This study aims to identify and evaluate the most common drugs associated with the risks of autoimmune hepatitis (AIH) using the FDA Adverse Event Reporting System (FAERS) database. Adverse drug events (ADEs) associated with drug-induced AIH (DI-AIH) were retrieved from the FAERS database (January 2004–June 2024). Disproportionality analysis was performed to identify drugs significantly linked to DI-AIH, and time-to-onset (TTO) analyses were conducted to evaluate the timing and risk profiles of DI-AIH adverse reactions. Our study identified 2,511 ADEs linked to autoimmune hepatitis. Disproportionality analysis identified 22 drugs significantly associated with AIH risk, including 4 antibiotics, 3 antivirals, 4 cardiovascular drugs, 5 antitumor agents, 2 immunomodulators, 2 nonsteroidal anti-inflammatory drugs, and 1 drug each from the respiratory and nervous system categories. The highest DI-AIH risks were observed with minocycline (ROR = 53.97), nitrofurantoin (ROR = 57.02), and doxycycline (ROR = 16.12). Antitumor drugs had the shortest median TTO (77.00 days), whereas cardiovascular drugs exhibited the longest (668.30 days). Through a comprehensive analysis of the FAERS database, our study identified drugs strongly associated with AIH. Preventing DI-AIH requires careful drug selection and monitoring. This study provides evidence-based insights into implicated drugs, aiming to optimize clinical management and mitigate risks.

This study aims to assess the risks associated with drug-induced macular edema and to examine the epidemiological characteristics of this condition. This study analyzed data from the U.S. Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) database from January 2004 to June 2024 to conduct a disproportionality analysis identifying drugs with positive signals of drug-induced ME. Additionally, the onset time of ME associated with these drugs was examined. In the FAERS database, a total of 490 drugs were reported to pose a risk of drug-induced ME. Disproportional analysis and screening further identified 8 drugs that significantly increased this risk. Among these, one is ophthalmic drugs, including Latanoprost (ROR = 5.51), and ten are non-ophthalmic drugs, including Cefuroxime (ROR = 75.93), Fingolimod (ROR = 30.69), and Siponimod (ROR = 20.51). This study utilizes the FAERS database to investigate potential associations between drug use and the occurrence of ME, rapidly identify drugs that may induce the condition, and propose research strategies. These findings hold significant value for guiding clinical medication practices.

Introduction: The role of cancer-associated fibroblasts (CAFs) in the progression, therapeutic resistance, and metastasis of castration-resistant prostate cancer (CRPC) remains incompletely understood. This study aimed to investigate how CAFs regulate the stemness of prostate cancer stem cells (PCSCs), with a focus on the Wnt/β-catenin and SDF-1/CXCR4 signaling pathways.Methods: We assessed the expression of CAF and PCSC markers in xenograft tumor tissues from hormone-sensitive prostate cancer and CRPC mouse models using immunohistochemistry and immunofluorescence. The impact of CAFs on stemness markers, SDF-1, CXCR4, and Wnt pathway activation was evaluated both in vitro and in vivo.Results: The expression levels of CAF and PCSC markers were significantly elevated in CRPC tissues compared to hormone-sensitive tumors. Bioinformatics analysis indicated high expression of CXCR4 and CTNNB1 (β-catenin) in CRPC, with positive correlations to disease progression. CAFs enhanced PCSC stemness, while inhibition of Wnt3a or SDF-1 led to reduced stemness and pathway activity. In vivo, CAFs promoted CRPC tumor growth and significantly increased the expression of Wnt3a, β-catenin, TCF4, LEF1, SDF-1, and CXCR4, along with an elevated p-GSK-3β/GSK-3β ratio. Conversely, β-catenin and CXCR4 inhibitors suppressed tumor growth and downregulated Wnt signaling components.Discussion: β-Catenin and CXCR4 showed strong co-localization in xenograft tumors. These findings suggest that CAFs promote PCSC stemness and CRPC progression by activating the Wnt/β-catenin and SDF-1/CXCR4 pathways via Wnt3a and SDF-1 expression. These insights provide potential targets for managing CRPC.

Objective: This study aimed to investigate the association between the Systemic Inflammatory Response Index (SIRI) and glaucoma using data from the 2005–2008 National Health and Nutrition Examination Survey (NHANES).Methods: We performed a cross-sectional analysis using data from NHANES (2005–2008). Among participants who underwent non-mydriatic retinal imaging and Frequency Doubling Technology (FDT) visual field testing, 4,514 were included after excluding those with missing key variable data. SIRI and other inflammatory indices, including the systemic immune-inflammation index (SII), platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte ratio (NLR), were calculated from blood samples. Logistic regression models were employed to assess the relationship between these indices and glaucoma, adjusting for demographic and health-related variables.Results: A significant positive association was found between elevated log₂SIRI levels and the prevalence of glaucoma (Model 3: OR 1.24, 95% CI 1.07–1.44, p < 0.005). We performed an in-depth analysis of the Log₂SIRI quartiles and found a significant association between Log₂SIRI Q4 and the occurrence of glaucoma (Model 3: OR1.62, 95%CI 1.12–2.34, p = 0.011). This correlation was further validated using the area under the receiver operator characteristic curve (AUC) in Model 3(AUC = 0.674).Conclusion: Elevated SIRI levels are significantly associated with the prevalence of glaucoma, highlighting the potential role of systemic inflammation in glaucoma pathogenesis. SIRI may serve as a useful biomarker for identifying individuals at risk of glaucoma, facilitating early detection and targeted intervention strategies. Further research is needed to validate these findings and explore their clinical applications.