BACKGROUND:Chronic hepatitis B virus (HBV) infection remains a major global health challenge and a leading cause of liver cirrhosis and hepatocellular carcinoma. Interleukin-6 (IL-6), a key pro-inflammatory cytokine, plays an important role in immune regulation and hepatic inflammation. However, its relationship with HBV viral load and disease severity remains incompletely understood. METHODS:A hospital-based cross-sectional study was conducted among 293 HBsAg-positive patients. Serum IL-6 levels were measured using ELISA, and HBV DNA was quantified using real-time quantitative PCR. Patients were stratified according to viral load. Statistical analyses included non-parametric tests, Spearman correlation, principal component analysis (PCA), and multiple linear regression. RESULTS:The median age was 45 years (IQR: 34-57), among which 54.6% were male. The median HBV DNA was 3.37 log10 IU/mL (IQR: 2.45-3.75), and IL-6 concentration was 2.38 log10 pg/mL (IQR: 2.21-2.49). IL-6 levels increased significantly across viral load categories (p < 0.001) and were higher in HBeAg-positive patients (p = 0.002), with no significant differences across age, sex, or cirrhosis. IL-6 levels correlated with HBV DNA (r = 0.40, p < 0.001). PCA identified distinct viral-inflammatory and biochemical axes. Regression analysis confirmed HBV DNA as the significant independent predictor (β = 0.461, p < 0.001; adjusted R2 = 0.206). CONCLUSION:IL-6 was closely associated with HBV DNA levels, while the association with conventional biochemical markers of hepatocellular injury was significantly less in this cohort, suggesting that IL-6 may serve as an adjunct biomarker of disease activity in patients with chronic hepatitis B.
Background: Hydatid disease, caused primarily by Echinococcus granulosus, remains a significant public health challenge in endemic regions. While hepatic (80-85%) and pulmonary (15-20%) involvements are common, multi-organ dissemination involving rare sites such as the pericardium, diaphragm, and mediastinum occurs in less than 0.1-2% of cases. Case presentation: We present a rare case of a 26-year-old male, a farmer for 10 years, with occupational exposure to dogs and horses, with a personal history of multiple surgically treated abdominal cysts in 2016, admitted after abdominal computed tomography revealed liver cysts greater than 5 cm, as well as mediastinal and diaphragmatic cysts. Histopathological examination of the surgically resected hepatic cyst material confirmed echinococcosis. Serology was also positive for echinococcosis. Echocardiography revealed a pericardial cyst, posterior to the left atrium. Under these circumstances, antiparasitic treatment was initiated by an infectious disease specialist, followed by surgical treatment of the abdominal cysts, confirming the final diagnosis of hydatid disease, and subsequently, surgical treatment of the thoracic hydatid cysts was performed. The postoperative course was complicated by bronchial superinfection with Stenotrophomonas maltophilia, identified from bronchial aspirate culture after extended incubation and managed with trimethoprim-sulfamethoxazole. Conclusions: This case underscores the necessity of lifelong surveillance in hydatid disease, the potential role of postoperative antiparasitic therapy in preventing long-term recurrence, and the vital role of a multidisciplinary team in managing complex, disseminated relapses.
BACKGROUND:Vector-borne diseases (VBDs) caused by Borrelia spp., Bartonella spp., and Babesia spp. are associated with neuropsychiatric morbidity. Cerebral folate deficiency (CFD), primarily caused by folate receptor-α autoantibodies (FRAAs) impairing folate blood-brain barrier transport, is a treatable contributor to neurodevelopmental disorders including pediatric acute-onset neuropsychiatric syndrome (PANS) and autism spectrum disorder. Despite overlapping clinical manifestations, FRAA prevalence in VBD populations has not been investigated. This study aimed to determine the prevalence of FRAA in patients with confirmed VBDs. METHODS:This retrospective cohort study included 68 VBD-positive patients with and without PANS evaluated at a single clinical practice. VBD testing was performed by IGeneX Laboratories; FRAA analysis including binding, blocking, and soluble folate receptor (sFR) testing was performed by Religen Laboratories (Plymouth Meeting, PA). Statistical associations were assessed using Fisher's exact test with Wilson 95% confidence intervals. RESULTS:Of the 68 VBD-positive patients, 42 (61.8%; 95% CI: 49.9-72.4%) were also FRAA-positive. Soluble folate receptor (sFR) was detected in eight patients (11.8%; 95% CI: 6.1-21.5%), all of whom were binding FRAA-positive, with 87.5% carrying confirmed evidence of Borrelia species infection. Neuropsychiatric symptoms were highly prevalent across both groups but did not significantly differentiate FRAA-positive from FRAA-negative patients (all p > 0.05). CONCLUSIONS:This study demonstrates a high prevalence of FRAA in a pediatric VBD cohort. The sFR was strongly associated with Borrelia species infection, suggesting a potential mechanistic link between spirochetal infection and folate receptor autoimmunity. These findings support the consideration of FRAA testing in patients with VBDs and warrant further investigation in larger prospective cohorts.
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease characterized by irreversible extracellular matrix deposition and high mortality, with aging representing its strongest risk factor. Increasing evidence suggests that cellular senescence is not merely a consequence of tissue injury but a central driver of disease progression. Senescent alveolar epithelial cells and fibroblasts contribute to impaired tissue repair and persistent fibrotic remodeling through the acquisition of a senescence-associated secretory phenotype (SASP), which promotes chronic inflammation and amplifies profibrotic signaling. This review provides a comprehensive synthesis of current evidence on the role of cellular senescence in IPF, focusing on key molecular mechanisms, including telomere attrition, mitochondrial dysfunction, oxidative stress, DNA damage response activation, and dysregulated transforming growth factor-β (TGF-β) signaling. A structured literature search was conducted using the PubMed, Scopus, and Web of Science databases to identify mechanistic, translational, and clinical studies related to cellular senescence in IPF. Relevant studies were selected based on conceptual relevance and scientific quality, and findings were qualitatively synthesized within a narrative-review framework. These interconnected pathways form self-reinforcing feedback loops that stabilize the senescent phenotype and sustain fibroblast activation. In addition, we critically evaluate emerging therapeutic strategies targeting senescence, including senolytic and senomorphic approaches, highlighting their potential to modify fundamental disease mechanisms rather than solely attenuating fibrotic progression. Preclinical and early clinical studies suggest that selective targeting of senescent cells may represent a promising avenue for intervention, although challenges related to specificity, safety, and biomarker development remain. Overall, this review positions cellular senescence as a central mechanistic link between aging and fibrosis and underscores its relevance as a translational target in IPF.
Background: Stunting remains a major public health problem among ethnic minority children in mountainous areas of Vietnam. Picky eating has been suggested as a potential behavioral risk factor for poor child growth, but evidence from vulnerable rural populations remains limited. This study examined the association between picky eating and stunting among ethnic minority children aged 12-35 months in Vietnam. Methods: This cross-sectional study was conducted from October to November 2025 in two communes of Phu Tho province, formerly part of Lac Son District, Hoa Binh Province, Vietnam. A total of 341 children aged 12-35 months and their caregivers were included. Data were collected using structured interviewer-administered questionnaires on feeding practices and child characteristics. Picky eating was assessed based on caregiver-reported behaviors. Anthropometric measurements were performed according to standard procedures, and height-for-age Z-scores were calculated using the WHO Child Growth Standards. Zinc status was assessed in a subsample of children. Bivariate and multivariable logistic regression analyses were conducted to identify factors associated with stunting. Adjusted odds ratios (AORs) with 95% confidence intervals (95% CIs) were reported. Results: The prevalence of picky eating was 39.6%, while 24.9% of children were stunted. Zinc deficiency was identified in 41.9% of children with available blood samples. In multivariable analysis, picky eating was significantly associated with increased odds of stunting (AOR = 3.63; 95% CI: 1.71-7.70). Snacking before main meals was also independently associated with stunting (AOR = 1.81; 95% CI: 1.01-3.24). In contrast, zinc deficiency was associated with stunting in crude analysis but was not statistically significant after adjustment. Other factors, including child age, sex, caregiver identity, and timing of complementary feeding, were not independently associated with stunting. Conclusions: Picky eating was common and was independently associated with stunting among ethnic minority children in this mountainous setting. These findings suggest that behavioral feeding practices, particularly picky eating and pre-meal snacking, warrant attention in nutritional programs targeting this population; however, longitudinal studies are needed to confirm the direction of this relationship.
