Microcephalic osteodysplastic primary dwarfism type II (MOPDII) is a form of primordial nanism characterized by extreme short stature, microcephaly, specific phenotype, maxillofacial dysmorphisms, skeletal dysplasia, disorders of carbohydrate metabolism, and neurovascular abnormalities. This article describes a patient with a Seckel syndrome phenotype presenting with left internal carotid artery aneurysms with intracerebral hemorrhages, thrombocytosis, arterial hypertension, and diabetes mellitus due to insulin resistance confirmed by a low Matsuda index. Target carbohydrate metabolism values were achieved on metformin therapy. Clinical exome sequencing revealed two rare heterozygous variants in the PCNT gene: c.6220C>T (p.Gln2074*) and c.4564-12T>A. Comparison of the results of the molecular genetic study and the patient's phenotype allowed us to verify the diagnosis of MOPDII. Hypergonadotropic hypogonadism was described for the first time in this syndrome.

Tamsulosin, a selective α1-adrenergic antagonist prescribed for benign prostatic hyperplasia and expulsion of ureteral stones, carries a rare risk of priapism. We present a 59-year-old male with hypogonadism, hypertension, and hyperlipidemia who developed painless priapism 72 hours after initiating tamsulosin for ureterolithiasis. Despite the atypical absence of pain, penile blood gas analysis confirmed ischemic priapism. Initial treatment with intracavernosal phenylephrine (1000 mcg) failed, requiring bilateral corpus spongiosum shunts for resolution. A literature review revealed that many of the 14 existing cases identified occurred within 24 hours of drug initiation in middle-aged or older patients without additional risk factors. Approximately half responded to intracavernosal vasoconstrictors, while refractory cases required surgical intervention. To our knowledge, this is the first reported case of painless tamsulosin-induced ischemic priapism, emphasizing the importance of patient counseling and prompt evaluation of persistent erections regardless of pain intensity.

Age-related hearing loss is a progressive bilateral sensorineural loss that increases steeply with age, contributing to communication disabilities and social isolation, impacting healthy aging. Across diverse cohorts, men tend to develop earlier and more severe high-frequency threshold elevations than age-matched women. This male disadvantage is partly explained by gender-related lifetime exposure (e.g., occupational noise, smoking), likely reflecting interactions with biological sex factors, including steroid signaling and mitochondrial susceptibility. Sex differences in cochlear physiology are detectable from infancy, including larger otoacoustic emissions in female newborns, supporting developmental endocrine influences. Adult men usually exhibit earlier and steeper high-frequency declines. Conversely, studies in menopausal women have indicated heterogeneity rather than a uniform female inflection point. Mechanistic studies have demonstrated inner-ear estrogen receptor expression and context-dependent otoprotection. However, human epidemiology does not support uniform auditory benefits from menopausal hormone therapy; rather, long-term oral estrogen or estrogen plus progestogen use may increase the risk of hearing loss. Evidence for androgen pathways is emerging, albeit limited. In older men, higher serum testosterone, but not dehydroepiandrosterone sulfate, is associated with lower odds of high-frequency hearing loss. The precise mechanisms and clinical effects of exogenous hormone therapies on auditory aging remain uncertain. This review synthesizes current evidence using a life-course "multi-hit" framework. Rather than pointing to a single biological driver, we describe how innate susceptibilities such as the aging endocrine axis and mitochondrial variation interact with male-predominant ototoxic exposure and cardiometabolic comorbidities to shape auditory dimorphisms. Addressing current knowledge gaps requires sex-stratified longitudinal research integrating precise endocrine profiling with functional auditory outcomes. Clinically, although endocrine pathways are not yet therapeutic targets, understanding this multidimensional vulnerability highlights the utility of risk-stratified screening. Incorporating proactive hearing assessment into routine evaluations of aging men, particularly those with late-onset hypogonadism, can facilitate early detection, timely rehabilitation, and possible downstream cognitive benefit.

Late-Onset Hypogonadism (LOH), also known as male menopause syndrome, is a common health problem plaguing middle-aged and elderly men. Its core pathophysiological change lies in the progressive decline of testosterone levels in men with age. This leads to a series of symptoms involving sexual function, physical, and psychological aspects, seriously affecting the quality of life and overall health of patients. The core pathophysiological link of LOH lies in the progressive decline of testosterone levels caused by the reduction in the number and functional decline of Leydig cells (LCs). As the cell source of LCs, Stem Leydig cells (SLCs) play an indispensable role in maintaining testosterone homeostasis and testicular endocrine function. Compared to other stem cells, the localization of SLCs in testicular tissue enables them to directly sense and respond to various paracrine factors and signaling molecules from adjacent somatic cells and the testicular interstitial fluid, thereby achieving precise regulation of their self-renewal and differentiation potential. The functional decline of SLCs and the impaired adaptability in the aging microenvironment are the key intrinsic mechanisms for the occurrence and development of LOH. The discovery of SLCs and the clarification of their biological characteristics have opened up a brand-new perspective for understanding the pathogenesis of LOH and exploring innovative treatment strategies. The aim of this review is to systematically sort out the research progress of SLCs in LOH, with a view to providing a deeper theoretical basis and potential targets for the prevention and treatment of LOH.

Pituitary metastases from pulmonary large cell neuroendocrine carcinoma (LCNEC) are exceedingly rare but should be considered in patients presenting with arginine vasopressin deficiency and panhypopituitarism in the context of known or suspected metastatic lung cancer. Early recognition and prompt initiation of hormonal replacement therapy are essential to prevent life-threatening endocrine crises and to improve symptom burden. We describe a case of a 43-year-old male who presented with dyspnea, weight loss, and weakness who was found to have metastatic LCNEC involving the liver. Endocrine evaluation revealed central hypothyroidism, central adrenal insufficiency, and later arginine vasopressin deficiency manifested by polyuria and hypernatremia. Additional pituitary testing demonstrated central hypogonadism and growth hormone deficiency consistent with panhypopituitarism. Magnetic resonance imaging showed a sellar mass with pituitary stalk thickening consistent with metastatic disease. Alternative infectious and infiltrative etiologies were excluded. Although the prognosis remains poor due to the aggressive nature of LCNEC, this case underscores the importance of a multidisciplinary approach with endocrinology, oncology, and palliative care to optimize management and quality of life in patients with advanced disease.

Rod-cone dystrophy (RCD) is an inherited retinal disorder primarily affecting rod photoreceptors, followed by cone degeneration. We present the case of a 26-year-old male with RCD and multiple systemic abnormalities (atrial septal defect, hypogonadism, liver disease with gastric varices, hypertriglyceredemia, hypothyroidism, adrenal insufficiency, and delayed epiphyseal closure) in the same individual. Ophthalmic evaluation revealed retinal pigment epithelial atrophy, bone spicule pigmentation, a macular hole in the right eye, and an epiretinal membrane in the left. Genetic testing identified a heterozygous ABCA4 c.3113C>T (p.Ala1038Val) mutation, previously associated with retinal dystrophies. We postulate that this case represents a unique blended phenotype, i.e., retinal disease due to ABCA4 and multiple systemic issues due to an unidentified syndrome.

Obesity is a major global health challenge strongly associated with increased cardiometabolic morbidity and mortality. In men, obesity is characterized by a predominance of visceral adiposity, which is metabolically active and closely linked to systemic inflammation, hormonal dysregulation, and adverse cardiovascular outcomes. Despite its clinical relevance, male obesity remains underrecognized as a distinct pathophysiological condition. This study aimed to analyze the inflammatory mechanisms underlying male obesity and their relationship with cardiometabolic risk. A structured narrative review was conducted based on a PICo-guided research question, with literature searches performed in PubMed/MEDLINE, Scopus, Web of Science, Embase, and ScienceDirect, covering publications from 2015 to 2026. Studies focusing on male obesity, inflammatory pathways, and cardiometabolic outcomes were included. Evidence indicates that visceral adipose tissue acts as an active endocrine organ, releasing pro-inflammatory cytokines such as TNF-α and IL-6, contributing to chronic low-grade inflammation. This inflammatory state is associated with insulin resistance (IR), endothelial dysfunction, and oxidative stress, mediated by intracellular pathways including NF-κB and JNK. Additionally, adipokine imbalance, characterized by reduced adiponectin and increased leptin levels, further exacerbates metabolic and vascular impairment. Hormonal alterations, particularly reduced testosterone levels, play a key role in amplifying visceral fat accumulation and inflammation, creating a bidirectional relationship between hypogonadism and metabolic dysfunction. Clinically, these mechanisms highlight the importance of integrating inflammatory biomarkers, body composition assessment, and hormonal evaluation into the management of male obesity. Emerging therapies, including GLP-1 receptor agonists and immunometabolic interventions, offer promising strategies for reducing cardiometabolic risk. In conclusion, male obesity represents a complex, inflammation-driven condition requiring a comprehensive and mechanism-based approach to improve clinical outcomes and guide future therapeutic developments.

Male hypogonadism is associated with metabolic and cardiovascular comorbidities, and emerging evidence implicates testosterone deficiency in immune dysregulation that may elevate cancer risk. To review current evidence on the relationship between male hypogonadism, immune function, and cancer risk, focusing on mechanisms linking testosterone deficiency to immune suppression and oncologic outcomes. PubMed/MEDLINE, Google Scholar, and SciSpace were systematically searched (through April 2026) using predefined search strings. After removal of duplicates (n = 1535 records screened), 156 full-text articles were assessed for eligibility; 20 studies met predefined inclusion criteria (comprising 4 experimental studies, 4 prospective/RCT studies, 7 observational studies, and 5 reviews used as secondary literature) and were included in a narrative synthesis. Testosterone deficiency was consistently associated with elevated IL-6, TNF-α, IL-1β, and CRP, impaired neutrophil maturation, and reduced NK-cell cytotoxicity. Androgen deprivation augmented thymic output and anti-tumor T cell responses in prostate cancer models, yet promoted chronic inflammation in other contexts. Epidemiologically, low testosterone correlated with increased colorectal cancer risk and poorer survival in advanced malignancies; the prostate cancer relationship followed a paradoxical saturation model. The immunological consequences of hypogonadism are context-dependent. Testosterone deficiency drives pro-inflammatory signaling that may promote carcinogenesis, while androgen-mediated immunosuppression can paradoxically impair anti-tumor surveillance. No simple linear relationship exists between hypogonadism and cancer risk via immune suppression. Prospective studies are needed to guide clinical decisions on testosterone replacement therapy in hypogonadal men.