One of the main objectives of the WHO is the elimination of viral hepatitis by 2030 (with targets of a 90% reduction in new infections and a 65% reduction in mortality). Globally, an estimated 50 million people are infected with HCV. Several reports demonstrate that the COVID-19 pandemic has reduced HCV diagnoses and treatments in most countries, with few countries on track to meet the 2030 HCV elimination targets, underscoring the need to scale up interventions to achieve viral hepatitis elimination. Based on these premises, this review evaluates the burden of HCV infection in Africa, disparities among population groups, and clinical outcomes observed over the past four years, based on a comprehensive search of the Scopus, Web of Science, PubMed, and African Index Medicus databases from 1 May 2022 to 1 May 2026. Recent studies are concentrated in a limited number of countries, while in many others, they appear to be confined to blood donors and specific clinical populations. The findings of clinical epidemiology studies show that chronic HCV infection continues to be a cause of liver-related morbidity and mortality in Africa, with notable differences across regions. A heavier disease burden appears in high‑risk groups, such as people with HIV infection, people who practice high‑risk sexual behaviours and people who inject drugs. These findings confirm the need to focus on interventions by policymakers and clinicians, including barrier reduction, screening, prevention, and linkage to care for at‑risk populations to reduce HCV transmission and its effects.
Benign recurrent intrahepatic cholestasis (BRIC) is a rare inherited cholestatic disorder whose diagnosis is usually confirmed by genetic testing. However, access to molecular diagnostics remains limited in many low- and middle-income countries. Here, we report a 38-year-old Cambodian man presenting with his first episode of severe cholestatic jaundice and pruritus. Extensive investigations excluded infectious, autoimmune, metabolic, and obstructive causes. Liver biopsy reviewed by a French expert reference center demonstrated isolated cholestasis, supporting the diagnosis of BRIC despite the absence of genetic confirmation. The patient achieved complete clinical and biochemical remission during follow-up. This case illustrates that BRIC can be diagnosed with high confidence using established clinical criteria when genetic testing is unavailable and highlights the value of international collaboration in improving rare disease diagnosis in resource-limited settings.
BACKGROUND:The coexistence of Pancreatic cancer (PC) with diabetes mellitus (DM) and metabolic disorders (MDs) may further exacerbate the disease burden; however, the long-term mortality trends remain unclear. METHODS:We utilized the CDC WONDER database to extract mortality data for PC and its comorbidities with diabetes mellitus and metabolic disorders among the U.S. population aged 25 and older from 1999 to 2023. We calculated the Age-Adjusted Mortality Rate (AAMR) and employed Joinpoint regression analysis to assess the average annual percentage change (AAPC), stratifying the data by sex, age, race, region, and urbanization level. RESULTS:The annual AAMR for PC in the United States increased from 16.41 (95% CI: 16.22 to 16.60) to 17.33 (95% CI: 17.17 to 17.48), with an AAPC of 0.24 (95% CI: 0.19 to 0.30). The AAMR of PC with DM also increased, with an AAPC of 2.21 (95% CI: 1.52 to 2.89; p < 0.001), while PC with MDs showed a steeper increase, with an AAPC of 5.45 (95% CI: 4.86 to 6.03; p < 0.001). The highest AAMR was observed among males, non-Hispanic blacks, and patients in Southern, Midwestern and nonmetropolitan areas, with a particularly notable increase in non-urban regions. CONCLUSIONS:The mortality rate associated with PC and its metabolic comorbidities continues to rise, indicating the need to strengthen early screening and metabolic management for high-risk populations.
BACKGROUND:Portal vein thrombosis (PVT) is a challenging complication of cirrhosis, associated with adverse outcomes. Clinical management of PVT remains complex and demanding. METHODS:We performed a retrospective study involving 1562 cirrhotic patients from six medical centers, among whom 222 were diagnosed with chronic non-tumoral PVT. These PVT patients were categorized into four primary treatment groups: watch-and-wait follow-up alone (n=38), anticoagulation monotherapy (n=85), isolated TIPS creation (n=32), and TIPS combined with postoperative warfarin anticoagulation (n=67). For secondary efficacy analyses, the anticoagulation group was further divided into three medication subgroups (warfarin, LMWH, rivaroxaban), resulting in five analytical subgroups in total. Risk factors for PVT were analyzed in the entire cirrhotic cohort. Therapeutic efficacy and safety were compared across subgroups. Outcomes were evaluated between patients with and without PVT, TIPS-treated PVT patients with and without post-TIPS anticoagulation, and PVT patients receiving different anticoagulants. RESULTS:Ascites, variceal disease, and the Model for End-Stage Liver Disease (MELD) score were associated with the development of chronic PVT. No significant differences in recanalization or rethrombosis rates were observed among patients receiving different anticoagulants. Adjunctive postoperative anticoagulation significantly improved early portal venous recanalization compared with TIPS monotherapy. The MELD score, but not anticoagulant use, was associated with an increased bleeding risk. After adjusting for confounding factors, PVT, anticoagulant type, and post-TIPS anticoagulation were not associated with poor outcomes. CONCLUSIONS:The severity of cirrhosis is linked to PVT development. Individualized PVT therapy enables safe and high-probability recanalization. TIPS expands therapeutic options for decompensated cirrhotic patients with PVT.
BACKGROUND:We studied the safety and effectiveness of glucagon-like peptide-1 receptor agonists (GLP1-RAs) and sodium-glucose co-transporter-2 inhibitors (SGLT2is) in liver transplant recipients with diabetes. METHODS:This retrospective single-center study included 41 patients treated with GLP1-RAs and/or SGLT2is after liver transplantation (LT) who were compared to a control group receiving antidiabetic treatment excluding GLP1-RAs and/ SGLT2is. RESULTS:The treatment group showed no serious adverse events, with 15.0% experiencing moderate side effects, primarily gastrointestinal disorders. The HbA1c target concentration was achieved in 90.0% (n=36) of patients in the GLP1-RA and/or SGLT2i group versus 74.0% (n = 42) in the control-group (p = 0.16). The fasting glycaemia target was reached by a higher proportion of patients in the GLP1-RA and/or SGLT2i group than in the control-group: 80.0% versus 55.0%, p = 0.033. Insulin withdrawal was greater in the group of patients receiving GLP1-RAs and/or SGLT2is treatment, in particular for those with post-transplant diabetes (80.0% vs. 0%, p < 0.01). The median time of follow-up was 11.0 months (IQR: 6-13). CONCLUSIONS:Our results suggest the safety of GLP1-RAs and SGLT2is treatment, with the remarkable benefit of insulin withdrawal for a subgroup of patients with new-onset diabetes. However, larger prospective studies are needed to assess the long-term impact on cardiovascular events, obesity, liver steatosis, and mortality.
BACKGROUND:Metabolic dysfunction-associated steatotic liver disease (MASLD) is now the leading cause of chronic liver disease and is tightly linked to obesity, insulin resistance and type 2 diabetes. There are limited drugs approved for MASLD, creating an urgent need to repurpose agents with favourable metabolic and organ-protective profiles. Empagliflozin, a sodium-glucose cotransporter-2 (SGLT-2) inhibitor with established cardiovascular and renal benefits, has emerged as a promising candidate, but trial-level evidence remains fragmented. METHODS:We performed a systematic review and meta-analysis of randomized controlled trials evaluating empagliflozin in adults with imaging-confirmed MASLD or related entities. Searches of PubMed/MEDLINE, Embase, Web of Science, Scopus, and major trial registries were conducted. Continuous outcomes were pooled as mean differences (MD) using mixed-effects models. Risk of bias and certainty of evidence were formally assessed. RESULTS:Eight RCTs were included. Empagliflozin significantly reduced liver fat content (MD -2.47%, 95% CI -3.79 to -1.16) and liver stiffness (MD -0.49 kPa, 95% CI -0.89 to -0.09). Alanine aminotransferase and aspartate aminotransferase (MD -4.85 U/L, -9.21 to -0.49) declined, while aspartate aminotransferase-to-platelet ratio index improved (MD -0.03, 95% CI -0.05 to -0.00). Body mass index, visceral adipose tissue and truncal fat mass fell significantly with preservation of skeletal muscle index. Fasting glucose improved, whereas homeostatic model assessment of insulin resistance, low-density lipoprotein cholesterol, and triglycerides remained neutral. Safety profiles were consistent with established SGLT2 inhibitor experience, with no hepatic safety signals. CONCLUSION:Empagliflozin confers coherent improvements in hepatic steatosis, fibrosis surrogates, insulin resistance and visceral adiposity in MASLD, without new safety concerns, supporting its further evaluation as a potential adjunctive therapeutic option for MASLD.
INTRODUCTION:Diagnosing Covert Hepatic Encephalopathy (CHE) in alcohol-related cirrhosis is complicated by potential overlap with alcohol-related cognitive impairment (ARCI), whose effect on recommended CHE tests remains poorly characterized. We aimed to assess the performance of PHES, MoCA and the Simplified Animal Naming Test (sANT) in patients with chronic alcohol exposure, with and without cirrhosis. METHODS:In this prospective single-center cohort, patients admitted for alcohol withdrawal or pre-liver-transplant workup were assessed with PHES (CHE if <-4), MoCA (impairment if <26) and sANT. Correlations and factors associated with CHE were analyzed by univariate and multivariate analysis; sANT diagnostic performance for CHE detection was evaluated by ROC analysis against PHES as the reference standard. RESULTS:236 patients were included, 137(58%) with cirrhosis (age 61 [54-64], MELD 14 [9-19]; 13% clinical HE) and 99 without (age 48 [42-55]). PHES<-4 occurred in 34(33%) non-cirrhotic versus 52(38%) cirrhotic patients; sANT was below the CHE cut-off in 27% and 27% respectively. sANT AUROC for CHE in cirrhosis was 0.77(0.69-0.85). sANT correlated significantly with PHES and MoCA in both groups (rho 0.44-0.56). In multivariate analysis, PHES was associated with sANT, MoCA, Creatinine and albumin; MoCA with sANT, PHES and education. CONCLUSION:A comparable proportion of patients crossed the PHES and sANT cut-offs whether or not they had cirrhosis, suggesting failure to distinguish ARCI from CHE in alcohol-related cirrhosis. Clinicians should interpret abnormal CHE tests with caution in this population. Further research is required to better disentangle ARCI from CHE. Magnetic resonance imaging and spectroscopy, therapeutic tests, or more accurate biomarkers, are promising opportunities.
BACKGROUND:Inflammatory bowel disease (IBD) and primary biliary cholangitis (PBC) have been reported to coexist in some patients, but the extent of this association remains to be further clarified. Clarifying their shared genetic architecture and intercellular interaction patterns may provide insight into the biological links between these two immune-mediated diseases and inform future disease monitoring strategies. METHODS:This study integrated summary statistics from genome-wide association studies (GWAS) of two independent IBD cohorts and one PBC cohort, along with spatially resolved single-cell transcriptomic data. Genetic correlations were examined using linkage disequilibrium score regression, genetic covariance estimation, and localized variant association analyses. Shared susceptibility loci were identified through conditional/joint false discovery rate (FDR) approaches and multi-trait joint analysis. Furthermore, a genetic information-guided cell-type spatial mapping strategy was applied to delineate disease-associated cellular populations at single-cell resolution. RESULTS:Genetic analyses revealed significant genome-wide correlations and extensive polygenic overlap between IBD, its subtypes, and PBC. Local variation analyses further identified multiple chromosomal regions exhibiting regional genetic associations shared by both diseases. Several putative shared susceptibility loci were discovered, with a subset validated using independent datasets. The genetic information-guided spatial mapping approach demonstrated comparable tissue-resident cell distribution patterns between IBD and PBC. CONCLUSION:By integrating GWAS data with single-cell transcriptomic profiling, this study provides a systematic characterization of the genetic relationships between IBD and PBC. These findings offer genetic and cellular-level insights that contribute to a deeper understanding of the molecular basis underlying their comorbidity.
