A different perspective on sofosbuvir-ledipasvir treatment of patients with HCV genotype 1b cirrhosis: The ital-c network study.

The effectiveness of a 12-week course of sofosbuvir-ledipasvir in treatment-experienced HCV genotype 1b-infected patients with cirrhosis is still under debate. Our primary endpoint was to compare the sustained virological response at post-treatment week 12 (SVR12) of sofosbuvir-ledipasvir in combination with ribavirin for 12 weeks, and sofosbuvir-ledipasvir alone for 24 weeks. This was a prospective observational study that enrolled 424 (195 naive, 229 experienced; 164 treated for 12 weeks with Ribavirin and 260 with sofosbuvir-ledipasvir alone for 24 weeks) consecutive HCV genotype 1b-infected patients with cirrhosis. The SVR12 rates were 93.9% and 99.2% in patients treated for 12 and 24 weeks, respectively (P = .002). The baseline characteristics of patients treated for 12 weeks were significantly different from those treated for 24 weeks as regards their younger age (P = .002), prevalence of Child-Pugh class A (P = .002), lower MELD scores (P = .001) and smaller number of nonresponders (P = .04). The shorter treatment was significantly associated with a lower SVR12 in univariate and multivariate analyses (P = .007 and P = .008, respectively). The SVR rate was unaffected by age, gender, BMI, Child-Pugh class, MELD score or previous antiviral treatment. Patients receiving ribavirin experienced more episodes of ascites and headache but less recurrence of hepatocellular carcinoma (HCC), and were prescribed more diuretics and cardiopulmonary drugs. No patient discontinued treatment. The therapeutic regimen of sofosbuvir-ledipasvir plus ribavirin administered for 12 weeks was less effective than sofosbuvir-ledipasvir alone given for 24 weeks. At odds with European guidelines, the recommended 12-week treatment with sofosbuvir-ledipasvir alone might be suboptimal for this setting of patients.

Worldwide prevalence, genotype distribution and management of hepatitis C.

Hepatitis C virus (HCV) is one of the leading causes of chronic liver disease, cirrhosis, and hepatocellular carcinoma, resulting in major global public health concerns. The HCV infection is unevenly distributed worldwide, with variations in prevalence across and within countries. The studies on molecular epidemiology conducted in several countries provide an essential supplement for a comprehensive knowledge of HCV epidemiology, genotypes, and subtypes, along with providing information on the impact of current and earlier migratory flows. HCV is phylogenetically classified into 8 major genotypes and 57 subtypes. HCV genotype and subtype distribution differ according to geographic origin and transmission risk category. Unless people with HCV infection are detected and treated appropriately, the number of deaths due to the disease will continue to increase. In 2015, 1.75 million new viral infections were mostly due to unsafe healthcare procedures and drug use injections. In the same year, access to direct-acting antivirals was challenging and varied in developing and developed countries, affecting HCV cure rates based on their availability. The World Health Assembly, in 2016, approved a global strategy to achieve the elimination of the HCV public health threat by 2030 (by reducing new infections by 90% and deaths by 65%). Globally, countries are implementing policies and measures to eliminate HCV risk based on their distribution of genotypes and prevalence.

Small intestinal bacterial overgrowth and celiac disease: A systematic review with pooled-data analysis.

BACKGROUND: A link between small intestinal bacterial overgrowth (SIBO) and celiac disease (CD) has been hypothesized. METHODS: Literature search was performed in main medical databases. Methods of analysis/inclusion criteria were based on Preferred Reporting Items for Systematic reviews and Meta-Analyses recommendations. The end-point was to estimate, by a pooled-data analysis, SIBO prevalence in CD. Proportions/percentages and their 95% confidence intervals (CI) were calculated by inverse variance method, whereas odd ratios (OR) and their 95% CI were estimated, where available, based on the Mantel-Haenszel method. Data were entered into the RevMan 5.3 software. KEY RESULTS: Eleven articles fulfilled considered criteria. The pooled mean prevalence of SIBO in CD was 20% (95% CI of 10%-30%). In comparison to asymptomatic controls, CD was associated to higher risk of SIBO, with an OR of 10.52 (95% CI 2.69-41.21, P=.0007). Jejunal aspirate culture assessed SIBO prevalence of 11% (95% CI 3%-19%) in CD, whereas breath tests detected a higher value (23%, 95% CI 10%-37%). The pooled prevalence of SIBO in CD patients who were symptomatic despite a GFD was 28% (95% CI 10%-47%), higher than in asymptomatic celiac patients (pooled prevalence of 10%, with a 95% CI of 3%-16%), despite not statistically significant (P=.06). When GFD-unresponsive CD was defined only by clinical persistence of symptoms, the prevalence of SIBO was higher than in the case of villous atrophy association (31% vs 16% P=.33). CONCLUSIONS: The heterogeneity of available studies may not support a relationship SIBO-CD. Nevertheless, SIBO could be more common in CD when symptoms do not improve after GFD.