Hepatic, oxidative, and immunological alterations in adults with concomitant Schistosoma mansoni infection and alcohol abuse in an endemic area of Cameroon

BACKGROUND: Schistosoma mansoni infection and chronic alcohol consumption are major public health concerns that predominantly affect the liver, yet their combined hepatic effects remain insufficiently understood. This study aimed to investigate the pathophysiological mechanisms associated with this co-exposure in an endemic setting in Cameroon. METHODS: A cross-sectional analytical study was conducted in Makenéné, Cameroon, including 310 adults stratified by parasitic status and level of alcohol exposure. Infection was diagnosed using Kato-Katz and POC-CCA assays. Alcohol exposure was assessed using the Alcohol Use Disorders Identification Test (AUDIT). Hematological, liver function, oxidative, inflammatory, and fibrogenic profiles were evaluated. RESULTS: Compared with alcohol abuse alone, combined S. mansoni infection and alcohol abuse was associated with reduced erythrocyte and platelet indices (p < 0.05), elevated activities of AST (p < 0.001), ALP (p < 0.01), GGT (p < 0.05), AST/ALT ratio (p < 0.001), and protein concentration (p < 0.001). Relative to schistosomiasis alone, the comorbidity was associated with higher ALT and AST (p < 0.01) and GGT (p < 0.05), but lower total protein (p < 0.05). Both schistosomiasis and alcohol abuse, independently, induced oxidative stress, evidenced by increased malondialdehyde levels (p < 0.001) and decreased catalase activity, GSH, and nitrite levels. This oxidative imbalance was exacerbated in co-exposed individuals who exhibited the lowest catalase activity (p < 0.01) and GSH concentration (p < 0.05). The comorbidity was also characterized by the lowest TNF-α levels (p < 0.05) and the highest TGF-β1 levels (p < 0.001). Procollagen type III N-terminal peptide (P3NP) peaked during S. mansoni infection (p < 0.001) but was less expressed during the comorbidity (p < 0.05). Both S. mansoni infection intensity and alcohol abuse correlate positively with transaminases and malondialdehyde, but negatively with nitrite, catalase, and TNF-α. Infection correlates positively with proteins, TGF-β1, IL-10, and P3NP, while alcohol abuse negatively correlates with IL-10 and SOD. CONCLUSION: S. mansoni infection and alcohol abuse comorbidity exacerbates liver injury beyond either condition alone, with increased liver enzymes, oxidative stress, immune imbalance, and fibrogenesis, highlighting the need for integrated public health strategies to reduce liver-related morbidity in endemic settings.