Aim: Dysbiosis of gut microbiota favors chronic hepatic inflammation with subsequent hepatic carcinogenesis. The current study aimed to evaluate the role of gut dysbiosis in the development of hepatocellular carcinoma in patients with chronic HCV infection.Methods: This descriptive cross-sectional cohort study carried out on 400 subjects recruited from the Internal Medicine Department and Tropical Medicine and Gastroenterology Department of Helwan and South Valley University Hospitals in Egypt. The study period was from January 2017 till January 2020. The subjects were divided clinically into three groups. Group I: One hundred patients with HCC, evaluated by Child Pugh, TNM and BCLC scoring systems. Group II: 200 chronic hepatitis C virus-infected patients. All patients infected with hepatitis C virus genotype 4. Group III: One hundred healthy control subjects with negative hepatitis marker and normal abdominal ultrasound. PCR of stool Microbiota, complete blood counts, complete liver function tests, INR, HCV antibodies and HBsAg were done for all included subjects. HCV PCR assessment and alpha-fetoprotein (AFP) were done for all patients.Results: No statistically significant difference was detected between HCC patients and control (p-value > 0.05) as regard Bacteroides fragilis & Akkermansia muciniphila. Faecalibacterium prausnitzii was less detected in HCC patients (51%), opposite to 70% of healthy control. With Statistically significant difference (p-value < 0.05). Bifidobacterium was less detected in HCC patients (43%), opposite to (76%) of healthy control. With highly statistically significant difference (p-value < 0.001). Lactobacillus & Enterobacteriaceae was more detected in HCC patients (80%) and (81%), in. Opposite to (36%) and (58%) in healthy control, respectively. With highly statistically significant difference (p-value < 0.001). no significant difference was detected between gut-microbiota and HCC progression with respect to Child or TNM systems. However, a significant difference was detected between number of positive stool isolate of Bacteroid Fragilis and BCLC staging system; where it was isolated from 66.7% of patients with BCLC stage IV opposite to 10.7% of patients with BCLC stage I.Conclusion: A characteristic pattern of Bifidobacterium, Lactobacillus and Enterobacteriaceae species in patients with chronic HCV and HCC was detected. Alteration of gut microbiota may be accused as a predisposing factor for liver disease progression.
This study aimed to evaluate the possible role of gut dysbiosis in the development of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C virus (HCV) infection. This study was carried out on 400 individuals categorized into three groups: group I included 100 patients with HCC; group II included 200 chronic HCV-infected patients; and group III included 100 healthy control subjects. The included patients were evaluated using Child-Pugh, tumor (T), nodes (N), and metastases (M) (TNM), and Barcelona Clinic Liver Cancer (BCLC) scoring systems. In addition to routine investigations (complete blood counts, complete liver function tests, international normalized ratio, HCV antibodies, and hepatitis B surface antigen), polymerase chain reaction of stool microbiota, HCV infection, and alphafetoprotein were assessed for all patients. The results revealed no significant difference between HCC patients and control patients (p > 0.05) regarding Bacteroides fragilis and Akkermansia muciniphila. Faecalibacterium prausnitzii and Bifidobacterium were detected in fewer patients with HCC (51% and 43%, resp.) compared with healthy controls (70% and 76%, resp.) (p < 0.05). Lactobacillus and Escherichia coli were detected in more patients with HCC (80% and 81%, resp.) compared with healthy controls (36% and 58%, resp.), p < 0.001. No significant differences were detected between gut microbiota and HCC progression with respect to Child-Pugh or TNM scores. However, B. fragilis was detected in stool isolates from 66.7% of BCLC stage IV patients compared with 10.7% of BCLC stage I patients. Thus, characteristic patterns of Bifidobacterium, Lactobacillus, and E. coli species in patients with chronic HCV and HCC were detected. Therapies targeting altered gut microbiota may be beneficial in reducing the risk of HCC in patients with HCV infection, as altered gut microbiota is a predisposing factor for liver disease progression.
Some studies reported a high prevalence of ischemic stroke in hepatitis C virus patients, other several studies have suggested that hepatitis C virus (HCV) may act as a trigger for autoimmune diseases and autoantibodies including Anti-Neutrophil Cytoplasmic Antibody (ANCA) which predispose to vasculitis. Because vasculitis is a risk factor for ischemic stroke, we investigated the association of the hepatitis C virus with ANCA in first-ever ischemic stroke patients. This study included 67 Egyptian patients with first-ever ischemic stroke. These patients were clinically examined and investigated for HCV infection by chemiluminescence & Real Time-PCR, and ANCA antibodies by ELISA. Forty-two patients (62.7%) had HCV infection. Twenty-nine (43.2%) of them were cytoplasmic- Antineutrophil Cytoplasmic Antibodies (c-ANCA) positive, while none was perinuclear- Antineutrophil Cytoplasmic Antibodies (p-ANCA) positive. Comparison between c-ANCA positive and ANCA negative patients showed that 82.8% and 47.4% had anti-HCV antibody, respectively, with P-value 0.003. The c-ANCA level correlated significantly with age, and HCV antibody level. No statistically significant difference was found in both the consciousness and stroke severity between the negative and positive c- ANCA patients. However, patients with positive c-ANCA had smaller and multiple cerebral infarctions with P-value 0.002 and 0.01 respectively. Multiple regression analysis showed that the number and size of cerebral infarctions were independent predictors of c-ANCA positivity with P value 0.02, and 0.03 respectively. In conclusion, c-ANCA level correlates with HCV antibody and may predispose to ischemic stroke by a possible ANCA associated vasculitis.
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