No evidence of association between inherited thrombophilia and increased risk of liver fibrosis.

BACKGROUND: Preliminary evidence suggests that inherited hypercoagulable disorders can lead to an increased risk of significant liver fibrosis. OBJECTIVE: We aimed to investigate the prevalence of significant fibrosis in patients with inherited thrombophilia, assessed by using liver stiffness (LS), and to compare this prevalence to that found in a large population-based cohort from the same region. METHODS: This was a single-center, cross-sectional study. A complete laboratory analysis for liver disease, LS by transient elastography and an abdominal ultrasound were performed in patients with inherited thrombophilia diagnosed between May 2013-February 2017. These patients were propensity score matched (ratio 1:4) with a population-based cohort from the same region (PREVHEP-ETHON study; NCT02749864; N = 5988). RESULTS: Of 241 patients with inherited thrombophilia, eight patients (3.3%) had significant fibrosis (LS ≥8 kPa). All of them had risk factors for liver disease and met diagnostic criteria for different liver diseases. After matching 221 patients with thrombophilia with 884 patients of the PREVHEP-ETHON cohort, the prevalence of significant fibrosis was similar between both cohorts (1.8% vs. 3.6%, p = 0.488). Multivariate analysis showed that age and liver disease risk factors, but not belonging to the thrombophilia cohort, were associated with the presence of significant fibrosis. The magnitude of the increased risk of significant fibrosis in patients with risk factors for liver disease was also similar in both cohorts. CONCLUSIONS: Our findings do not provide evidence supporting an association between inherited thrombophilia and an increased risk of significant liver fibrosis, independent of the presence of liver-related causes of fibrosis.

Infliximab-induced hypoglycemia, a rare but relevant side effect.

Tumor necrosis factor (TNF) inhibitors are part of the therapeutic arsenal for many immune-mediated diseases and, especially in inflammatory bowel disease (IBD), have led to a change in the management of this disease.

Management of haemostatic alterations and associated disorders in cirrhosis in Spain: A national survey.

BACKGROUND: Knowledge of haematological abnormalities in cirrhosis has greatly improved in recent years. AIMS: To evaluate how Spanish Digestive Disease specialists manage haemostatic alterations and associated disorders in patients with cirrhosis. METHODS: All members of the Spanish Association for the Study of the Liver and Spanish Society of Digestive Pathology were invited to fill in a web-based questionnaire. RESULTS: 135 professionals, 93 hepatologists and 42 non-hepatologists responded to the survey. The concept of rebalanced haemostasis was known by 74.8% of them. Most specialists corrected the INR and thrombocytopenia before invasive procedures with moderate risk of bleeding or major surgery and in severe gastrointestinal bleeding. The threshold of platelets and, especially, INR used to administer blood products varied greatly. Pharmacological prophylaxis of venous thromboembolism prevailed, but it was highly dependent on the INR and platelet figures. Most participants initiated anticoagulation regardless of the degree of portal vein thrombosis, even in patients ineligible for transplantation. In potential candidates, only 56% maintained it indefinitely or until liver transplantation. No major differences between hepatologists and non-hepatologists were found. CONCLUSIONS: A significant variability and certain deviation from current guidelines was observed among Spanish Digestive Disease specialists regarding management of haemostatic alterations and associated disorders in cirrhosis.

Impact of an acute hemodynamic response-guided protocol for primary prophylaxis of variceal bleeding.

AIM: To evaluate the long-term outcome of an acute hemodynamic response-guided protocol in which acute responders to intravenous propranolol received traditional nonselective beta-blockers (NSBBs) and acute nonresponders received carvedilol. METHODS: Retrospective review of a protocol for primary prophylaxis of variceal bleeding guided by the acute hemodynamic response to intravenous propranolol. Fifty-two acute responders treated with traditional NSBB (i.e. propranolol or nadolol) were compared with 24 acute nonresponders receiving carvedilol. A second hemodynamic study was performed in 27 and 13 patients, respectively. The primary endpoint was development of first or further decompensation. Secondary endpoints included death from any cause, association between acute and chronic hemodynamic response, and baseline clinical and laboratory variables related to the acute hemodynamic response. RESULTS: Acute responders and acute nonresponders presented similar 1, 2, and 3-year probabilities of first decompensation (NSBB: 0%, 13.7%, 26.1% vs carvedilol: 0%, 20%, 20%, P = 0.968) or further decompensation (21.2%, 26.1%, 40.9% vs 21.2%, 50.0%, 50.0%, P = 0.525). A previous episode of hepatic encephalopathy was the only independent predictor of decompensation [hazard ratio (95% confidence interval): 8.03 (2.76-23.37)]. Mortality rates were similar in acute responders and acute nonresponders with compensated (P = 0.428) or decompensated cirrhosis (P = 0.429). No clinical, laboratory, endoscopic or hemodynamic parameter predicted the acute hemodynamic response. In patients receiving traditional NSBB, the acute and chronic changes of hepatic venous pressure gradient were correlated (r = 0.59, P = 0.001). Up to 69.2% of acute nonresponders gained chronic response with carvedilol. CONCLUSION: Early identification and treatment with carvedilol of acute nonresponders to intravenous propranolol improves the clinical outcome of this high-risk group of patients, probably due to its greater effects for reducing portal pressure.