Ashley Denisse Ayala Ochoa

Endocrine-metabolic disorders are increasingly recognized as major determinants of cardiovascular risk because their effects extend beyond alterations in glucose and lipid metabolism and involve inflammatory, vascular, and hemostatic pathways. This review analyzed the interaction between endocrine-metabolic abnormalities, the development of a prothrombotic state, and cardiovascular risk, with particular emphasis on obesity, insulin resistance, type 2 diabetes mellitus, metabolic syndrome, thyroid dysfunction, and hypercortisolism. A structured integrative review was conducted using scientific evidence from clinical guidelines, systematic reviews, meta-analyses, mechanistic studies, and epidemiological investigations. The findings showed that obesity, diabetes mellitus, and metabolic syndrome presented the greatest overlap of pathophysiological mechanisms, particularly chronic inflammation, oxidative stress, endothelial dysfunction, platelet hyperreactivity, coagulation activation, and impaired fibrinolysis. Coagulation activation was one of the most consistently identified pathways, while reduced fibrinolytic capacity, frequently associated with increased plasminogen activator inhibitor-1 activity, contributed to thrombus persistence. Diabetes was additionally associated with structural alterations of fibrin and increased platelet responsiveness, whereas visceral adiposity was linked to inflammatory and procoagulant signaling. Thyroid dysfunction and hypercortisolism also demonstrated relevant hemostatic alterations, supporting the broader relationship between endocrine regulation and thrombosis. Overall, the evidence indicates that cardiovascular risk in endocrine-metabolic disease results from an interconnected network in which metabolic dysfunction promotes inflammation and oxidative stress, followed by endothelial injury, platelet and coagulation activation, impaired fibrinolysis, and ultimately atherothrombotic events. The prothrombotic state therefore represents an important intermediate pathophysiological phenotype between endocrine-metabolic dysfunction and cardiovascular disease. These findings support comprehensive cardiovascular prevention and highlight the need for future studies evaluating integrated metabolic and hemostatic biomarkers for improved risk stratification.

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) has emerged as one of the most prevalent chronic liver diseases worldwide and represents a growing challenge for healthcare systems due to its close relationship with obesity, insulin resistance, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome. This review aimed to integrate current scientific evidence regarding the epidemiology, pathophysiology, clinical progression, diagnosis, treatment, and emerging role of precision medicine in MASLD. International scientific literature was reviewed through recognized biomedical databases, incorporating original studies, systematic reviews, meta-analyses, clinical practice guidelines, and international consensus statements relevant to the disease. The evidence demonstrates a substantial global burden of MASLD, with particularly high prevalence estimates reported in Latin America and other regions experiencing rapid growth in cardiometabolic disorders. Disease progression is heterogeneous, ranging from hepatic steatosis to metabolic dysfunction-associated steatohepatitis, advanced fibrosis, cirrhosis, and hepatocellular carcinoma, with fibrosis representing one of the most important predictors of adverse clinical outcomes. Advances in non-invasive biomarkers, serum-based fibrosis scores, transient elastography, and magnetic resonance-based techniques have improved risk stratification and reduced dependence on liver biopsy. Lifestyle modification remains fundamental to treatment, while emerging pharmacological therapies provide additional opportunities for patients with specific metabolic and hepatic profiles. The integration of clinical characteristics, metabolic phenotype, fibrosis stage, imaging findings, and biological markers supports the transition toward precision medicine. MASLD should therefore be approached as a multisystem metabolic disease requiring early identification, multidisciplinary management, comprehensive cardiometabolic control, and individualized therapeutic strategies to reduce progression and long-term complications.

Chronic kidney disease (CKD) without diabetes mellitus has become an increasingly recognized clinical entity whose progression cannot be explained exclusively by traditional hemodynamic mechanisms. Growing evidence indicates that endocrine dysregulation, metabolic remodeling, mitochondrial dysfunction, chronic inflammation, oxidative stress, and altered communication between the kidney and other organ systems play fundamental roles throughout disease development and progression. The present review critically analyzes current scientific evidence regarding the endocrine and metabolic mechanisms involved in non-diabetic CKD, integrating findings from nephrology, endocrinology, and internal medicine while incorporating information relevant to Latin American populations. A narrative review based on the Scientific Method was conducted using high-quality publications retrieved from internationally recognized databases and clinical practice guidelines. The available evidence demonstrates that persistent activation of the renin–angiotensin–aldosterone system, disruption of the fibroblast growth factor 23–Klotho axis, impaired vitamin D metabolism, insulin resistance, obesity-related endocrine alterations, mitochondrial dysfunction, and gut–kidney interactions contribute substantially to renal fibrosis, progressive loss of kidney function, and cardiovascular complications. Contemporary therapeutic approaches, particularly sodium–glucose cotransporter-2 inhibitors, have significantly modified disease management by providing nephroprotective effects beyond glycemic control. Emerging biomarkers and precision medicine strategies also show considerable potential for improving early diagnosis, individualized risk assessment, and targeted therapeutic interventions. Nevertheless, additional multicenter studies, particularly involving underrepresented regions such as Latin America, remain necessary to strengthen the current evidence base. Overall, non-diabetic CKD should be regarded as a complex multisystem disorder requiring an integrated clinical approach that combines endocrine, metabolic, cardiovascular, and nephrological perspectives to optimize patient outcomes.

Hidden hearing loss (HHL) has emerged as an important topic in auditory medicine because many individuals experience significant communication difficulties despite presenting normal pure-tone audiometric thresholds. This review critically analyzes current international evidence regarding the epidemiology, pathophysiology, clinical manifestations, diagnostic challenges, and therapeutic perspectives associated with HHL, with particular emphasis on cochlear synaptopathy and its implications for clinical practice. A narrative literature review was conducted using the Scientific Method as the methodological framework. Scientific publications indexed in PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar were reviewed, prioritizing original investigations, systematic reviews, meta-analyses, and clinical guidelines published in peer-reviewed journals. The evidence indicates that speech-in-noise perception deficits, tinnitus, listening fatigue, and temporal auditory processing impairments represent the most frequently reported manifestations among individuals with suspected HHL. Occupational and recreational noise exposure, together with physiological aging, were consistently identified as the principal risk factors. Although conventional pure-tone audiometry remains essential for hearing assessment, it demonstrates limited sensitivity for detecting early neural dysfunction. Complementary evaluations, including speech-in-noise testing, auditory brainstem responses, extended high-frequency audiometry, and other electrophysiological techniques, provide additional diagnostic information; however, no single method currently constitutes a definitive diagnostic standard. The reviewed literature supports the implementation of multimodal diagnostic strategies integrating behavioral, physiological, and clinical findings. Furthermore, the analysis highlights the need for standardized diagnostic criteria, objective biomarkers, multicenter investigations, and increased scientific participation from Latin America. Hidden hearing loss represents an evolving multidisciplinary concept that expands the understanding of auditory dysfunction beyond conventional audiometry and emphasizes the importance of comprehensive patient-centered evaluation to improve early recognition, clinical management, and future research.