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Corresponding author: Li Hong Tao, 13979211776@163.com

DOI: 10.12201/bmr.202608.00023

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  Abstract: Schistosomiasis is an important neglected tropical parasitic disease affecting approximately 250 million people worldwide, with the digestive system being its primary target organ. Following deposition of parasite eggs in the liver and intestinal wall, granulomatous inflammatory responses are triggered, leading to severe consequences including hepatic fibrosis, portal hypertension, and colorectal malignancy. This article systematically reviews the etiological basis, pathophysiological mechanisms, clinical spectrum, diagnostic strategies, and therapeutic advances of digestive system injury induced by schistosome infection. In terms of pathological mechanisms, soluble egg antigen activates type 2 immune responses, driving M2 macrophage polarization and hepatic stellate cell activation, thereby promoting collagen deposition through TGF-beta/Smad and JAK2/STAT3 signaling pathways. Clinical manifestations include hepatic fibrosis, esophagogastric variceal bleeding, colorectal polyps, and malignant transformation. Regarding diagnosis, parasitological detection remains the gold standard, while immunological assays (CAA/CCA) and molecular techniques (PCR, CRISPR-Cas13a) have improved sensitivity. Praziquantel is the first-line therapeutic agent, though challenges of reinfection and emerging resistance persist; traditional Chinese medicine shows unique advantages in anti-fibrotic therapy, and vaccine development remains an active area of investigation. Future efforts should focus on elucidating key molecular nodes in fibrogenesis, developing early diagnostic biomarkers, and optimizing integrated prevention and control strategies.

  Key words: schistosomiasis; digestive system; hepatic fibrosis; portal hypertension; colorectal neoplasms

  Submit time: 9 August 2026

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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  1	2026-05-25	10.12201/bmr.202608.00023V1	Download

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