Primary aldosteronism (PA) and obstructive sleep apnea (OSA) are both considered independent risk factors for hypertension, which can lead to an increase in cardiovascular disease incidence and mortality. Clinical studies have found a bidirectional relationship between OSA and PA. However, the underlying mechanism between them is not yet clear. This study aims to investigate the shared genetic characteristics and potential molecular mechanisms of PA and OSA. We obtained microarray datasets of aldosterone-producing adenoma (APA) and OSA from the gene expression omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was used to select co-expression modules associated with APA and OSA, and common genes of the two diseases were obtained by intersection. Subsequently, hub genes for APA and OSA were identified through functional enrichment analysis, protein-protein interaction (PPI), datasets, and public database. Finally, we predicted the transcription factors (TFs) and mirRNAs of the hub genes. In total, 52 common genes were obtained by WGCNA. The Gene Ontology (GO) of common genes includes interleukin-1 response, cytokine activity, and chemokine receptor binding. Functional enrichment analysis highlighted the TNF, IL-17 signaling, and cytokine-cytokine receptor interactions related to APA and OSA. Through PPI, datasets, and public databases verification, we identified 5 hub genes between APA and OSA (IL6, ATF3, PTGS2, CCL2, and CXCL2). Our study identified shared 5 hub genes between APA and OSA (IL6, ATF3, PTGS2, CCL2, and CXCL2). Through bioinformatics analysis, we found that the 2 disorders showed relative similarity in terms of inflammation, stress, and impaired immune function. The identification of hub genes may offer potential biomarkers for the diagnosis and prognosis of PA and OSA.

Hypertension does not recognize obvious pathogenic causes in the majority of patients (essential hypertension). However, a secondary underlying cause of hypertension can be recognized in 5-10% of unselected hypertensive patients, and this prevalence may increase to more than 20% in patients with hypertension that is difficult to control or frankly resistant to treatment. In children, secondary hypertension is most often due to aortic coarctation, distal thoracic or abdominal aortic stenosis, or specific gene mutations. In adults or elderly individuals, secondary hypertension is most often due to atherosclerotic renal artery stenosis, primary hyperaldosteronism, and Cushing\'s disease or syndrome. Parenchymal nephropathy and hyperparathyroidism can cause hypertension at all ages, while pheochromocytoma and paraganglioma tend to occur more often in adolescents or young adults. In general, secondary hypertension should be suspected in subjects with: (a) onset of hypertension under 30 years of age especially if in the absence of hypertensive family history or other risk factors for hypertension; (b) treatment-resistant hypertension; c) severe hypertension (>180/110 mmHg), malignancy, or hypertensive emergencies; d) rapid rise in blood pressure values in previously well controlled patients. Any clinical signs suspicious or suggestive of hypertension from endocrine causes, a \"reverse dipping\" or \"non-dipping\'\" profile at 24 h ambulatory blood pressure monitoring not justified by other factors, signs of obvious organ damage may be helpful clues for diagnosis. Finally, patients snoring or with clear sleep apnea should also be considered for possible secondary hypertension.

We report a case of a ruptured triple hormone-secreting adrenal mass with hyperaldosteronism, hypercortisolism, and elevated normetanephrine levels, diagnosed as adrenal cortical carcinoma (ACC) by histology. A 53-year-old male patient who initially presented with abdominal pain was referred to our hospital for angiocoagulation of an adrenal mass rupture. Abdominal computed tomography revealed a heterogeneous 19×11×15 cm right adrenal mass with invasion into the right lobe of the liver, inferior vena cava, retrocaval lymph nodes, and aortocaval lymph nodes. Angiocoagulation was performed. Laboratory evaluation revealed excess cortisol via a positive 1-mg overnight dexamethasone suppression test, primary hyperaldosteronism via a positive saline infusion test, and plasma normetanephrine levels three times higher than normal. An adrenal mass biopsy was performed for pathological confirmation to commence palliative chemotherapy because surgical management was not deemed appropriate considering the extent of the tumor. Pathological examination revealed stage T4N1M1 ACC. The patient started the first cycle of adjuvant mitotane therapy along with adjuvant treatment with doxorubicin, cisplatin, and etoposide, and was discharged. Clinical cases of dual cortisol- and aldosterone-secreting ACCs or ACCs presenting as pheochromocytomas have occasionally been reported; however, both are rare. Moreover, to the best of our knowledge, a triple hormone-secreting ACC has not yet been reported. Here, we report a rare case and its management. This case report underscores the necessity of performing comprehensive clinical and biochemical hormone evaluations in patients with adrenal masses because ACC can present with multiple hormone elevations.

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BACKGROUND: Primary aldosteronism (PA) is the most common secondary endocrine cause of hypertension with familial hyperaldosteronism type 1 (FH-1), a rare heritable subtype. Timely identification of FH-1 is important because of an increased risk of vascular events in affected individuals and because it provides the opportunity to guide appropriate treatment. Genetic testing is recommended if onset is at a young age (<20 years), there is a family history of PA or early cerebrovascular events occur.
OBJECTIVE: To assess national rates of testing for FH-1, whether this varied over time and by region.
METHODS: De-identified data were obtained on genetic testing performed for FH-1 from 1 April 2010 to 30 October 2023 (163 months) from the Canterbury Health Laboratories database, the sole national testing laboratory for FH-1.
RESULTS: A total of 147 tests were performed, of which 19 (12.9%) were positive. Eleven of the positive tests were requested by one region. Testing rates varied from 0.00 to 0.63 per 100 000 people per annum. Most tests were requested by endocrinology services. Testing increased over time from an average of 4.6 tests per annum in the first 5 years of the period studied to 17.7 tests in the most recent 5 years. Limitations include lack of ethnicity data, information on testing indications and testing rates for other familial PA subtypes.
CONCLUSIONS: Testing for FH-1 has increased over time but remains low. Testing for familial forms of PA should be considered in those in whom PA was diagnosed at a young age or with a suggestive family history.

Hypokalaemia is a common electrolyte disorder affecting hospitalised patients. It is associated with adverse outcomes including increased mortality. Inpatients with hypokalaemia need a different approach to workup and management as the aetiologies and progression of the hypokalaemia are distinct to outpatients. Potassium homeostasis is predominantly maintained by renal potassium handling. The clinical manifestations of hypokalaemia depend on the severity of hypokalaemia, however, most of the findings are non-specific. The approach to management is guided by the severity of the hypokalaemia and the underlying aetiology. Oral potassium replacement can be used in many cases of mild hypokalaemia. Intravenous replacement of potassium is necessary for many inpatients. Close monitoring is essential to ensure adequacy and to prevent adverse outcomes. An interdisciplinary approach with critical care input is needed in severe cases, and in patients where routine intravenous replacement may not be feasible (e.g., patients with heart failure). In addition to replacement, the cornerstone of management is a comprehensive review of the patient to identify the underlying cause of the hypokalaemia and the factors sustaining it. In patients in whom the cause is not apparent, or the potassium does not improve as anticipated, a referral to nephrology or endocrinology should be considered. This paper reviews the assessment of hypokalaemia in a hospital setting. It is aimed at early career doctors on the wards to help carry out a thorough evaluation. It also provides a useful framework for management.

BACKGROUND: Adrenal vein sampling (AVS), integral to identifying surgically remediable unilateral primary aldosteronism (PA), is technically challenging and subject to fluctuations in cortisol and aldosterone secretion. Intra-procedural adrenocorticotropic hormone (ACTH), conventionally administered as a 250-μg bolus and/or 50 μg per hour infusion, increases cortisol and aldosterone secretion and can improve AVS success, but may cause discordant lateralisation compared to unstimulated AVS.
OBJECTIVE: To assess if AVS performed with ultra-low dose ACTH infusion causes discordant lateralisation.
METHODS: Here, we describe our preliminary experience using an ultra-low dose ACTH infusion AVS protocol. We retrospectively reviewed the results of consecutive AVS procedures (n = 37) performed with and without ultra-low dose ACTH (1-μg bolus followed by 1.25 μg per hour infusion).
RESULTS: Bilateral AV cannulation was successful in 70% of procedures pre-ACTH and 89% post-ACTH (p < 0.01). Sixty-nine percent of studies lateralised pre-ACTH and 55% post-ACTH, improving to 79% when both groups were combined. Lateralisation was discordant in 11 cases, including eight in which lateralisation was present only on basal sampling, and three in which lateralisation occurred only with ACTH stimulation.
CONCLUSIONS: Overall, the decrease in lateralisation rates with ACTH was higher than previously reported for some protocols utilising conventional doses of ACTH. Our results suggest that AVS performed with ultra-low dose ACTH can cause discordant lateralisation similar to AVS performed with conventional doses of ACTH.
CONCLUSIONS: Prospective studies directly comparing low and conventional dose ACTH AVS protocols and long-term patient outcomes are needed to help define the optimal ACTH dose for accurate PA subtyping.

BACKGROUND: Primary aldosteronism is the most frequent cause of hypertension although is undetected. The 2016 Endocrine Society guidelines (2016-ESG) recommendations for primary aldosteronism detection are unfulfilled. We aimed to ascertain the prevalence of primary aldosteronism, following the screening criteria endorsed by the 2016-ESG.
METHODS: All adult patients tested for primary aldosteronism at an endocrine hypertension unit of a tertiary hospital during 2021-2023 were studied. Primary aldosteronism investigation was performed when at least one reason for its screening based on 2016-ESG was detected. When screening was positive, confirmatory tests were executed. Rates and diagnostic accuracy of the reasons for primary aldosteronism screening were analyzed.
RESULTS: Two hundred and sixty-five patients were included. Mean age was 55 ± 14 years, 124 of 265 (46.8%) were women, 24.6% had hypokalemia, and 16% adrenal incidentaloma(s) as indication for screening. Primary aldosteronism was diagnosed in 122 of 265 (46%). The presence of each reason for primary aldosteronism screening increased the probability of primary aldosteronism in 2.2-fold [95% confidence interval (CI): 1.63 to 2.97; P < 0.001]. The most frequent reason for primary aldosteronism screening was a blood pressure at least 150/100 mmHg on three measurements on different days, and had a sensitivity of 95%. Hypertension with spontaneous or diuretic-induced hypokalemia was the most specific reason (87.5%) but was not frequent. Adrenal incidentaloma(s) was not associated with primary aldosteronism diagnosis.
CONCLUSIONS: Primary aldosteronism prevalence is markedly high when the 2016-ESG recommendations are rigorously implemented. The greater the number of indications for primary aldosteronism investigation, the higher its prevalence. Further studies are needed to corroborate this observed primary aldosteronism prevalence.

Aldosterone-producing adenoma is a subtype of primary aldosteronism. Recent advancements in multi-omics research have led to significant progress in understanding primary aldosteronism at the genetic level. Among the various genes associated with the development of aldosterone-producing adenomas, the KCNJ5 (potassium inwardly rectifying channel, subfamily J, member 5) gene has received considerable attention due to its prevalence as the most common somatic mutation gene in primary aldosteronism. This paper aims to integrate the existing evidence on the involvement of KCNJ5 gene in the pathogenesis of aldosterone-producing adenomas, to enhance the understanding of the underlying mechanisms of aldosterone-producing adenomas from the perspective of genetics, and to provide novel insights for the clinical diagnosis and treatment of aldosterone-producing adenomas.

原发性醛固酮增多症（原醛症）的诊断分为筛查、确诊及分型3个步骤，其中筛查是实现早期诊断的关键。而降压药是最常见的影响因素，但常用降压药是否影响醛固酮/肾素筛查效能，能否不停常用降压药进行原醛症筛查，是目前原醛症的热点讨论话题之一。本文就这一话题进行文献复习和总结，探索筛查原醛症的高效、可行的策略和路径。.