Portal cavernoma cholangiopathy: consensus statement of a working party of the Indian national association for study of the liver.

Portal cavernoma cholangiopathy (PCC) is defined as abnormalities in the extrahepatic biliary system including the cystic duct and gallbladder with or without abnormalities in the 1st and 2nd generation biliary ducts in a patient with portal cavernoma. Presence of a portal cavernoma, typical cholangiographic changes on endoscopic or magnetic resonance cholangiography and the absence of other causes of these biliary changes like bile duct injury, primary sclerosing cholangitis, cholangiocarcinoma etc are mandatory to arrive a diagnosis. Compression by porto-portal collateral veins involving the paracholedochal and epicholedochal venous plexuses and cholecystic veins and ischemic insult due to deficient portal blood supply or prolonged compression by collaterals bring about biliary changes. While the former are reversible after porto-systemic shunt surgery, the latter are not. Majority of the patients with PCC are asymptomatic and approximately 21% are symptomatic. Symptoms in PCC could be in the form of long standing jaundice due to chronic cholestasis, or biliary pain with or without cholangitis due to biliary stones. Endoscopic retrograde cholangiography has no diagnostic role because it is invasive and is associated with risk of complications, hence it is reserved for therapeutic procedures. Magnetic resonance cholangiography and portovenography is a noninvasive and comprehensive imaging technique, and is the modality of choice for mapping of the biliary and vascular abnormalities in these patients. PCC is a progressive condition and symptoms develop late in the course of portal hypertension only in patients with severe or advanced changes of cholangiopathy. Asymptomatic patients with PCC do not require any treatment. Treatment of symptomatic PCC can be approached in a phased manner, coping first with biliary clearance by nasobiliary or biliary stent placement for acute cholangitis and endoscopic biliary sphincterotomy for biliary stone removal; second, with portal decompression by creating portosystemic shunt; and third, with persistent biliary obstruction by performing second-stage biliary drainage surgery such as hepaticojejunostomy or choledochoduodenostomy. Patients with symptomatic PCC have good prognosis after successful endoscopic biliary drainage and after successful shunt surgery.

Minimal hepatic encephalopathy: consensus statement of a working party of the Indian National Association for Study of the Liver.

Hepatic encephalopathy (HE) is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Overt HE occurs in approximately 30-45% of cirrhotic patients. Minimal HE (MHE), the mildest form of HE, is characterized by subtle motor and cognitive deficits and impairs health-related quality of life. The Indian National Association for Study of the Liver (INASL) set up a Working Party on MHE in 2008 with a mandate to develop consensus guidelines on various aspects of MHE relevant to clinical practice. Questions related to the definition of MHE, its prevalence, diagnosis, clinical characteristics, pathogenesis, natural history and treatment were addressed by the members of the Working Party.

Endoscopic sclerotherapy of gastric variceal bleeding with N-butyl-2-cyanoacrylate.

BACKGROUND: bleeding from gastric varices is a life-threatening complication of portal hypertension. Fundal and isolated gastric varices are at high risk for variceal bleeding. In this study, we report our experience with n-butyl-2-cyanoacrylate (BC) in patients with large gastric varices. STUDY: twenty-nine patients (15 male, 14 female) with large fundal varices (active bleed, 5; passive bleed after eradication of esophageal varices, 13; unbled fundal varices with red color sign, 11) underwent endoscopic sclerotherapy with BC. Cirrhosis was present in 13 patients; extrahepatic portal venous obstruction, in 13; and noncirrhotic portal fibrosis, in 3. N-Butyl-2-cyanoacrylate after mixing with lipiodol (1:1) was given to the initial 10 patients and was given in undiluted form to the remaining patients, followed by injection of 0.7 mL of distilled water to rinse the injection catheter. One to three injections (0.5-1 mL) were given until all gastric varices became hard. All patients were on long-term endoscopic sclerotherapy or variceal ligation programs for eradication of esophageal varices. RESULTS: acute variceal bleeding was controlled in all five patients with BC injections. Eradication of gastric varices was achieved in 27 (93.1%) patients (20 patients in 1 session, 4 patients in 2, and 3 patients in 3-6). Rebleeding occurred in three (10.3%) patients who responded to repeat BC injections. Complications related to the procedure occurred in two (6.9%) patients. In one patient, the needle became impacted into the tissue adhesive. This patient died 5 days later because of massive upper gastrointestinal bleeding. In the other patient, there was distal embolization. CONCLUSIONS: sclerotherapy of gastric varices with BC is a safe and an effective treatment for control of bleeding and eradication. The needle should be withdrawn immediately after the BC injection to prevent its impaction into the tissue adhesive.

Reevaluation of a North India isolate of hepatitis E virus based on the full-length genomic sequence obtained following long RT-PCR.

The genomic cloning and sequence of hepatitis E virus (HEV) from an epidemic in North India is reported. We describe here a simple method wherein the viral RNA was reverse transcribed and then amplified in a single step using an extra long polymerase chain reaction procedure. The full genome nucleotide sequence of this HEV isolate (called Yam-67) was made up of 7191 nucleotides, excepting the poly(A) tail and had three open reading frames: ORF1 coding for 1693 amino acids (aa), ORF2 coding for 659 aa and ORF3 coding for 122 aa. This North Indian isolate of HEV showed close sequence homology to other HEV isolates from India and Asia, but was distant from the Chinese genotype 4, Japanese, Mexican and US isolates. There is no indication from sequence analysis that this may be an atypical strain of HEV, as reported earlier.