Helicobacter pylori Infection Increases Thrombocytopenia and Inflammation in Patients With Hepatitis B and/or C: An Analytical Study in Cameroon

幽门螺杆菌感染加重乙型和/或丙型肝炎患者的血小板减少症和炎症:喀麦隆的一项分析研究

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Abstract

BACKGROUND AND AIMS: Helicobacter pylori infection is associated with increased intestinal permeability. It promotes the passage of bacterial endotoxin through the portal vein and reaches the liver, constituting a factor in the aggravation of hepatitis. This study aims to investigate the impact of H. pylori coinfection with HBV/HCV on the progression of hepatic pathophysiology, specifically the inflammatory system and hematological parameters, with the goal of enhancing the care of patients with hepatitis. METHODS: An analytical cross-sectional study was carried out for 6 months in 2023. This study was carried out in people infected with the hepatitis B and/or C virus who were being monitored at Laquintinie Hospital. After having informed the participants about the objective of the study and obtaining their consent, we collected sociodemographic data and clinicobiological history. Subsequently, the diagnosis of H. pylori infection was made by testing for immunoglobulins G and M using the ELISA method. Then, inflammation was explored through the determination of C-reactive protein (CRP) and the cytokines Interleukin-6 and Interleukin-8 (IL-6, and IL-8). Finally, the hemogram was carried out by the flow cytometry method. The data obtained were analyzed using SPSS statistical software. RESULTS: The study population consisted of 184 patients with hepatitis, including 113 (61.4%) cases of hepatitis B and 71 (38.6%) cases of hepatitis C. A total of 94 (51.1%) patients were male and 90 (48.9%) female for a mean age of 41.55 ± 16.90 years. The frequency of coinfection was 37.5%. The mean CRP was 3.79 ± 3.5 mg/dL and 2.4 ± 2.1 mg/dL in coinfected and non-coinfected patients, respectively (p = 0.057). IL-6 was significantly associated with coinfection (p = 0.001). Furthermore, elevated IL-6 was a predictive sign of H. pylori infection in patients with viral hepatitis B/C (OR = 2.88 [0.82-10.11]; p = 0.01). Furthermore, 22 (12.0%) patients presented thrombocytopenia, including 21 (30.4%) in the coinfected group and 1 (0.9%) in the non-coinfected group (p = 0.01). Moreover, the reduction in platelets is a predictive factor of H. pylori infection (OR = 2.34[0.11-7.6]; p = 0.09). CONCLUSION: These results suggest that hepatitis B/C and H. pylori coinfection is a factor in worsening inflammation and thrombocytopenia in patients. Hence, the a need to prevent H. pylori coinfection and control the progression of the disease in patients with hepatitis.

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