Alcohol-related liver disease phenotype impacts survival after an acute variceal bleeding episode.

BACKGROUND & AIMS: Alcohol-related hepatitis (AH) encompasses a high mortality. AH might be a concomitant event in patients with acute variceal bleeding (AVB). The current study aimed to assess the prevalence of AH in patients with AVB and to compare the clinical outcomes of AH patients to other alcohol-related liver disease (ALD) phenotypes and viral cirrhosis. METHODS: Multicentre, observational study including 916 patients with AVB falling under the next categories: AH (n = 99), ALD cirrhosis actively drinking (d-ALD) (n = 285), ALD cirrhosis abstinent from alcohol (a-ALD) (n = 227) and viral cirrhosis (n = 305). We used a Cox proportional hazards model to calculate adjusted hazard ratio (HR) of death adjusted by MELD. RESULTS: The prevalence of AH was 16% considering only ALD patients. AH patients exhibited more complications. Forty-two days transplant-free survival was worse among AH, but statistical differences were only observed between AH and d-ALD groups (84 vs. 93%; p = 0.005), when adjusted by MELD no differences were observed between AH and the other groups. At one-year, survival of AH patients (72.7%) was similar to the other groups; when adjusted by MELD mortality HR was better in AH compared to a-ALD (0.48; 0.29-0.8, p = 0.004). Finally, active drinkers who remained abstinent presented better survival, independently of having AH. CONCLUSIONS: Contrary to expected, AH patients with AVB present no worse one-year survival than other patients with different alcohol-related phenotypes or viral cirrhosis. Abstinence influences long-term survival and could explain these counterintuitive results.

Occurrence of the JAK2 V617F mutation in the Budd-Chiari syndrome.

Myeloproliferative diseases represent a major risk factor for Budd-Chiari syndrome. In 32 patients with Budd-Chiari syndrome, the JAK2 V617F mutation was detected, in heterozygous state, in 11 individuals (34.4%; 95% confidence interval: 18.6-53.2). Eight patients with (72.7%; 95% confidence interval: 39.0-94.0) and six without (28.6%; 95% confidence interval: 11.3-52.2) the JAK2 V617F mutation had a diagnosis of myeloproliferative diseases before or at the occurrence of the venous thrombotic event. In three patients carrying the JAK2 V617F mutation, a myeloproliferative disease was not detected. Determination of the JAK2 V617F mutation may be useful to recognize patients with Budd-Chiari syndrome with or at risk for the subsequent development of overt myeloproliferative diseases.

Splanchnic vein thrombosis and variceal rebleeding in patients with cirrhosis.

OBJECTIVES: Splanchnic vein thrombosis (SVT) affects the short-term prognosis of acute variceal bleeding in cirrhotic patients. This study evaluated whether SVT also affects the rebleeding rate of patients included in a program of secondary prophylaxis after variceal bleeding. PATIENTS AND METHODS: A total of 387 patients with variceal bleeding were included from January 2001 to December 2010. Band ligation was carried out every 3-4 weeks. Follow-up included endoscopy at 1, 3, and every 6 months, Echo-Doppler, and biochemical examination every 6 months. From 2005, patients with SVT received anticoagulation with enoxaparin 200 UI/kg/day for at least 6 months. The therapy was started after variceal eradication. RESULTS: SVT was diagnosed in 41 patients at variceal bleeding, in eight before and in 18 patients during the follow-up. Variceal eradication was achieved in 89.2 and 86.6% in no-SVT and SVT patients. Rebleeding occurred in 9.5 and 11.9% of no-SVT and SVT patients at 12 months. Varices relapsed more frequently in SVT than in no-SVT patients (25.4 vs. 14.67%, P=0.03). The rates of variceal rebleeding and relapse were similar in patients who received or did not receive anticoagulation, but mortality was significantly lower in patients who received anticoagulation. CONCLUSION: SVT favors the relapse of esophageal varices, but rebleeding can be effectively prevented by standard scheduled band ligations. Anticoagulation does not prevent variceal relapse. The improvement in the survival of patients treated with anticoagulation needs to be confirmed in future studies.

Coagulation disorders in liver disease.

The liver plays a central role in the clotting process, and acute and chronic liver diseases are invariably associated with coagulation disorders due to multiple causes: decreased synthesis of clotting and inhibitor factors, decreased clearance of activated factors, quantitative and qualitative platelet defects, hyperfibrinolysis, and accelerated intravascular coagulation. The bleeding tendency accounts for increased risk of morbidity and mortality in patients with liver disease undergoing diagnostic or therapeutic invasive procedures. Peculiar coagulation disorders are prevalent in patients with acute fatty liver of pregnancy or undergoing liver transplantation. Emerging evidence shows that sepsis further impairs hemostasis in patients with liver cirrhosis bleeding from esophageal varices. Thrombotic events, even if rare in cirrhotic patients, occur mainly in the portal and mesenteric veins. The therapeutic approach to coagulative disorders is also discussed.