Inhibitors of the renin-angiotensin-aldosterone system remain foundational therapies for arterial hypertension across major international guidelines. Their effectiveness, however, may be partially attenuated by the phenomenon of aldosterone escape, characterized by chronic elevation of adrenal aldosterone due to activation of alternative enzymatic pathways. Mineralocorticoid receptor antagonists are recommended as first-line therapy for resistant hypertension, yet their clinical utility is limited by poor adherence and high discontinuation rates, driven largely by hyperkalaemia and sex hormone-related adverse effects such as gynaecomastia, impotence, and menstrual irregularities. Recent pharmacologic research has focused on alternative strategies for suppressing aldosterone activity, particularly through the development of selective aldosterone synthase inhibitors (ASIs). This approach has led to the emergence of highly selective agents such as baxdrostat and lorundrostat. Clinical studies have demonstrated meaningful reductions in blood pressure among patients with resistant or uncontrolled hypertension, with favourable tolerability and without clinically significant adverse events. Further studies are required to determine the impact of ASIs on hypertensive-mediated organ damage, major cardiovascular events, nephrovascular outcomes, and long-term safety.

BACKGROUND Kennedy disease, also known as spinal and bulbar muscular atrophy (SBMA), is a rare and incurable X-linked neuromuscular disorder mainly affecting men aged 30 to 60 years. Polymyositis can present similarly, but can be excluded by measuring muscle enzymes, performing muscle imaging, and electromyography. This report describes the case of a 52-year-old man with a 10-year history of progressive limb weakness due to Kennedy disease, established by genetic testing. CASE REPORT A 52-year-old man presented with a 10-year history of gradually progressive proximal limb weakness and persistently elevated creatine kinase levels ranging from 808-2300 U/L (normal 39-308 U/L). One year prior to this admission, the limb weakness had worsened, but initial electromyography, neuroimaging, and muscle biopsy showed no specific abnormalities. Despite a trial of immunosuppressive therapy due to suspected polymyositis, there was no clinical improvement. Neurological examination later revealed gynecomastia, proximal muscle atrophy, and bilateral tongue atrophy with tremor. Electromyography showed chronic neurogenic changes and reduced sensory nerve action potentials. Repeat expansion analysis identified a hemizygous pathogenic CAG repeat expansion in exon 1 of the androgen receptor gene using a short-read next-generation sequencing-based repeat detection algorithm (ExpansionHunter), with an estimated repeat number of 51 (range 50-53). At 6-month follow-up, the patient demonstrated mild progression of motor symptoms but remained functionally stable. CONCLUSIONS This report presents a rare case of Kennedy disease, initially diagnosed as polymyositis, and highlights the importance of follow-up with genetic testing when neurological and electromyography investigations are not typical for polymyositis. Early identification of Kennedy disease helps avoid unnecessary immunosuppressive treatments.

End-stage kidney disease (ESKD) patients receiving dialysis bear a heavy burden of cardiovascular disease (CVD), the leading cause of mortality. Mineralocorticoid receptor antagonists (MRAs) have cardiovascular protective effects in non-dialysis patients, but their efficacy and safety in dialysis-dependent individuals remain controversial. This study aimed to clarify their clinical value via an updated systematic review and meta-analysis. Following preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines, we systematically searched PubMed, EMBASE, and The Cochrane Library up to 25 August 2025. Eligible studies were parallel-design randomized controlled trials (RCTs) enrolling adults (≥18 years) on maintenance dialysis, comparing MRAs with placebo or no intervention. Two reviewers independently screened studies, extracted data, and assessed quality using the Cochrane Risk of Bias Tool 2.0. Meta-analysis was performed with Cochrane Review Manager 5.4. The results showed that a total of 14 RCTs involving 4,525 patients were included (13 used spironolactone, one used eplerenone; follow-up: 3-40.8 months). MRAs significantly reduced nonfatal CVD events (RR 0.68, p = 0.04) but had no significant effect on cardiovascular mortality (RR 0.75, p = 0.14) or all-cause mortality (RR 0.76, p = 0.05). They significantly elevated risks of severe hyperkalemia (RR 1.35, p = 0.009) and gynecomastia and breast pain (RR 4.23, p < 0.001). In conclusion, MRAs can reduce the incidence of nonfatal cardiovascular events in dialysis patients; however, clinicians also need to be mindful of the risks of severe hyperkalemia as well as gynecomastia and breast pain in men when prescribing them.

Gynecomastia is a relatively common condition arising from disproportionate concentrations of estrogen and androgen. Most cases of bilateral gynecomastia in men are idiopathic or drug-induced but can rarely arise secondary to malignancy. We present the case of a 57-year-old male who presented with new-onset gynecomastia and recurrent episodes of hematuria. Laboratory testing revealed elevated estradiol, free testosterone, and β-human chorionic gonadotropin (β-hCG) with suppressed luteinizing hormone (LH) and follicle stimulating hormone (FSH), concerning for ectopic β-hCG secretion. Mammography, breast and testicular ultrasonography, and chest computed tomography demonstrated no evidence of breast, testicular, or lung malignancy. Concurrent evaluation of hematuria with cystoscopy identified a 6-cm tumor on the posterior bladder wall. The patient underwent transurethral resection of the bladder tumor and was diagnosed with papillary high-grade T1 urothelial carcinoma. The β-hCG immunohistochemical staining of the tumor was positive, and the patient's β-hCG level was undetectable 1 month postoperatively. A review of the literature revealed there are only a few reports detailing urothelial carcinomas capable of secreting β-hCG. To the best of our knowledge, this is the first case of a β-hCG-secreting papillary T1 urothelial carcinoma initially presenting as gynecomastia.

Gynecomastia is the most common breast condition in pediatric and young adult males, yet large-scale studies evaluating its etiologies, risk factors, and management remain scarce. In adolescents, gynecomastia is most frequently idiopathic or obesity-related, while secondary causes are rarer. Persistent presentations may cause psychosocial distress and lead to surgical correction, though the optimal diagnostic approach remains controversial. We conducted a retrospective, population-based study of 19,640 males aged 10-25 years with documented gynecomastia diagnosis, extracting demographic and clinical variables including age, body mass index (BMI) Z-scores, family history, comorbidities, medication exposure, and surgical status. Reporting was in accordance with the STROBE guidelines. Most patients were idiopathic (74.3%), followed by medication-related (23.1%) and pathology-associated (3.4%). For patients with pathology-associated cases compared with other etiologies, the mean age and mean BMI Z-score were higher, and surgeries were more frequent (all p < 0.001). The prevalence of pathology increased with age, whereas obesity-related and familial cases predominated in younger children. Morbid obesity was significantly associated with higher surgical rates (5.2% vs. 2.1% in non-obese, p < 0.001). Independent associations with surgical intervention included older age (odds ratio (OR 1.20), higher BMI Z-score (OR 1.30), ≥2 affected siblings (OR 8.35), and testicular tumors (OR 14.06). Model discrimination (area under the curve = 0.973) was excellent. In conclusion, gynecomastia in younger boys is primarily idiopathic or obesity-related, while older adolescents are more often diagnosed with secondary causes. Age- and risk-tailored diagnostic strategies, including early screening for obesity, family history, and medication exposure may optimize management and guide surgical decision-making.

Nonmedical anabolic-androgenic steroid (AAS) use is increasingly encountered in sexual medicine practice, often presenting through sexual symptoms or fertility concerns rather than overt systemic illness. This review summarizes the major health consequences of AAS abuse with emphasis on sexual and reproductive sequelae and provides a pragmatic approach to evaluation and recovery after cessation. AAS exposure commonly suppresses the hypothalamo-pituitary-gonadal axis, leading to hypogonadism and hormonal imbalance that may manifest as reduced libido, erectile dysfunction, gynecomastia, and impaired spermatogenesis ranging from severe oligozoospermia to azoospermia. Recovery after discontinuation is heterogeneous: endocrine parameters frequently normalize earlier than semen parameters, and prolonged/high-dose exposure is associated with delayed or incomplete recovery in a clinically meaningful subset. Beyond sexual and reproductive harm, convergent observational evidence supports increased cardiovascular risk (remodeling, dysfunction, and adverse events), hepatic injury (particularly with 17α-alkylated agents), hematologic/prothrombotic changes, tendon pathology, neuropsychiatric symptoms, and dermatologic complications, with risk shaped by dose, duration, and polypharmacy. In the absence of robust randomized trials, management should prioritize AAS cessation and relapse prevention. Clinicians should actively screen for organ-specific sequelae and individualize follow-up based on symptom burden, hormonal status, fertility goals, and time since last exposure, with selective use of pharmacological induction of recovery when clinically appropriate.

Limited information indicates that maternal doses of aripiprazole up to 15 mg daily produce low levels in milk. Aripiprazole can lower serum prolactin in a dose-related manner, and cases of poor milk supply and lactation cessation have been reported. Weight loss and poor weight gain have been reported in breastfed infants whose mothers were taking aripiprazole. Monitor the breastfed infant for dehydration and lack of appropriate weight gain. Cases of gynecomastia and galactorrhea have also been reported. Until more data become available, an alternate drug may be preferred, especially while nursing a newborn or preterm infant.[1]

Gynecomastia is a frequent cause of male breast enlargement and may result from physiological, pathological, or drug-induced mechanisms. Ultrasound offers a dynamic, non-invasive assessment that goes beyond image depiction, helping to differentiate gynecomastia from pseudogynecomastia and identify morphological stages. Typical sonographic patterns support clinical decisions, guide additional laboratory or imaging workup, and allow early recognition of suspicious features suggestive of malignancy. While mammography retains value in older patients or when cancer is suspected, ultrasound is generally the preferred first-line modality, providing essential information for accurate diagnosis and individualized management.

We report a rare case of a 72-year-old man with prostatic adenocarcinoma metastasizing to gynecomastia breast tissue with ipsilateral axillary lymph node involvement. This presentation is notable for the absence of disseminated metastatic disease or prolonged androgen deprivation therapy. The clinical and radiological features initially suggested a primary breast carcinoma, highlighting the diagnostic challenge in such presentations. The patient had a history of high-risk prostate adenocarcinoma resected in 2020. A prostate-specific membrane antigen (PSMA) PET scan, performed for rising prostate-specific antigen (PSA) levels, demonstrated a new avid left breast lesion within longstanding bilateral gynecomastia tissue. The pattern of PSMA uptake, including involvement of ipsilateral axillary lymph nodes, further increased suspicion for a locally advanced primary breast carcinoma. Core biopsy of the breast lesion and fine-needle aspiration of the axillary lymph node were consistent with metastatic prostate adenocarcinoma, which was subsequently confirmed on surgical excision. This case adds to the limited literature describing prostate cancer metastasis to the breast and underscores the diagnostic challenges such presentations can create. It demonstrates how metastatic disease can closely mimic primary breast malignancy, reinforcing the importance of histopathological confirmation when imaging findings suggest a primary breast lesion.

We report the case of a 52-year-old man with a metastatic right testicular Sertoli cell tumor. The patient presented with fatigue, anorexia, unintentional weight loss, and bilateral gynecomastia. Staging computed tomography revealed pleural, hepatic, and bone metastases. Laboratory evaluation demonstrated markedly elevated estradiol and testosterone levels with suppressed gonadotropins. Histopathological analysis of a metastatic soft-tissue lesion confirmed the diagnosis. A multidisciplinary approach combining BEP (bleomycin, etoposide, and cisplatin) chemotherapy with hormonal therapy using letrozole and goserelin was initiated. Despite treatment, disease progression was observed, and enrollment in a clinical trial was considered. The patient ultimately died one month later due to respiratory failure. This case highlights the aggressive behavior of metastatic Sertoli cell tumors and underscores the challenges in managing rare, hormone-producing, treatment-refractory testicular neoplasms.