Prevalence of H. Pylori Infection in Non-Cirrhotic Patients with Chronic Delta Hepatitis

Objective: The relationship between Hepatitis Delta infection and Helicobacter infection in patients with non-cirrhotic hepatitis B infection was retrospectively investigated. Material and Methods: Stool samples of 117 patients included with Delta hepatitis infection in the study At total 36 of them were tested for H. Pylori infection. To detect H. Pylori, stool samples were tested using a commercial stool H. Pylori antigen assay. Results: Of these, 13 (19%) patients had H. Pylori seropositivity in the Hepatitis B infection group and 23 (48%) patients tested positive for H. Pylori infection in hepatitis delta infection group. There was a statistically significant difference between groups regarding H. Pylori seropositivity by the faecal test (p= 0.001). Conclusion: This study provides new knowledge on H. Pylori infection and reflects the need for evidence-based and comorbid dieases-oriented guidelines in the field of gastroenterology.

Number of Endoscopic Sessions to Eradicate Varices Identifies High Risk of Rebleeding in Cirrhotic Patients

Background and aims: Risk stratification to identify patients with high risk of variceal rebleeding is particularly important in patients with decompensated cirrhosis. In clinical practice, eliminating gastroesphageal varices thoroughly after sequential endoscopic treatment reduces the rebleeding rate, however, no simple method has been build to predict high risk of variceal rebleeding. We conducted this study to explore the value of the number of endoscopic sessions required to eradicate gastroesphageal varices in identifying high risk of rebleeding.Patients and methods: Consecutive cirrhotic patients received sequential endoscopic therapy between January 2015 to March 2020 were enrolled. Endoscopic treatment was performed every 1-4 weeks until the eradication of varices. The primary endpoint was variceal rebleeding.Results: A total of 146 patients were included of which 60 patients received standard therapy and 86 patients underwent sequential endoscopic treatment alone. The cut-off value of the number of sequential endoscopic sessions is 3.5 times. Variceal rebleeding was significant higher in patients with endoscopic sessions > 3 times vs. ≤ 3 times (61.5% vs. 17.5%, p<0.001). Variceal rebleeding of patients with endoscopic sessions ≤3 times was significant lower than patients with > 3 times in group of standard therapy (19.6% vs. 88.9%, p<0.001) and endoscopic therapy (15.9% vs. 47.1%, p=0.028) respectively. Conclusion: The number of sequential endoscopic sessions required to eradicate the varices is related to the risk of variceal rebleeding in patients with cirrhosis. If three times of endoscopic treatment can not eradicate the varices, a more aggressive treatment such as TIPS should be seriously considered.

Role of portal color Doppler ultrasonography as noninvasive predictive tool for esophageal varices in cirrhotic patients

Background Esophageal varices (EV) is the most common apprehensive complication of portal hypertension in patients with cirrhotic liver. Guidelines recommend Upper gastro-intestinal endoscopic screening for EV in patients with newly diagnosed chronic cirrhosis (Imperiale et al. in Hepatology 45(4):870–878, 2007). Yet, it is invasive, time consuming and costly. To avoid unnecessary endoscopy, some studies have suggested Doppler ultrasound examination as simple, and noninvasive tool in prediction and assessment of severity of EV (Agha et al. in Dig Dis Sci 54(3):654–660, 2009). Our study was to assess the role of different Doppler indices of portal vein, hepatic and splenic arteries as a noninvasive tool for prediction of esophageal varices in cirrhotic patients. Results This prospective case control study was conducted on 100 cirrhotic liver patients and 100 of healthy volunteers as control group. Patients were subjected to clinical examination, upper gastrointestinal tract endoscopy, abdominal ultrasonography with duplex Doppler evaluation of different portal Doppler hemodynamic indices were done for each patient. The results revealed that portal vein diameter, hepatic artery pulsatility index, portal hypertensive index, portal vein flow velocity, portal congestion index have high sensitivity for prediction of EV. However, Splenic artery resistance index, hepatic artery resistance index HARI, liver vascular index and platelet count/spleen diameter have less sensitivity for prediction of EV. Conclusion Measuring the portal hemodynamic indices can help physicians as noninvasive predictors of EV in cirrhotic patients to restrict the need for unnecessary endoscopic screening especially when endoscopic facilities are limited.

Plasma Cyclic Guanosine Monophosphate Is a Promising Biomarker of Clinically Significant Portal Hypertension in Patients With Liver Cirrhosis

Introduction: Despite intensive research, reliable blood-derived parameters to detect clinically significant portal hypertension (CSPH) in patients with cirrhosis are lacking. As altered homeostasis of cyclic guanosine monophosphate (cGMP), the central mediator of vasodilatation, is an essential factor in the pathogenesis of portal hypertension, the aim of our study was to evaluate plasma cGMP as potential biomarker of cirrhotic portal hypertension.Methods: Plasma cGMP was analyzed in cirrhotic patients with CSPH (ascites, n = 39; esophageal varices, n = 31), cirrhotic patients without CSPH (n = 21), patients with chronic liver disease without cirrhosis (n = 11) and healthy controls (n = 8). cGMP was evaluated as predictor of CSPH using logistic regression models. Further, the effect of transjugular intrahepatic portosystemic shunt (TIPS) placement on plasma cGMP was investigated in a subgroup of cirrhotic patients (n = 13).Results: Plasma cGMP was significantly elevated in cirrhotic patients with CSPH compared to cirrhotic patients without CSPH [78.1 (67.6–89.2) pmol/ml vs. 39.1 (35.0–45.3) pmol/l, p &lt; 0.001]. Of note, this effect was consistent in the subgroup of patients with esophageal varices detected at screening endoscopy who had no prior manifestations of portal hypertension (p &lt; 0.001). Cirrhotic patients without CSPH displayed no significant elevation of plasma cGMP compared to patients without cirrhosis (p = 0.347) and healthy controls (p = 0.200). Regression analyses confirmed that cGMP was an independent predictor of CSPH (OR 1.042, 95% CI 1.008–1.078, p = 0.016). Interestingly, portal decompression by TIPS implantation did not lead to normalization of plasma cGMP levels (p = 0.101).Conclusions: Plasma cGMP is a promising biomarker of CSPH in patients with cirrhosis, especially with respect to screening for esophageal varices. The lacking normalization of plasma cGMP after portal decompression suggests that elevated plasma cGMP in cirrhotic portal hypertension is mainly a correlate of systemic and splanchnic vasodilatation, as these alterations have been shown to persist after TIPS implantation.

Molecular mechanisms of liver carcinogenesis related to metabolic syndrome

Global prevalence of non-alcoholic fatty liver disease (NAFLD) and of NAFLD-hepatocellular carcinoma (HCC) is estimated to grow in the next years. The burden of NAFLD and the evidence that NAFLD-HCC arises also in non-cirrhotic patients, explain the urgent need of a better characterization of the molecular mechanisms involved in NAFLD progression. Obesity and diabetes cause a chronic inflammatory state which favors changes in serum cytokines and adipokines, an increase in oxidative stress, DNA damage, and the activation of multiple signaling pathways involved in cell proliferation. Moreover, a role in promoting NAFLD-HCC has been highlighted in the innate and adaptive immune system, dysbiosis, and alterations in bile acids metabolism. Several dietary, genetic, or combined mouse models have been used to study nonalcoholic steatohepatitis (NASH) development and its progression to HCC, but models that fully recapitulate the biological and prognostic features of human NASH are still lacking. In humans, four single nucleotide polymorphisms (PNPLA3, TM6SF2, GCKR, and MBOAT7) have been linked to the development of both NASH and HCC in cirrhotic and non-cirrhotic patients, whereas HSD17B13 polymorphism has a protective effect. In addition, higher rates of somatic ACVR2A mutations and a novel mutational signature have been recently discovered in NASH-HCC patients. The knowledge of the molecular pathogenesis of NAFLD-HCC will be helpful to personalized screening programs and allow for primary and secondary chemopreventive treatments for NAFLD patients who are more likely to progress to HCC.