The advent of direct antiviral agents (DAAs) has radically changed the natural history of hepatitis C virus (HCV) chronic liver disease. Even patients with cirrhosis may display improvements in liver function or features of portal hypertension following viral eradication. The aim of this study was to assess whether a HCV cure would lead to improvements in cirrhotic patients using simple, readily available tools in clinical practice, together with liver stiffness (LS) measurement. This is a retrospective study of cirrhotic patients with cured HCV infection, with or without previous decompensation. Clinical and biochemical parameters as well as LS measurements were collected before antiviral treatment with DAAs and after 6 months following sustained virological response. Hepatic synthesis was assessed by serum albumin levels. Portal hypertension was indirectly assessed by platelet count. Liver function was determined by the CHILD score. A total of 373 cirrhotic patients with successful HCV eradication were retrospectively included. After 6 months of follow-up, a significantly higher proportion of patients showed improved liver function, shifting from the CHILD B/C to CHILD A group, (71.4%, p < 0.001). Similarly, LS improved from a median of 19.3 kPa (14.7–27) at the baseline vs. a median of 11.6 (7.7–16.8 kPa) at follow-up (p < 0.001). The proportion of patients who showed improved hepatic synthesis was 66.0%, which was statistically different when compared to that of patients who had a worsened condition (0.3%) (p < 0.001). Moreover, when classifying the cohort according to the RESIST-HCV score, we found that a significant proportion of patients shifted into the “low risk” group following DAA treatment (52% baseline vs. 45.6% at follow-up, p = 0.004). Even in the decompensated patients, LS improved from 1.6 to 2-fold from the baseline. Antiviral treatment is effective in improving indirect signs of hepatic synthesis and portal hypertension. Similarly, the LS values displayed significant improvements, even in decompensated patients.

Helicobacter pylori (H. pylori) is a bacterium that selectively colonizes gastric epithelium in more than 50% people over the world. The infection is usually acquired in early childhood and rarely resolved spontaneously; transmission is mostly person to person, and occurs by fecal-oral or oraloral modality. Diagnosis and antibiotic treatment may lead to eradication of H. pylori, improving the prevention and the outcome of gastric and extragastric diseases. Many tests are currently available for the diagnosis of H. pylori infection and the choice depends on several clinical aspects including symptoms, age, indications for testing, concomitant medications and comorbidities.Invasive tests (i.e. endoscopy with histologic assessment) are considered the gold standard, but they are expensive and should be performed only in an appropriate context. The most common noninvasive tests are urea breath test (UBT), stool antigens test and serology. UBT is non-invasive, quick, safe, accurate and cheap. This test is performed mainly with 13 C and is based on the presence of H. pylori urease, an enzyme that converts urea (labelled with an isotope) into CO2. Labelled CO2 is then exhaled and measured by dedicated spectrophotometers. This review analyses with special emphasis UBT, focusing on its molecular aspects.

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