Persistent advanced periductal fibrosis is associated with cagA‐positive Helicobacter pylori infection in post‐praziquantel treatment of opisthorchiasis

Abstract

Background Liver fluke infection caused by Opisthorchis viverrini is associated with several hepatobiliary diseases including advanced periductal fibrosis (APF) and cholangiocarcinoma. Recently, we demonstrated a persistent APF in over one‐third of opisthorchiasis patients after worm removal by praziquantel (PZQ) treatment. However, the underlying mechanism(s) of this phenomena is unclear. Given a co‐infection with Helicobacter pylori (H. pylori) especially cagA‐positive strain enhances APF, we hypothesized that H. pylori with CagA virulent factor contributes to persistent APF. Materials and methods Seventy‐five opisthorchiasis patients who underwent ultrasonography and treatment with PZQ were recruited in the 2‐year follow‐up study. Helicobacter and its cagA in the feces were examined by conventional and qPCR. Correlations between prevalence or bacterial loads of Helicobacter spp., H. pylori, and cagA‐positive H. pylori before and after PZQ treatment were analyzed among resolved, slowly resolved, relapsed, and persistent APF groups. Results Overall, prevalence of Helicobacter spp., H. pylori, and cagA‐positive H. pylori declined after PZQ treatment. However, only the prevalence and bacterial loads of cagA‐positive H. pylori detected at 2‐year post‐treatment were significantly lower than those before treatment (p < .05). In addition, both prevalence and bacterial loads of cagA‐positive H. pylori were significantly lower in the resolved APF group after PZQ treatment, while there were no significant changes in the slowly resolved, relapsed, and persistent APF groups. Among the APF subgroups, cagA‐positive H. pylori prevalence in both relapsed and persistent APF groups were significantly higher than the resolved APF group. Conclusion The results support our hypothesis that H. pylori, especially cagA‐positive strain, contributes to the relapsed and persistent APF. A supplementary antibiotic treatment for H. pylori to reduce persistent APF and eventually CCA is warranted.

Persistent advanced periductal fibrosis is and helicobacter pylori infection in post‐treatment of opisthorchiasis: Correspondence

“…The interrelationship among several factors might be theoretically possible and it can be the main pathobiological process for cholangiocarcinoma development. 4 The current study by Phung et al 1 can still not rule out the effect of other confounding factors.…”

Elevated circulating TLR4+ monocytes in patients with liver fluke Opisthorchis viverrini is associated with advanced periductal fibrosis

“…There is now a great deal of evidence to show that Ov may serve as a reservoir of H. pylori, a Gram-negative bacterium, resulting in coinfection with the two pathogens in endemic areas [19]. Furthermore, a long-term follow-up study following praziquantel treatment to clear Ov infection has shown that those with relapsed or persistent APF have a statistically-significant higher incidence of infection with cagA-positive H. pylori [20]. However, the mechanism by which cagA-positive H. pylori drives APF is still undefined.…”

Opisthorchis viverrini—Current Understanding of the Neglected Hepatobiliary Parasite

“…The existing literature proposes that a carcinogenic bacterium, Helicobacter pylori ( H. pylori ), also contributes to the development of cholangiocarcinoma by enhancing the severity of hepatobiliary abnormalities [ 67 ]. A study by Hang et al found that even after completion of therapy with praziquantel, patients with co-infection by H. pylori , especially cagA-positive strain, continued to have persistent APF [ 68 ]. Hence, this suggests the need for concurrent H. pylori treatment for better outcomes.…”