Gastro­oesophageal reflux disease in liver cirrhosis: Possible pathogenesis and clinical intervention (Review).

Oesophageal variceal bleeding is a common complication of decompensated liver cirrhosis (LC). Some studies have reported that reflux oesophagitis (RE) is a risk factor for upper gastrointestinal bleeding, and greatly impacts the quality of life. However, the frequency and mechanism of gastro-oesophageal reflux disease (GERD) in LC remain unclear. The present review explored the possible pathogenesis, and analysed the advantages and disadvantages of the interventional measures and the need for implementation of these measures. By combining the comprehensive terms associated with LC, GERD and RE, EMBASE, Medline/PubMed and the Cochrane Library were systematically searched. The underlying pathological mechanism of GERD in LC was summarized: Transient relaxation of the lower oesophageal sphincter, delayed gastric emptying, increased intra-abdominal pressure, increased intragastric pressure and excessive nitric oxide production destroyed the 'anti-reflux barrier', causing gastric content reflux. Proton pump inhibitors (PPIs) have been widely used empirically to lower the risk of oesophageal venous rupture and bleeding. However, long-term use of acid inhibitors in patients with LC may induce complications, such as spontaneous bacterial peritonitis. The metabolic half-life of PPIs is prolonged in patients with severe liver function impairment. Therefore, the indications for using acid inhibitors lack clarity. However, after endoscopic oesophageal variceal eradication, additional benefits may be gained from the long-term use of PPIs in small doses.

An Open-Label Exploratory Clinical Trial Evaluating the Effects of GLS (Coptidis Rhizoma-Evodiae Fructus 2 : 1) on Fibroblast Growth Factor 21 in Patients with Nonalcoholic Fatty Liver Disease.

Methods: In a 12-week, open-label, exploratory clinical trial, 126 NAFLD patients were randomly divided into the GLS group (lifestyle intervention plus GLS) or the polyene phosphatidylcholine (PPC) group (lifestyle intervention plus PPC). Random numbers generated by DPS software were used in combination with opaque, sealed envelopes for allocation concealment. At baseline as well as at the end of the study, anthropometric parameters, glucose, lipids, hepatic enzymes, and FGF 21 were measured, with hepatic fat accumulation assessed by ultrasound (US) and US-based controlled attenuation parameter (CAP). Results: 119 patients completed the study. Baseline parameters did not significantly differ between the two groups (P > 0.05). Compared with PPC, GLS decreased more significantly in hepatic fat accumulation, body weight index, waist circumference, waist-to-hip ratio, serum glucose, total cholesterol, triglyceride, low-density lipoprotein cholesterol, alanine transaminase, aspartate transaminase, gamma-glutamyl transferase, and FGF 21 (P < 0.05). The effects of GLS on waist circumference, waist-to-hip ratio, CAP, and gamma-glutamyl transferase (GGT) were positively correlated with serum FGF 21 (r = 0.343, 0.342, 0.315, and 0.374, respectively, P < 0.05). The GGT and FGF-21 changes were also confirmed by multiple linear regression analysis (B, 0.777; 95% CI: 0.307-1.247, P < 0.05). Conclusion: GLS has a significant hepatoprotective effect on NAFLD patients, causing a decrease in FGF-21 secretion in response to the damage itself.