Reports from Asian populations have suggested that chronic hepatitis B virus (HBV) infection may predispose patients to hearing impairment, particularly sudden sensorineural hearing loss, yet evidence from Europe has been lacking. To address this gap, we conducted a nationwide, retrospective analysis of the prevalence of ear and hearing disorders among patients hospitalized with HBV infection in Poland between 2012 and 2023, using the national hospital discharge database. Hospital records with ICD-10 codes for acute or chronic HBV infection were examined, and cases with concomitant ear or hearing disorders were identified. In total, 80,181 HBV-related hospitalizations were recorded, of which 36.6% represented first-time admissions, while the remainder were repeat hospitalizations. Diagnoses of hearing loss were rare, occurring in only 0.05% of first-time and 0.04% of all hospitalizations, and all affected patients were adults. Hearing loss diagnoses, including those encompassing both conductive and sensorineural forms, were exceptionally uncommon. Notably, conditions most frequently discussed in the context of HBV, such as sensorineural hearing loss, were rare and showed no tendency to recur across repeated admissions. Importantly, the prevalence of hearing disorders in this HBV-infected cohort was substantially lower than that reported for the general population, suggesting no increased prevalence of auditory disorders among patients with HBV infection in this setting. These findings indicate that, in contrast to observations from parts of Asia, chronic HBV infection is not associated with an increased prevalence of hearing impairment in this European population. Discrepancies with Asian studies likely reflect multiple regional factors, including differences in HBV genotype distribution, disease characteristics, healthcare practices, and host or environmental influences, rather than genotype alone.

Drug-induced renal injury (DIRI) remains a substantial issue in clinical practice, contributing to high morbidity, mortality, socioeconomic and healthcare cost. Traditional markers, such as serum creatinine or blood urea nitrogen, have low specificity and sensitivity for early identification, underscoring the need for new reliable biomarkers. This chapter investigates biomarker improvements for DIRI, focusing on clinical uses, limitations, and future possibilities. The chapter examines biomarkers such as neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, cystatin C, β2-microglobulin and clusterin for diagnosing nephrotoxicity. In addition, we highlight the role of proteomics and metabolomics in facilitating the identification and development of novel biomarker candidates via high-throughput ultra-sensitive technology in investigating DIRI mechanisms. The chapter discusses validation frameworks, regulatory criteria for biomarker adoption in clinical settings, and how they are integrated into treatment monitoring and personalized medicine. Case examples demonstrate the real-world applicability in early diagnosis, risk classification, and therapy optimization. Standardization, cost, and translational gaps are discussed, as well as the potential for artificial intelligence and machine learning to improve biomarker processing and interpretation. Finally, this chapter emphasizes the transformative potential of DIRI biomarkers in providing a pathway to more accurate and timely identification of renal injury, improved patient outcomes, and reduced healthcare costs. Future research and global collaboration are required to fully realize the potential of these advances in clinical and regulatory settings.

This issue of the Biomedical Journal explores emerging perspectives across neuropsychiatry, metabolism, aging, regenerative medicine, artificial intelligence, and chronic inflammatory disease. Featured contributions examine epigenetic and neuroendocrine mechanisms in depression, including the antidepressant-like effects of magnolol in chronic stress-induced models and the potential relevance of short-chain fatty acids as biomarkers and therapeutic targets in major depressive disorder. Additional reviews address evolutionary and metabolic dimensions of liver disease, artificial intelligence-assisted imaging approaches in lymphedema, immunological senotherapeutic strategies, developmental origins of cardiovascular-kidney-metabolic syndrome, and the risks associated with short-term corticosteroid exposure. Original investigations further examine dopaminergic signaling during acute deprivation, molecular mechanisms of axonal regeneration, lipid peroxidation in pulmonary fibrosis, hypothalamic NPFFR2 signaling in metabolic dysfunction, neurobehavioral consequences of occlusal disharmony, and fall risk following cataract surgery with blue-light-filtering intraocular lenses. A correspondence exchange additionally discusses the diagnostic scope and limitations of elastase pretreatment in ALK fluorescence in situ hybridization analysis for non-small cell lung cancer.

Cytomegalovirus (CMV) is a ubiquitous herpesvirus infecting a large proportion of the population worldwide. Clinical manifestations range from asymptomatic infection to severe disease with multi-organ involvement, depending primarily on host immune status. CMV hepatitis is an uncommon clinical presentation. In pregnancy, infection is usually asymptomatic in immunocompetent women; however, transplacental transmission may occur, leading to congenital infection. Congenital CMV is the most common congenital viral infection. This report describes the case of a 30-year-old pregnant woman with acute CMV infection acquired during the first trimester. The disease manifested as hepatitis, with ALT and AST levels reaching up to 31-fold and 15-fold above the upper limits of normal, respectively. Gradual improvement was observed with supportive treatment, and the outcome was favourable for both mother and child. The infant was delivered at term and has shown normal development; at 8 years of age, the only reported condition is lactose intolerance.

Miscellaneous equine liver conditions not covered in other chapters include chronic active hepatitis, Tyzzer's disease, seasonal idiopathic hepatitis, neoplasia, and idiopathic persistent hyperbilirubinemia. Chronic active hepatitis refers to inflammatory and fibrotic liver disease with an unknown cause. Treatment is aimed at reducing inflammation. Tyzzer's disease is caused by Clostridium piliforme infection and causes acute necrotizing hepatitis in foals. Successful treatment with antimicrobial therapy and supportive care is rare. Seasonal idiopathic hepatitis is a winter disease of Midwestern horses. The cause is unknown but the prognosis is excellent with supportive care. Primary hepatic neoplasia and idiopathic persistent hyperbilirubinemia are rare.

Hepatitis E virus (HEV) is a recognized cause of acute hepatitis and a potential trigger of acute decompensation (AD) and acute-on-chronic liver failure (ACLF) in patients with cirrhosis in hyperendemic regions; however, its clinical relevance in low-endemic settings remains poorly defined. We conducted a combined cross-sectional and prospective longitudinal study to evaluate the prevalence and clinical impact of HEV infection among patients with cirrhosis in Argentina. Adult patients with mild-to-moderate cirrhosis (Child-Pugh score 6-12) of different etiologies were tested for anti-HEV IgG and IgM antibodies by ELISA and HEV RNA by RT-PCR in serum samples. Epidemiological data were collected using a structured questionnaire. In the longitudinal cohort, patients were followed for up to 24 months with serial sampling at baseline, every 6 months, and during episodes of hepatic decompensation. Anti-HEV IgG seroprevalence was 5.2% (95% CI: 2.2-11.5%), comparable to that observed in healthy blood donors, with no significant differences across cirrhosis etiologies. No patient had detectable anti-HEV IgM or HEV RNA at baseline. During follow-up, 19 patients developed hepatic decompensation, including six cases of ACLF; three patients showed anti-HEV IgG positivity, including one seroconversion, but none had evidence of acute HEV infection. These findings indicate limited HEV exposure among patients with cirrhosis in this low-endemic region and suggest that HEV infection is unlikely to represent a major trigger of AD or ACLF, although continued surveillance remains warranted.

This study investigated the role of microglia-derived insulin-like growth factor 1 (IGF-1) in modulating host defense and disease progression in a viral model of neuroinflammation and demyelination. Intracranial infection of susceptible mice with the glial-tropic JHM strain of mouse hepatitis virus (JHMV) induces acute encephalomyelitis, followed by an immune-mediated demyelinating disease that mimics many clinical and histologic features of multiple sclerosis (MS). Utilizing an inducible fractalkine receptor (Cx3cr1) promoter-driven Cre-loxP recombinant system, we performed timed ablation of Igf1 in microglia to assess its impact on the central nervous system (CNS) response to JHMV. While the loss of microglial IGF-1 did not impair the control of viral replication, it significantly exacerbated spinal cord demyelination. CyTOF and imaging mass cytometry analysis of spinal cords indicated increased myelin damage was associated with increased accumulation of CD8[+]Ly6C[+] effector T cells and reduced expression of TREM2 that impaired transition into a disease-associated microglia (DAM) phenotype capable of sensing and potentially mitigating myelin damage. Collectively, these findings argue that microglial IGF-1 is a non-redundant coordinator of the CNS immune responses that occur in response to CNS viral infection.