Background: Despite a general improvement in the HIV burden over the past two decades, gendered social determinants including intimate partner violence (IPV) continue to affect women’s vulnerability to HIV, which could be further exacerbated as resources dwindle over the coming years. Our study aimed to quantify recent trends in the HIV burden, the magnitude of the HIV burden associated with IPV, and the potential impact of declining financial support globally.

Methods: Using the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2023 framework, we estimated annual HIV incidence, prevalence, and mortality for 204 countries and territories from 1990 to 2023, disaggregated by age and sex. Input data included national HIV programme reports, population-based serosurveys, clinical and vital registration data, and systematically reviewed literature. Countries and territories were grouped according to the availability and completeness of HIV prevalence and mortality data, with tailored modelling approaches applied for each group. To characterize the potential contributions of IPV to the HIV burden, time series estimates of IPV prevalence by location and effect size estimates were combined to generate population attributable fractions of the HIV burden. To forecast future trends and assess the potential impact of reductions in development assistance for health, we used a non-parametric stochastic frontier approach to estimate how funding levels could affect antiretroviral therapy (ART) coverage. Adjustments in future ART coverage were integrated into our forecasts, altering projected rates of HIV-related incidence and mortality. We compared scenarios with and without funding cuts, quantifying the potential epidemiological effects of reduced ART availability by sex.

Findings: Between 2003 and 2023, the annual number of new HIV infections declined globally, from 2·85 million (95% uncertainty interval [UI] 2·76–2·96) to 2·06 million (1·88–2·29). Meanwhile, HIV-related deaths decreased from a peak of 1·71 million (1·61–1·83) in 2004 to 0·83 million (0·73–0·96) in 2023. The number of people living with HIV rose from 26·3 million (25·5–27·3) in 2003 to 42·4 million (40·3–44·4) in 2023, reflecting improved survival associated with ART expansion. Although females continued to have higher prevalence of HIV than males in 2023 (23·4 million [22·2–24·6] vs 19·1 million [17·6–20·5]), the gap in incidence between females and males has substantially declined. Regionally, sub-Saharan Africa had the greatest declines in both incidence (64·3%; 58·0–68·6) and mortality (74·6%; 70·4–78·5) between 2003 and 2023, while central Europe, eastern Europe, and central Asia recorded the highest increases in incidence rates (232·1%; 146·5–299·1) and mortality rates (37·8%; 31·2–45·5) during this period. IPV was associated with an estimated 10·7% (1·6–20·4) of HIV-related deaths among females aged 15 years and older globally in 2023, corresponding to 40 700 (6400–80 600) deaths, with the highest population attributable fractions observed in Oceania (17·4%; 2·8–33·1), central sub-Saharan Africa (14·2%; 2·1–29·4), and eastern sub-Saharan Africa (13·2%; 2·0–25·3). Forecasts indicate that funding reductions could decrease ART coverage by 8·1% globally between 2025 and 2030, resulting in approximately 1·6 million new HIV infections among females and 1·3 million new HIV infections among males, alongside 790 600 and 670 600 HIV-related deaths, respectively. These impacts are primarily concentrated in sub-Saharan Africa.

Interpretation: Despite two decades of substantial progress, the global HIV response remains highly sensitive to gendered social determinants and funding stability. The potential contribution of IPV to HIV-related mortality among women underscores the need for integrated interventions that address violence prevention and post-violence care alongside HIV treatment. The projected effects of funding cuts—millions of additional infections and deaths—highlight the fragility of the gains achieved and the urgent need to protect HIV financing. Achieving and sustaining the UNAIDS 2030 targets will require renewed investment, gender-responsive programming, and resilient health systems capable of providing equitable access to care.

A middle-aged adult presented with non-severe alcoholic hepatitis after 3 years of daily whisky intake (80–100 mL/day). He was noted to have persistent erythrocytosis (haemoglobin 186 g/L; haematocrit 53.8%) without leucocytosis or thrombocytosis and with normal serum erythropoietin. Secondary causes were evaluated, including hypoxia, cardiac and renal disease, and myeloproliferative neoplasms; Janus Kinase 2 Valine 617 Phenylalanine (JAK2 V617F) and JAK 2 exon 12 testing were negative. Despite intravenous hydration and reported complete alcohol abstinence, erythrocytosis persisted for several weeks after hepatic biochemistry improved. A bone marrow biopsy was planned but deferred when haemoglobin and haematocrit normalised spontaneously by 10 weeks. Overall, the presentation was most consistent with presumed alcohol-associated stress (relative) erythrocytosis, which may show delayed resolution after cessation, and careful longitudinal follow-up may avoid premature invasive investigations once polycythaemia vera and clinically important secondary causes have been reasonably excluded.

Intravenous albumin has established roles in decompensated cirrhosis, particularly following large-volume paracentesis and in patients with spontaneous bacterial peritonitis or hepatorenal syndrome-acute kidney injury. Emerging evidence suggests that albumin may also improve hepatic encephalopathy through its antioxidant, immunomodulatory, endothelial-stabilizing, and toxin-scavenging effects. A recent systematic review and meta-analysis of four randomized controlled trials involving 306 patients reported improved recovery from hepatic encephalopathy and reduced mortality with albumin administration, without a significant increase in adverse events. However, the available evidence remains promising rather than definitive because the required information size for mortality was not achieved. In patients with decompensated cirrhosis, multiple albumin indications frequently coexist, creating important questions regarding clinical prioritization, particularly in resource-limited settings where cost and availability restrict treatment. Albumin may be most justifiable when hepatic encephalopathy occurs alongside established indications such as spontaneous bacterial peritonitis, acute kidney injury, hepatorenal syndrome, systemic inflammation, or circulatory dysfunction. Routine administration for isolated hepatic encephalopathy should remain cautious until larger trials identify the patients most likely to benefit. Future studies should evaluate hepatic encephalopathy severity, renal dysfunction, infection, inflammatory status, volume status, albumin dosage, pulmonary complications, hospitalization outcomes, readmissions, affordability, and cost-effectiveness. Albumin represents a promising adjunctive treatment for hepatic encephalopathy, but future research must determine not only its efficacy but also where its use is most necessary, safe, and feasible.

Intravenous albumin has established roles in decompensated cirrhosis, particularly following large-volume paracentesis and in patients with spontaneous bacterial peritonitis or hepatorenal syndrome-acute kidney injury. Emerging evidence suggests that albumin may also improve hepatic encephalopathy through its antioxidant, immunomodulatory, endothelial-stabilizing, and toxin-scavenging effects. A recent systematic review and meta-analysis of four randomized controlled trials involving 306 patients reported improved recovery from hepatic encephalopathy and reduced mortality with albumin administration, without a significant increase in adverse events. However, the available evidence remains promising rather than definitive because the required information size for mortality was not achieved. In patients with decompensated cirrhosis, multiple albumin indications frequently coexist, creating important questions regarding clinical prioritization, particularly in resource-limited settings where cost and availability restrict treatment. Albumin may be most justifiable when hepatic encephalopathy occurs alongside established indications such as spontaneous bacterial peritonitis, acute kidney injury, hepatorenal syndrome, systemic inflammation, or circulatory dysfunction. Routine administration for isolated hepatic encephalopathy should remain cautious until larger trials identify the patients most likely to benefit. Future studies should evaluate hepatic encephalopathy severity, renal dysfunction, infection, inflammatory status, volume status, albumin dosage, pulmonary complications, hospitalization outcomes, readmissions, affordability, and cost-effectiveness. Albumin represents a promising adjunctive treatment for hepatic encephalopathy, but future research must determine not only its efficacy but also where its use is most necessary, safe, and feasible.

Background: Tuberculosis (TB) involving the central nervous system (CNS) can present as tuberculoma and may mimic neoplasms or vascular lesions, particularly when the brainstem is involved. Early recognition is critical in endemic settings such as India.

Case presentation: A previously healthy female in late adolescence presented with a one-month history of headache followed by progressive left-sided weakness and multiple cranial nerve deficits, producing a crossed brainstem syndrome. Magnetic resonance imaging (MRI) of the brain revealed conglomerated ring-enhancing lesions in the midbrain and pons, accompanied by surrounding edema. Magnetic resonance spectroscopy (MRS) demonstrated a lipid–lactate peak. Cerebrospinal fluid (CSF) analysis and systemic laboratory investigations were within normal limits. Empirical anti-tubercular therapy (ATT) with adjunctive corticosteroids was initiated, with clinical improvement noted within two weeks and continued gains on follow-up.

Discussion: Brainstem tuberculoma can closely mimic brainstem stroke and other mass lesions. In endemic regions, characteristic MRI/MRS findings should prompt consideration of tuberculoma even when CSF findings are normal. Early treatment may prevent the need for invasive diagnostic procedures and improve outcomes.

Conclusion: Brainstem tuberculoma should be considered an important differential diagnosis in young patients presenting with crossed brainstem signs in TB-endemic regions. A combination of characteristic imaging findings and high clinical suspicion can support the early initiation of ATT with adjunctive corticosteroids, which, in this case, was associated with prompt and favorable neurological recovery.

Aluminium phosphide is a highly lethal pesticide that liberates phosphine gas, leading to mitochondrial dysfunction, distributive shock and cardiotoxicity, but guidance on late pulmonary complications is limited. We report a previously healthy adolescent who ingested ~1.5 g of aluminium phosphide in a suicide attempt and initially presented haemodynamically stable with metabolic acidosis and elevated lactate. By 72–96 hours, she developed progressive hypoxemic respiratory failure with bilateral infiltrates fulfilling Berlin criteria for moderate acute respiratorydistress syndrome (ARDS) (PaO?/FiO? nadir ?115 on FiO? 1.0), preceded by fever and culture-proven lower respiratory and urinary tract infections, resulting in sepsis and disseminated intravascular coagulation (DIC). She required escalation from non-invasive to invasive mechanical ventilation, with lung-protective strategies, targeted antibiotics, component therapy for DIC and early magnesium and calcium supplementation. Despite markedly elevated N-terminal pro-B type natriuretic peptide with preserved biventricular function on echocardiography and transient acute kidney injury, she made a full clinical recovery and was discharged with normal oxygenation and functional status. This case underscores that delayed moderate ARDS with superimposed sepsis and DIC can complicate initially stable aluminium phosphide poisoning and highlights that meticulous, protocol-based supportive care can still result in survival in this rarely reported scenario.

Gallbladder ascariasis is an uncommon manifestation of ascaris lumbricoides infection, typically seen in the endemic regions. Even rarer is the concurrent presence of Löffler’s syndrome. We report the two cases – the first, a 92?year?old male, presented with typical biliary colic and was diagnosed with gallbladder ascariasis. The second, a 38?year?old female, presented with respiratory symptoms and was found to have ground?glass opacities on high?resolution computed tomography and peripheral eosinophilia, later associated with gallbladder ascariasis on imaging. Both cases were managed conservatively with anthelminthic therapy and supportive care. This series highlights both the hepatobiliary and pulmonary presentations of ascaris lumbricoides infection.

Introduction A comprehensive evaluation of metabolic dysfunction-associated steatotic liver disease (MASLD) prevalence among hypothyroid patients and its correlation with hepatic stiffness, particularly using advanced diagnostic tools like transient elastography (TE) and serological parameters, has yet to be fully explored. Methods A cross-sectional study was conducted involving patients with subclinical or overt hypothyroidism.MASLD was diagnosed by ultrasonography, and hepatic stiffness was assessed by TE. Patients were stratified by MASLD severity and hepatic stiffness, and statistical analyses, including logistic regression, were performed. Results We found a high prevalence (47%) of MASLD in hypothyroid patients. A positive correlation was found between TSH levels and both the severity of fatty liver and hepatic stiffness. Hepatic steatosis was found in 34.38% of people who were subclinical hypothyroid (SCH), and 60.29% of people who were overt hypothyroid. The prevalence of hepatic stiffness was 27.3% (9.38% in SCH and 44.12% in overt hypothyroid). Serum total thyroxine (T4) levels were inversely associated with MASLD severity, and logistic regression revealed a positive association between TSH and hepatic steatosis and fibrosis. Conclusion In this cohort of individuals with hypothyroidism, MASLD and fibrosis markers were common, and higher TSH levels were associated with greater steatosis and fibrosis severity, including after adjustment for body mass index within the cohort. Controlled studies with matched euthyroid comparators are required to confirm whether hypothyroidism independently increases MASLD risk at the population level.