateral PA.     

The Influence of a Heparin-Like Compound on Hypertension,Electrolytes and Aldosterone in Man

The mechanisms of the aldosterone-inhibiting and antihypertensive actions of heparin and certain other sulfated mucopolysaccharides were investigated in 13 hypertensive patients. N-formyl chitosan polysulfuric acid (RO 1-8307) was used rather than heparin because of its low anticoagulant activity. RO 1-8307 lowered aldosterone secretion in one patient with proved and one with probable primary aldosteronism; this indicates that the mucopolysaccharide does not inhibit aldosterone secretion via the renin-angiotensin mechanism. In six hypertensive patients RO 1-8307 caused a fall in the secretion of aldosterone and its probable immediate precursor, 18-hydroxycorticosterone; therefore it does not act at the last step in the synthesis of aldosterone. RO 1-8307 produced a prolonged clinical and biochemical remission in the two patients considered to have primary aldosteronism but did not influence blood pressure in five of seven patients in whom excessive aldosterone was probably not a major factor in the hypertension. It is concluded that the antihypertensive action of RO 1-8307, and perhaps of heparin as well, is largely due to suppression of aldosterone secretion.     

Adrenal aldosterone-producing adenoma: use of colonic potential in diagnosis and subtraction scanning technique for localisation.

Primary hyperaldosteronism is a potentially curable cause of hypertension, and much interest has been shown in methods of diagnosing the associated hypokalaemic hypertension and localising the adrenal adenoma. In two patients the diagnosis of primary aldosteronism was confirmed by colonic potential measurement and the adenoma localised by a new subtraction technique for early adrenal imaging applied to the use of 131I-19-iodocholesterol. Both patients underwent adrenalectomy and in each case an adenoma was removed. Blood pressure and electrolyte levels returned to normal after operation. In one patient bilateral adrenal phlebography had failed to show the tumour, and sampling of aldosterone concentrations in the adrenal veins had been unsatisfactory.     

分侧肾上腺静脉取血与肾上腺CT对原发性醛固酮增多症诊断的价值比较研究

摘要 目的：研究原发性醛固酮增多症（PA）患者行分侧肾上腺静脉取血（AVS）、肾上腺CT诊断的效果。方法：数据遴选本院2018年1月-2021年11月收治的70例原发性醛固酮增多症患者,所有患者均行肾上腺CT、AVS诊断,对最终诊断结果比较分析。结果：收缩压、舒张压、空腹血糖、总胆固醇在单双侧间无差异（P＞0.05）,双侧肾素活性、血清醛固酮肾素比值较单侧存在差异（P＜0.05）;肾上腺CT与AVS诊断的符合率情况：肾上腺CT显示为单侧异常、双侧异常及双侧正常患者,AVS符合率分别为65.00 %、31.25 %、50.00 %;单独肾上腺CT诊断：灵敏度为57.1 %,特异度为25.7 %,肾上腺静脉采血诊断：灵敏度为74.3 %,特异度为42.9 %;并联联合诊断灵敏度为100.0 %,特异度为26.3 %,串联诊断灵敏度为19.5 %,特异度为100.0 %。结论：PA是临床常见疾病,具有患病率高、预后差等特点,临床依靠临床表现、血液生化检查诊断PA疾病,但仅借助血液生化检验进行诊断治疗较困难,功能定位是治疗关键。实际工作中,可以临床通过CT检查及AVS检查功能定位诊断,但对于PA患者来说,仅借助肾上腺CT诊断结果制定治疗方案,可能导致手术侧选择错误,建议愿意接受肾上腺手术治疗者,推荐先行AVS,正确选择治疗方案,达到改善预后作用,效果较理想、值得临床借鉴推广。     

Prevalence,Subtype Classification,and Outcomes of Treatment of Primary Aldosteronism: A Prospective Study in China

ObjectiveTo investigate the prevalence of primary aldosteronism (PA) among participants with hypertension, evaluate the concordance of PA classification between adrenal computed tomography and adrenal venous sampling, and compare the outcomes of surgery and medication for unilateral PA.MethodsA prospective study was conducted among all inpatients with hypertension (n = 7594) at the National Center for Cardiovascular Diseases, China, from May 2016 to April 2018.ResultsOf the 7594 participants, 8.12% (n = 617) with plasma aldosterone-renin ratio ≥3.7 were possible PA cases. Three hundred sixty-seven cases with plasma aldosterone-renin ratio ≥3.7 and plasma aldosterone concentration ≥10 ng/dL were confirmed using the recumbent saline infusion test (69.20%, 182 of 263) or the captopril challenge test (66.5%, 69 of 104, P > .05). The prevalence of PA was 3.31% (n = 251). Of the 251 patients with PA, all of them had multiple comorbidities, and 49.40% (n = 124) had spontaneous hypokalemia. The concordance of PA classification between adrenal computed tomography and adrenal venous sampling was only 47.11%. The patients’ blood pressure declined to normal ranges in the adrenalectomy (85.71%, 30 of 35) and spironolactone (63.04%; 29 of 46) groups (P < .05). Furthermore, hypokalemia was normalized in the adrenalectomy (100.00%; 26 of 26) and spironolactone (94.74%; 18 of 19) groups.ConclusionIt is necessary to incorporate PA screening into routine practice for those with hypertension in the Chinese population. This will assist in ensuring that the best therapeutic schedule based on PA subtypes is devised. Additionally, as a result, it may contribute to restoring the blood pressure levels and reducing the prevalence of comorbidities in these patients with PA.     

Unilateral adrenal hyperplasia is a usual cause of primary hyperaldosteronism. Results from a Swedish screening study

ABSTRACT: BACKGROUND: The existence of unilateral adrenal hyperplasia (AH) has been considered a rare cause of primary hyperaldosteronism (PA). METHODS: In a prospective study we screened for PA in a non-selected (NSP) and selected hypertensive population (SP), to define the cause of PA. We included 353 consecutive patients with hypertension; age 20 to 88 years, 165 women and 188 men, from a university-based Hypertension and Nephrology Outpatient clinics (123 SP) and two primary care centres, (230 NSP) from the same catch-up area. Serum aldosterone and plasma renin activity (PRA) were measured and the ARR calculated. Verifying diagnostic procedure was performed in patients with both elevated aldosterone and ARR. Patients diagnosed with PA were invited for adrenal venous sampling (AVS) and offered laparoscopic adrenalectomy when AVS found the disease to be unilateral. RESULTS: After screening, 46 patients, 13% of the whole population (22.8% SP and 7.8% NSP) had aldosterone and ARR above the locally defined cut-off limits (0.43 nmol/l and 1.28 respectively). After diagnostic verification, 20 patients (6%) had PA, (14.5% SP and 1.4% NSP). Imaging diagnostic procedures with CT-scans and scintigraphy were inconclusive. AVS, performed in 15 patients verified bilateral disease in 4 and unilateral in 10 patients. One AVS failed. After laparoscopic adrenalectomy, 4 patients were found to have adenoma and 5 unilateral AH. One patient denied operation. CONCLUSION: The prevalence of PA was in agreement with previous studies. The study finds unilateral PA common and unilateral AH as half of those cases. As may be suspected PA is found in much higher frequency in specialised hypertensive units compared to primary care centers. AVS was mandatory in diagnosis of unilateral PA.     

Familial Hyperaldosteronism Type 3 with a Rapidly Growing Adrenal Tumor: An In Situ Aldosterone Imaging Study

Primary aldosteronism is most often caused by aldosterone-producing adenoma (APA) and bi-lateral adrenal hyperplasia. Most APAs are caused by somatic mutations of various ion channels and pumps, the most common being the inward-rectifying potassium channel KCNJ5. Germ line mutations of KCNJ5 cause familial hyperaldosteronism type 3 (FH3), which is associated with severe hyperaldosteronism and hypertension. We present an unusual case of FH3 in a young woman, first diagnosed with primary aldosteronism at the age of 6 years, with bilateral adrenal hyperplasia, who underwent unilateral adrenalectomy (left adrenal) to alleviate hyperaldosteronism. However, her hyperaldosteronism persisted. At the age of 26 years, tomography of the remaining adrenal revealed two different adrenal tumors, one of which grew substantially in 4 months; therefore, the adrenal gland was removed. A comprehensive histological, immunohistochemical, and molecular evaluation of various sections of the adrenal gland and in situ visualization of aldosterone, using matrix-assisted laser desorption/ionization imaging mass spectrometry, was performed. Aldosterone synthase (CYP11B2) immunoreactivity was observed in the tumors and adrenal gland. The larger tumor also harbored a somatic β-catenin activating mutation. Aldosterone visualized in situ was only found in the subcapsular regions of the adrenal and not in the tumors. Collectively, this case of FH3 presented unusual tumor development and histological/molecular findings.     

Comprehensive Re-Sequencing of Adrenal Aldosterone Producing Lesions Reveal Three Somatic Mutations near the KCNJ5 Potassium Channel Selectivity Filter

Background

Aldosterone producing lesions are a common cause of hypertension, but genetic alterations for tumorigenesis have been unclear. Recently, either of two recurrent somatic missense mutations (G151R or L168R) was found in the potassium channel KCNJ5 gene in aldosterone producing adenomas. These mutations alter the channel selectivity filter and result in Na⁺ conductance and cell depolarization, stimulating aldosterone production and cell proliferation. Because a similar mutation occurs in a Mendelian form of primary aldosteronism, these mutations appear to be sufficient for cell proliferation and aldosterone production. The prevalence and spectrum of KCNJ5 mutations in different entities of adrenocortical lesions remain to be defined.

Materials and Methods

The coding region and flanking intronic segments of KCNJ5 were subjected to Sanger DNA sequencing in 351 aldosterone producing lesions, from patients with primary aldosteronism and 130 other adrenocortical lesions. The specimens had been collected from 10 different worldwide referral centers.

Results

G151R or L168R somatic mutations were identified in 47% of aldosterone producing adenomas, each with similar frequency. A previously unreported somatic mutation near the selectivity filter, E145Q, was observed twice. Somatic G151R or L168R mutations were also found in 40% of aldosterone producing adenomas associated with marked hyperplasia, but not in specimens with merely unilateral hyperplasia. Mutations were absent in 130 non-aldosterone secreting lesions. KCNJ5 mutations were overrepresented in aldosterone producing adenomas from female compared to male patients (63 vs. 24%). Males with KCNJ5 mutations were significantly younger than those without (45 vs. 54, respectively; p<0.005) and their APAs with KCNJ5 mutations were larger than those without (27.1 mm vs. 17.1 mm; p<0.005).

Discussion

Either of two somatic KCNJ5 mutations are highly prevalent and specific for aldosterone producing lesions. These findings provide new insight into the pathogenesis of primary aldosteronism.     

Primary aldosteronism caused by unilateral adrenal hyperplasia

In the hypertensive population, primary aldosteronism has been reported to have a prevalence of 0.1% to 2%, with the main causes being aldosterone-producing adenomas and bilateral hyperplasia. However, there is a third rare entity, called unilateral adrenal hyperplasia, that contributes to primary aldosteronism. Unilateral hyperplasia and primary aldosteronism are the subjects of this case review.     

HPLC isolation and GC-MS characterization of a compound strongly cross reacting with tetrahydroaldosterone antiserum

Urines from patients with hypertension and elevated aldosterone levels, i.e. primary aldosteronism due to adrenal adenoma or hyperplasia or carcinoma were extracted, paper chromatographed and thereafter chromatographed repeatedly with normal phase and repeatedly with reversed phase HPLC systems in an attempt to find new metabolites of aldosterone. Specific 3 alpha-hydroxy-5 beta-tetrahydroaldosterone antiserum was used in a radioimmunoassay system to detect possible aldosterone metabolites in the HPLC fractions after each isolation step. The immunoactive HPLC fractions were derivatized and analysed by GC-MS. A relatively nonpolar compound, 11 beta:18(S),18:20 alpha-diepoxy-5 beta-pregnan-3 alpha-ol, was isolated and identified in this manner. This material was originally described by Kelly et al., in 1962 after loading human subjects with huge amounts (25-160 mg) of exogenous aldosterone. This material has not yet been described from endogenously produced aldosterone. Very small amounts, if any, were similarly isolated from the urine of a control subject. Therefore, this compound could prove to be a new marker for hypertension due to hyper-production of aldosterone.     

Personalized Treatment of Patients With Primary Aldosteronism

Primary aldosteronism (PA) is a highly prevalent yet underdiagnosed secondary cause of hypertension. PA is associated with increased cardiovascular and renal morbidity compared with patients with primary hypertension. Thus, prompt identification and targeted therapy of PA are essential to reduce cardiovascular and renal morbidity and mortality in a large population with hypertension. Unilateral adrenalectomy is preferred for lateralized PA as the only potentially curative therapy. Surgery also mitigates the risk of cardiovascular and renal complications associated with PA. Targeted medical therapy, commonly including a mineralocorticoid receptor antagonist, is offered to patients with bilateral PA and those who are not surgical candidates. Novel therapies, including nonsteroidal mineralocorticoid receptor antagonists and aldosterone synthase inhibitors, are being developed as alternative options for PA treatment. In this review article, we discuss how to best individualize therapy for patients with PA.     

Hypertension outcomes of adrenalectomy in patients with primary aldosteronism: a systematic review and meta-analysis

Background

The hypertension cure rate of unilateral adrenalectomy in primary aldosteronism (PA) patients varies widely in existing studies.

Methods

We conducted an observational meta-analysis to summarize the pooled hypertension cure rate of unilateral adrenalectomy in PA patients. Comprehensive electronic searches of PubMed, Embase, Cochrane, China National Knowledge Internet (CNKI), WanFang, SinoMed and Chongqing VIP databases were performed from initial state to May 20, 2016. We manually selected eligible studies from references in accordance with the inclusion criteria. The pooled hypertension cure rate of unilateral adrenalectomy in PA patients was calculated using the DerSimonian–Laird method to produce a random-effects model.

Results

Forty-three studies comprising approximately 4000 PA patients were included. The pooled hypertension cure rate was 50.6% (95% CI: 42.9–58.2%) for unilateral adrenalectomy in PA. Subgroup analyses showed that the hypertension cure rate was 61.3% (95% CI: 49.4–73.3%) in Chinese studies and 43.7% (95% CI: 38.0–49.4%) for other countries. Furthermore, the hypertension cure rate at 6-month follow-up was 53.3% (95% CI: 36.0–70.5%) and 49.6% (95% CI: 40.9–58.3%) for follow-up exceeding 6 months. The pooled hypertension cure rate was 50.9% (95% CI: 40.5–61.3%) from 2001 to 2010 and 50.2% (95% CI: 39.0–61.5%) from 2011 to 2016.

Conclusions

The hypertension cure rate for unilateral adrenalectomy in PA is not optimal. Large clinical trials are required to verify the utility of potential preoperative predictors in developing a novel and effective prediction model.

     

Twenty-Four hour blood pressure profile in subjects with different subtypes of primary aldosteronism

The aim of our study was to evaluate the potential differences in blood pressure (BP) profile in subjects with different forms of primary aldosteronism (PA). Simultaneously, we studied the effects of PA treatment on BP curve. We therefore monitored 24-hour ambulatory blood pressure values in 22 subjects with aldosterone-producing adenoma (APA), 22 subjects with idiopathic hyperaldosteronism (IHA) and 33 subjects with essential hypertension (EH) as controls. We found a significantly attenuated nighttime systolic BP decline in the APA group (P=0.02). Patients with IHA had lower nighttime systolic BP values (P=0.01) and also a diastolic BP decline (P=0.02) during the night in comparison with EH. We did not detect any significant differences in BP profile characteristics between APA and IHA. Specific treatment of primary aldosteronism (adrenalectomy, treatment with spironolactone) led to the normalization of the BP curve with a marked BP decline. Our study thus demonstrates a blunted diurnal BP variability in patients with primary aldosteronism the specific treatment of which normalized previously attenuated nocturnal BP fall.     

Prolonged pseudoaldosteronism induced by glycyrrhizin.

We describe the natural recovery from the aggravated hypertension, hypokalemia and suppression of the renin-aldosterone axis after the glycyrrhizin discontinuation in two mild hypertensive women aged 71 and 68 years, who had been administered 273 to 546 mg glycyrrhizin daily for 1.5 and 6 months, respectively, for the treatment of liver disease. About one month after the glycyrrhizin discontinuation, acceleration of hypertension, hypokalemia and suppression of the renin-aldosterone system still continued in both patients. At this stage, sodium restriction resulted in the normalization of blood pressure with weight loss and the subsequent sodium repletion produced a rapid increase in blood pressure to hypertensive levels observed before sodium restriction, with weight gain. Plasma renin activity and plasma aldosterone were low and did not respond to sodium restriction. Inappropriately excessive amounts of potassium were also excreted in the presence of hypokalemia. About one and a half months later, the improvements of aggravated hypertension, hypokalemia and suppressed renin-aldosterone system gradually occurred in both patients. Sodium restriction performed about three months later in case 2 no longer produced the changes in blood pressure and body weight. Plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. These results demonstrate that both patients had a prolongation of the syndrome resembling primary aldosteronism except the low plasma aldosterone level about one month after the glycyrrhizin discontinuation. The possible mechanisms by which this prolongation was caused are discussed.     

Long-term consequences of surgical excision of cortisol producing adrenocortical adenoma

INTRODUCTION: Surgical excision of adrenocortical tumour in patients with ACTH-independent Cushing syndrome gives a chance for their entire cure. However in some patients after adrenalectomy persistent arterial hypertension, obesity and diabetes mellitus is observed. The aim of the study was to analyse long term consequences of surgical excision of cortisol producing adrenocortical adenoma with a special attention on the influence of adrenalectomy on arterial blood pressure. MATERIAL AND METHODS: 15 patients (mean age 54 years) suffering from arterial hypertension (n = 15), obesity or overweight (n = 12) and diabetes mellitus (n = 7) were subjected to analysis. Mean follow up time was 45 months. RESULTS: Improvement of blood pressure control after unilateral adrenalectomy was observed in 66.7% of patients. The risk factor of no improvement of blood pressure control was BMI > 30.5 kg/m(2) (RR = 4.0 [1.07-14.90]). During the follow up period decrease of maximal values of systolic and diastolic blood pressure was observed (34 [17-50] and 25 [16-35] mm Hg respectively; p < 0.01). In the entire group of patients a 3.4 kg/m(2) decrease of BMI was observed p = 0.01. BMI decreased significantly (more than 1 kg/m(2)) in 66.7% of patients. Only in 2 patients a complete regression of diabetes was observed. 46.7% of patients required supplementation with adrenal steroids. 40% of patients reported a subjective withdrawal of all symptoms of the disease after surgery and 46.7% only partial remission. CONCLUSION: Surgical excision of cortisol producing adrenocortical adenoma results in improvement of blood pressure control and body weight reduction in a large percentage of patients with Cushing syndrome. Obesity before adrenalectomy is the factor that reduces a chance for improvement of blood pressure control after surgery.