Combined *Schistosoma mansoni* infection and alcohol abuse severely worsen hepatic damage and oxidative stress

Schistosoma mansoni infection and chronic alcohol abuse are global health burdens, particularly impacting liver health. While both conditions independently cause significant hepatic damage, the synergistic effects of their co-occurrence remain poorly understood. Current interventions often target these conditions separately, leaving a gap in understanding and managing the compounded pathophysiological mechanisms when they coexist. This study addresses this by investigating the combined hepatic, oxidative, and immunological alterations in co-exposed individuals.

A cross-sectional analytical study was conducted in Makenéné, Cameroon, involving 310 adults stratified by parasitic status and alcohol exposure. Schistosoma mansoni infection was diagnosed using Kato-Katz and POC-CCA assays. Alcohol exposure was assessed via the Alcohol Use Disorders Identification Test (AUDIT). Researchers evaluated hematological, liver function (e.g., AST, ALT, GGT, ALP), oxidative stress (e.g., malondialdehyde, catalase, GSH, nitrite), inflammatory (TNF-α), and fibrogenic (TGF-β1, P3NP) profiles.

Combined S. mansoni infection and alcohol abuse significantly exacerbated liver damage, showing elevated AST (p < 0.001), ALP (p < 0.01), GGT (p < 0.05), and AST/ALT ratio (p < 0.001) compared to alcohol abuse alone. Relative to schistosomiasis alone, the comorbidity led to higher ALT and AST (p < 0.01) and GGT (p < 0.05), alongside lower total protein (p < 0.05). Both conditions independently induced oxidative stress, marked by increased malondialdehyde (p < 0.001) and decreased catalase, GSH, and nitrite. This oxidative imbalance was further worsened in co-exposed individuals, who exhibited the lowest catalase activity (p < 0.01) and GSH concentration (p < 0.05). Immunologically, the comorbidity featured the lowest TNF-α levels (p < 0.05) but 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).