FibroTest (FT) has similar accuracy for cirrhosis in ‘intention‐to‐diagnose’ which is superior to transient elastography (TE) in chronic hepatitis B.

ICU are gastrointestinal haemorrhage, sepsis and hepatic encephalopathy (HE); Simplified Acute Physiology Score II (SAPS II) or Sequential Organ Failure Assessment (SOFA), also mentioned by the authors (1), predict ICU mortality (2). Specifically, bacterial infections in cirrhotic patients are mainly caused by Gram-negative bacteria from intestine, although Gram-positive bacteria are a common cause of infection in hospitalized patients (3), also reported by the authors (1). Bacterial infections may be a trigger for HE, and ICU mortality of cirrhotic patients with HE is high. In this respect, hepatitis B (HBV) and C (HCV) infections are among the commonest causes of cirrhosis worldwide and the association between a widespread environmental agent [i.e. Helicobacter pylori (Hp)] and chronic viral hepatitis and/or cirrhosis has been recognized in different parts of the world; Hp infection (Hp-I) is strongly associated with HBVand HCV-related cirrhosis and is commoner in cirrhotic patients with HE than in those without. Moreover, HE is not a fully reversible condition (4,5). Helicobacter pylori-I has been frequently detected in neurological diseases including Alzheimer’s disease (AD) (6). In this regard, we found that Hp eradication may positively influence AD manifestations at 5-year clinical endpoints (7), thereby supporting a role for this common infection in the pathobiology of AD. Apart from Hp-induced increased ammonia and endotoxins circulating levels andHp bacteremia with sepsis that might contribute to HE, Hp may be further involved in cirrhosis-related cognitive dysfunction pathophysiology by several mechanisms including the release of large amounts of pro-inflammatory and vasoactive substances, such as interleukin 6, 8 and tumour necrosis factor (TNF)-a, also mentioned by the authors (1), involved in a number of vascular disorders including AD (6) and possibly HE (1). Specifically, a series of factors have been implicated in inducing blood–brain barrier disruption including inflammatory mediators (e.g. cytokines such as TNF-a and chemokines induced by Hp-I) and oxidative stress (6, 8), thereby leading to encephalopathy. Therefore, Hp eradication therapy in ICU Hp-positive cirrhotic patients might exert beneficial effects on the aforementioned Hp-induced HE-related contributors. However, further large-scale relative studies are needed to elucidate these fields.