Hepatitis C virus antibodies in acute and chronic liver disease in India.

The prevalence of serum antibodies to hepatitis C virus was assessed by an enzyme-linked immunosorbent assay in patients with epidemic non-A, non-B hepatitis (14), sporadic non-A, non-B hepatitis (42), chronic hepatitis (14) and cirrhosis (26). None of the patients with epidemic non-A, non-B hepatitis (14) and acute self-limiting sporadic non-A, non-B hepatitis without prior parenteral exposure (38) tested positive for hepatitis C virus antibody. Based on epidemiologic features, hepatitis E virus is presumably the etiologic agent for both these entities. Hepatitis C virus (HCV) antibody was positive in none of the patients with cryptogenic chronic hepatitis (11) and in 2(8%) patients with cryptogenic cirrhosis (25). It was concluded that cryptogenic chronic hepatitis and cirrhosis in India may be caused by alternative viral agents of the non-A, non-B type or by hepatotoxins to which the population may be exposed. Of 8 patients with prior parenteral exposure (transfusions 6, needle pricks 2) 5 (62.5%) patients tested positive for HCV antibody. HCV antibody was detected in 1 (25%) patient with acute self-limiting, parenterally transmitted non-A, non-B hepatitis and in 4 (100%) patients with chronic parenterally transmitted non-A, non-B hepatitis.

Serial cholangiographic appearances in recurrent pyogenic cholangitis.

From December 1982 to December 1991, cholangiograms were obtained in 227 patients with recurrent pyogenic cholangitis. Cholangiographic abnormalities included biliary dilation, calculi, sludge, excessive branching, and arrowhead formation of intrahepatic ducts and biliary strictures. In 21 patients, previous evidence of biliary ascariasis was seen. Repeat cholangiograms were performed in 55 patients in a follow-up period of 18.0 +/- 1 months. Of these patients, 12 treated conservatively continued to get recurrent cholangitis and revealed worsening abnormalities on repeat cholangiograms. Another 25 patients had successful endoscopic sphincterotomy and extraction of biliary calculi. These patients remained free of symptoms on follow-up, with significant resolution of abnormalities on repeat cholangiograms. The remaining 18 patients with failed surgical or endoscopic interventions continued to get recurrent episodes of cholangitis and worsening of abnormalities on repeat cholangiograms. This retrospective study indicates that the natural course of recurrent pyogenic cholangitis is a progressive, destructive cholangiopathy. Ascaris lumbricoides invasion of the biliary tree is an initiating event in a sub-group of patients.

Worm extraction and biliary drainage in hepatobiliary and pancreatic ascariasis.

From December 1989 to March 1992, 50 (32%) of 156 patients with hepatobiliary and pancreatic ascariasis underwent various endoscopic interventional procedures. Endoscopic intervention was performed when patients did not respond to energetic symptomatic treatment within the first few days of hospitalization (n = 45) or when worms had not moved out of the ducts into the duodenum at 3 weeks (n = 5). Worm extraction was successful in all 18 patients from the ampullary orifice and in 34 (89.5%) of 38 patients from the bile or pancreatic duct. In five patients with pyogenic cholangitis, endoscopic nasobiliary drainage was performed to decompress the bile ducts. After worm extraction/nasobiliary drainage, 41 (91%) of the 45 patients with biliary disease (n = 42) or acute pancreatitis (n = 3) had rapid relief of symptoms. Three patients developed complications related to endoscopy, including cholangitis (n = 2) and hypotension (n = 1).

Oddi's sphincter motor activity in patients with recurrent pyogenic cholangitis.

Oddi's sphincter motor activity was studied in 15 healthy subjects and 15 patients with recurrent pyogenic cholangitis. No significant difference was found in the common bile duct pressures, the Oddi's sphincter basal pressures or the amplitude, frequency and duration of phasic contractions between the controls and patients. However, a significant difference was found in the percentage of antegrade and retrograde phasic wave sequences between the two groups. In control patients 64.0% +/- 5.3% of phasic wave sequences were antegrade, and 20% +/- 3.6% were retrograde. In patients with recurrent pyogenic cholangitis, 37% +/- 3.6% of phasic wave sequences were antegrade, and 42% +/- 5.5% were retrograde. No significant difference was found in the percentage of simultaneous phasic wave sequences (16% +/- 1.5% vs. 18.5% +/- 2.8%, respectively) between the two groups. In all, five (33%) patients with recurrent pyogenic cholangitis had abnormal propagation of phasic contractions of Oddi's sphincter (retrograde phasic wave sequences greater than 50%), two (13%) patients had elevated Oddi's sphincter basal pressures (greater than 40 mm Hg) and one (7%) patient had increased frequency of Oddi's sphincter phasic contractions (more than 9/min). Six of the 15 patients had evidence of papillitis on duodenoscopy. We believe papillitis could induce motor abnormalities in these patients, thus resulting in delayed biliary drainage and recurrent attacks of cholangitis.

Sonographic findings in gallbladder ascariasis.

Invasion of the adult roundworm, Ascaris lumbricoides, into the gallbladder is rare and was seen in 14(2.1%) of the 665 cases with hepatobiliary ascariasis. The diagnosis was suggested in all 13 cases in which sonography was performed and in 5 of the 11 cases at endoscopic retrograde cholangiography. Sonographic findings included a nonshadowing, long, echogenic structure in the form of a coil, an echogenic strip with central anechoic tube, an echogenic structure extending across the gallbladder giving it a septate appearance, and characteristic erratic, nondirectional, zig-zag movements of these echogenic structures in the gallbladder. Serial sonograms accurately predicted spontaneous exit of the worm. Pregnancy and anomalous origin of the cystic duct directly from the papilla of Vater facilitated worm invasion into the gallbladder. We conclude that real-time sonography offers a simple, rapid approach for the diagnosis and follow-up of patients, whereas endoscopic retrograde cholangiography has limited diagnostic value in this disorder.

Biliary abnormalities associated with extrahepatic portal venous obstruction.

We prospectively studied 21 consecutive patients with extrahepatic portal venous obstruction for evidence of biliary tract disease. Two patients were first seen with extrahepatic cholestasis; another had recurrent cholangitis. All three patients with clinically manifest biliary disease were adults. Another five patients had icterus on clinical examination. Liver function tests revealed elevated bilirubin levels in 14 patients (66.6%), elevated alkaline phosphatase levels in 17 (80.9%) and elevated serum ALT levels in 8 (38.0%). Endoscopic retrograde cholangiography revealed abnormal findings in 17 patients (80.9%). The changes involved the common bile duct (66.6%) more often than they did the hepatic bile ducts (38.1%). Cholangiographic abnormalities included strictures (52.4%), caliber irregularity (23.8%), segmental upstream dilatation (42.8%), ectasia (9.5%), collateral veins causing extraluminal bile duct impressions (14.3%), displacement of ducts (9.5%), angulation of ducts (4.7%) and pruning of intrahepatic ducts (9.5%). The pathogenesis of such cholangiographic abnormalities is unknown. However, possible factors in such changes include collateral veins bridging the blocked portal vein, causing bile duct impressions; fibrous scarring of porta hepatis, causing angulation of bile duct; and ischemic injury to bile duct, leading to stricture formation and caliber irregularity. Biliary disease is important in the clinical outcome of patients with extrahepatic portal venous obstruction because variceal sclerotherapy has prolonged the life expectancies of such patients.

Percutaneous drainage versus albendazole therapy in hepatic hydatidosis: a prospective, randomized study.

BACKGROUND: Recently, drug treatment and percutaneous drainage have been used successfully when treating hepatic hydatid cysts. Until now, there is no published study comparing the relative safety and efficacy of these two forms of treatment. METHODS: In a prospective study, 33 hepatic hydatid cysts were randomly distributed to receive percutaneous drainage (10), albendazole (10 mg.kg-1.day-1 for 8 weeks) plus percutaneous drainage (12), and albendazole alone (11). Patients were serially assessed by clinical and biochemical examinations, ultrasonography, and hydatid serology. RESULTS: On serial ultrasonography, cysts attained heterogeneous echopattern in 18, uniform echogenicity in 11, and disappearance in 3. All 22 cysts treated with percutaneous drainage and only 2 (18.2%) cysts treated with albendazole alone reduced in size and change in echopattern (P < 0.01). Maximum size reduction was observed in cysts treated with a combination of percutaneous drainage and albendazole (P < 0.05). Complications observed with drainage were cyst infection in 2 patients, fever in 3, cyst biliary rupture in 1, and urticaria in 2. These were managed successfully without any mortality. Three patients who received albendazole developed reversible elevation of liver cell enzymes. CONCLUSIONS: It was concluded that percutaneous drainage with albendazole therapy is an effective form of management for hepatic hydatid cysts.