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The adverse relationship between viral hepatitis and pregnancy in developing countries had been interpreted as a reflection of retrospectively biased hospital-based data collection by the West. However, the discovery of hepatitis E virus (HEV) as the etiological agent of an epidemic of non-A, non-B hepatitis in Kashmir, and the documenting of the increased incidence and severity of hepatitis E in pregnancy via a house-to-house survey, unmasked this unholy alliance. In the Hepeviridae family, HEV-genotype (gt)1 from genus Orthohepevirus A has a unique open reading frame (ORF)4-encoded protein which enhances viral polymerase activity and viral replication. The epidemics caused by HEV-gt1, but not any other Orthohepevirus A genotype, show an adverse relationship with pregnancy in humans. The pathogenesis of the association is complex and at present not well understood. Possibly multiple factors play a role in causing severe liver disease in the pregnant women including infection and damage to the maternal-fetal interface by HEV-gt1; vertical transmission of HEV to fetus causing severe fetal/neonatal hepatitis; and combined viral and hormone related immune dysfunction of diverse nature in the pregnant women, promoting viral replication. Management is multidisciplinary and needs a close watch for the development and management of acute liver failure. (ALF). Preliminary data suggest beneficial maternal outcomes by early termination of pregnancy in patients with lower grades of encephalopathy.

Background: The long-term outcome of Budd‐Chiari syndrome (BCS) with transjugular intrahepatic portosystemic shunts (TIPS) is not well studied. To address this, the records of 47 consecutive patients with BCS evaluated in one center from January 1989 to April 2004, were analyzed. Results: Seven patients with liver tumors were excluded from analyses. Eleven patients had Bechet’s disease, 14 had thrombophiliac disorders, four had myeloproliferative diseases and 11 patients had other or unknown causes. The site of block was hepatic vein in 16 patients, in the suprhepatic inferior vena cava in 19 and not known in five. The majority of patients (21/40; 52.5%) presented with subacute disease with massive ascites and abdominal pain as the dominant manifestations. Eight patients with membranes or segemental block were treated with transluminal angiopalsty, and six were treated with clinical and biochemical recovery. The TIPS was placed through a transcaval puncture in eight patients with progressive liver disease who were on medical therapy and had thrombosis limited to hepatic veins. One patient bled from portal vein puncture, which was managed by placing stent across the punctured site. The TIPS was very effective in decreasing portal pressure gradient, improving synthetic functions, reducing transaminase levels and controlling ascites. Five patients had TIPS dysfunction needing revision. In two patients it was difficult to maintain TIPS patency due to repeated TIPS dysfunction. However, both these patients were asymptomatic with normal liver function tests. Long-term follow up revealed that patients with TIPS had significantly better survival than those treated with medical therapy alone (log‐ rank test, P = 0.04). In a multivariate Cox-model analysis four variables, namely, more florid presentation, male sex, no treatment with TIPS and increasing Child‐Pugh‐Turcotte score, adversely affected the survival. Conclusions: Budd‐Chiari syndrome needs an individualized multidisciplinary approach and TIPS is indicated in a subgroup of patients with progressive liver disease. It is safe, feasible and improves survival.

Aim: To address the issue of whether or not hepatitis E virus (HEV) is transmitted parenterally. Methods: We conducted a retrospective study which involved 145 multiple transfused patients and 250 healthy controls. A prospective study was also undertaken involving 50 hospitalized patients, 25 of whom were transfused with 107 blood units, while the other 25 did not receive any transfusions. Results: In our retrospective study, markers of acute HEV infection (IgM anti-HEV and HEV RNA) were detected in a significantly higher number of multiple transfused patients (13 of 145) compared to controls (two of 250) (P

Hepatitis E causes large-scale epidemics in endemic areas. The disease, during epidemics, has increased incidence and severity in pregnant women. Sporadic acute viral hepatitis (AVH) is common in endemic areas. The relationship of sporadic AVH and pregnancy has not been well studied. Over a 3-year period we prospectively studied 76 pregnant women and 337 non-pregnant women of childbearing age with sporadic acute viral hepatitis for aetiology, clinical course and outcome of disease. The aetiology in sporadic AVH was hepatitis A virus (HAV) in six (1.5%), hepatitis B virus (HBV) in 62 (15%), hepatitis C virus (HCV) in seven (1.7%), hepatitis D virus (HDV) co-infection in six (1.5%), hepatitis E virus (HEV) in 205 (49.6%), and hepatitis non-A-to-E (HNAE) in 127 (30.7%). Sixty-five (85.5%) pregnant women and 140 (41.5%) nonpregnant women had hepatitis E. The proportion of pregnant women was 31.7% in HEV group and 5.3% in non-HEV group [P < 0.001; OR=8.3 (95%C1 4.2-16.3)]. The prevalence of HEV in pregnant women in first trimester (76.9%), second trimester (88.9%), third trimester (83.8%) and puerperium (100%) did not differ significantly (P=0.09). Forty-seven (61.8%) of the 76 pregnant women developed fulminant hepatic failure (FHF), 69.2% in HEV group and 10% in non-HEV group (P < 0.001). Thirty-four (10.1%) nonpregnant women developed fulminant hepatic failure, 10% in HEV group and 9.7% in non-HEV group (P=0.86). FHF had occurred in four (40%) of 10 patients with HE in first trimester as against 41 (74.5%) of 55 patients in second trimester and beyond (P=0.015). Amongst the major complications of fulminant hepatic failure, cerebral oedema (53.2%) and disseminated intravascular coagulation (21.3%) occurred more often in pregnant women than in nonpregnant women (29.4% and 2.8%; P=0.03 and 0.016, respectively) while infections occurred more often in nonpregnant women (36.1%) than in pregnant women (10.6%; P=0.003). Fifty (61.7%) patients with FHF died [25 (53.2%) pregnant women and 25 (69.5%) nonpregnant women (P=0.06)]. Cerebral oedema and HEV aetiology were independent variables of survival in patients with FHF. Patients with cerebral oedema had worse prognosis and patients with HEV aetiology had best chances of survival. Hence HEV was the most common cause of sporadic AVH in this endemic area. High proportion of pregnant women and increased severity of disease in pregnancy were limited to patients with hepatitis E. Sporadic AVH caused by agents other than HEV did not show any special predilection to or increased severity in pregnancy. FHF in pregnant women caused by HEV was an explosive disease with short pre- encephalopathy period, rapid development of cerebral oedema and high occurrence of disseminated intravascular coagulation and may represent a severe manifestation of a Schwartzmann-like phenomenon.

present in the fundus of the stomach and worms were seen entering the cardiac orifi ce and esophagus. We believe the symptoms were caused by movement of the worms into the esophagus in search of food, especially at night. Th ree patients had repeated episodes of cough and choking during night. EGD showed worms in the esophagus and fundus in one patient ( Figure 2 ) and in the fundus of the stomach in two patients. Th e remaining three patients had associated diseases as detected on EGD (cirrhosis with esophageal varices and hypertensive gastropathy-1, gastric carcinoma-1, and nodular lymphoid hyperplasia-1). Mucosa of the stomach in fi ve patients and the duodenal bulb in four patients showed multiple hemorrhagic erosions. Th ese were localized lesions presumably caused by injury at the site at which the mouth of the ascaride was biting or holding the mucosa. None of the patients presented with gastrointestinal bleeding. All patients reported to have vomited worms during the illness. Gastric ultrasound showed actively motile ascarides in the stomach. Ascarides were recognized by their characteristic long echogenic strips

In recent years percutaneous drainage has been used successfully to treat the hepatic hydatid cysts of echinococcal disease. We performed a controlled trial to compare the safety and efficacy of percutaneous drainage with those of surgical cystectomy, the traditional treatment.In a prospective study, we randomly assigned 50 patients with hepatic hydatidosis to treatment with percutaneous drainage (25 patients) or cystectomy (25). Albendazole (10 mg per kilogram of body weight per day for eight weeks) was administered to the patients who underwent percutaneous drainage. Serial assessments included clinical and biochemical examinations, ultrasonography, and serologic tests of echinococcal-antibody titers.The mean (+/-SD) hospital stay was 4.2+/-1.5 days in the drainage group and 12.7+/-6.5 days in the surgery group (P0.001). Over a mean follow-up period of 17 months, the mean cyst diameter decreased from 8.0+/-3.0 to 1.4+/-3.5 cm (P0.001) after percutaneous drainage and from 9.1+/-3.0 to 0.9+/-1.8 cm (P0.001) after surgery. The final cyst diameter did not differ significantly between the two groups (P=0.20). The cysts disappeared in 22 patients (88 percent) in the drainage group and in 18 (72 percent) in the surgery group (P=0.29). After an initial rise, the echinococcal-antibody titers fell progressively and at the last follow-up were negative (1:160) in 19 patients (76 percent) in the drainage group and 17 (68 percent) in the surgery group (P=0.74). There were procedure-related complications in 8 patients (32 percent) in the drainage group and 21 (84 percent) in the surgery group, 17 of whom had fever postoperatively (P0.001).Percutaneous drainage, combined with albendazole therapy, is an effective and safe alternative to surgery for the treatment of uncomplicated hydatid cysts of the liver and requires a shorter hospital stay.

The role of medical treatment for patients with bleeding peptic ulcers is uncertain.We conducted a double-blind, placebo-controlled trial in 220 patients with duodenal, gastric, or stomal ulcers and signs of recent bleeding, as confirmed by endoscopy. In 26 patients the ulcers showed arterial spurting, in 34 there was active oozing, in 35 there were nonbleeding, visible vessels, and in 125 there were adherent clots. The patients were randomly assigned to receive omeprazole (40 mg given orally every 12 hours for five days) or placebo. The outcome measures studied were further bleeding, surgery, and death.Twelve of the 110 patients treated with omeprazole (10.9 percent) had continued bleeding or further bleeding, as compared with 40 of the 110 patients who received placebo (36.4 percent) (P0.001). Eight patients in the omeprazole group and 26 in the placebo group required surgery to control their bleeding (P0.001). Two patients in the omeprazole group and six in the placebo group died. Thirty-two patients in the omeprazole group (29.1 percent) and 78 in the placebo group (70.9 percent) received transfusions (P0.001). A subgroup analysis showed that omeprazole was associated with significant reductions in recurrent bleeding and surgery in patients with nonbleeding, visible vessels or adherent clots, but not in those with arterial spurting or oozing.In patients with bleeding peptic ulcers and signs of recent bleeding, treatment with omeprazole decreases the rate of further bleeding and the need for surgery.

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.

There are limited data on response and long-term follow-up of octreotide therapy in type-I gastric neuroendocrine tumors. The objective of the present study was to assess the response of type-I gastric neuroendocrine tumors to octreotide-long acting, repeatable (LAR) therapy and evaluate long-term follow up of such patients after therapy.Three patients with documented type-I gastric neuroendocrine tumors from a tertiary gastroenterology centre were studied. Octreotide-LAR therapy 20 mg intramuscularly every 28 days was administered for one year. Serum gastrin and chromogranin levels, gastroscopies and biopsies from tumor nodules at 6 months and one year on therapy and every 6 months after completion of drug therapy were taken. Follow-up after completion of therapy extended for 3 years in two and 2.5 years in one patient.During octreotide therapy there was normalization of serum gastrin levels and serum chromogranin levels. Tumors in all three patients had regressed at 6 months of treatment. Following cessation of therapy, there was progressive rise of serum gastrin to pre-treatment levels. Serum chromogranin levels remained within normal limits. Gastroscopic and histologic examination of gastric biopsies did not reveal recurrence of tumors in any patients. All patients tolerated therapy well and became asymptomatic soon after drug therapy.Octreotide-LAR therapy causes regression of type-I gastric neuroendocrine tumors. After completion of drug therapy there was no recurrence of tumors even with continued hypergastrinemia. Octreotide therapy should be considered as one of the treatment options in such patients.

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.

Background There are few published reports of Trichuris dysentery syndrome (TDS) in children. The disease has not been reported in adults. Objective To report the clinical, colonoscopic, and histologic findings of TDS in adults in an endemic area. Design Case series. Setting Tertiary gastroenterology center. Patients Eighty-four consecutive adult patients with chronic iron deficiency anemia over a 3-year period were investigated. Ten patients had severe Trichuris trichiura infection and received a diagnosis of TDS. Interventions and Main Outcome Measurements Colonoscopy and colonic biopsies. Patients received anthelmintic treatment, and their response was assessed. Results Ten patients with TDS were studied, including 8 female and 2 male patients with a mean (± standard deviation) age of 43 (± 15.5) years (range 15-65 years) and a hemoglobin level (± standard deviation) of 6.0 ± 1.5 g/dL (range 4-8 g/dL); the duration (± standard deviation) of disease was 2.1 ± 1.1 years (range 1.5-8.5 years). None of the patients had growth retardation, malnutrition, or immunodeficiency. Abdominal symptoms included abdominal pain, diarrhea, and hematochezia in 1 patient. Nine other patients had no abdominal symptoms. Colonoscopy revealed actively motile T trichiura worms in large numbers in the right colon in 7 patients, in the ileum in 1, in the left colon in 1, and worms carpeting of the whole colonic mucosa in 1. Associated mucosal changes included petechial lesions, blotchy mucosal hemorrhages, and active mucosal oozing. Biopsy of the colon revealed worm segments with a thick outer cuticle. The posterior segment of the worm contained gravid uterus with numerous characteristic T trichiura eggs. There was paucity of associated mucosal changes in most of the sections. Limitations Similar studies in other endemic areas are lacking. Conclusion TDS should be considered in all patients in endemic areas with chronic iron deficiency anemia and/or occult blood loss.

Ultrasonically (US) guided fine-needle aspiration biopsy was performed in 88 patients who had gallbladder masses. All masses were less than 4.8 cm in diameter. A 22- or 23-gauge, Teflon-coated needle was placed into the mass with the transhepatic or transperitoneal route. By means of this technique, gallbladder malignancy was confirmed in 69 of the 78 cases of malignancy (88.5%). Ten of 10 benign lesions were properly categorized. One patient developed bile peritonitis following a single needle pass with the transperitoneal approach. Pain, a minor complication of the procedure, was noted in four cases. No instances of hemorrhage or vasovagal reactions occurred. From their experience in this large series, the authors conclude that US-guided fine-needle aspiration biopsy of gallbladder masses is a safe, reliable, and accurate technique for the diagnosis of malignancy.

Preduodenal portal vein (PDPV) may occur as an isolated event and result in no symptoms, or it may found at autopsy as an incidental finding; associated preduodenal common bile duct (PDCBD) is an extremely rare event. To the 8 reported cases of PDPV with PDCBD, we add this rare case. Such a discovery is often incidental and of little import; however, it takes on major importance for hepatobiliary surgeons because the accidental damage of PDPV with PDCBD can lead to serious consequences. In addition to describing and illustrating this case, we discuss its relevant anatomy, embryology and associated malformations.

Background and Aim: The biliary tract has been referred to as the ‘Achilles heel’ of liver transplantation. The aim of this study was to document the frequency, clinical presentation and management of biliary complications after liver transplantation in the King Faisal Specialist Hospital and Research Center (KFSH&RC), Riyadh, Saudi Arabia. Methods: The liver transplant clinic at KFSHR age 40.6 ± 18.6 years; pediatric 33, adult 187) during the period from 1987 to June 2003. A total of 235 transplants were carried out on these patients. Cadaveric liver transplants had been carried out on 202 patients, non-heart beating liver transplant in three patients, live donor liver transplants in 11 and split transplant in four. Biliary reconstruction was duct-to-duct anastomosis in 147 patients and Roux-en-Y in 73. Biliary complications were suspected on clinical and biochemical parameters and confirmed using imaging techniques. Results: Forty patients (18.2%) developed 53 biliary complications. These included bile leak in 16, strictures in 25, calculi in eight, and sphincter of Oddi dysfunction and possible recurrence of primary sclerosing cholangitis in the donor duct in two patients each. Bile leaks were observed in the early postoperative period (median period 30 days, range 1–150 days, 95% confidence interval [CI] 8–51). Leakage occurred at the anastomotic site in 13 patients. Patients presented with bilious drainage (n = 6), abdominal pain at T-tube removal (n = 3), fever (n = 2), sepsis (n = 1), dyspnea (n = 1) and abnormal liver tests (n = 3). Eleven patients had intra-abdominal bilious collections. Two patients were treated conservatively, eight patients had ultrasound-guided aspiration of biloma, five had biliary stenting at endoscopic retrograde cholangiopancreatography and two patients needed surgery. There were four deaths, two of which were related to bile leak, one patient was left with permanent external biliary drainage and four patients had biliary strictures in the follow-up period. Biliary strictures occurred at a median period of 360 days (range 4–2900 days; 95% CI 50–670) after the transplant. Hepatic artery thrombosis caused biliary strictures in three, while 21 strictures were localized to the anastomotic site. Biliary strictures presented with elevated liver tests in five patients, progressive cholestasis in five, cholangitis (with septicemia in five) in 11, abdominal pain in two and acute pancreatitis in three patients. Repeat sessions of endoscopic or percutaneous dilatation and stenting (mean sessions 4.4/patient, range 3–7) were attempted in 20 patients to relieve strictures, with success in only nine patients. Seven patients had surgery. Four patients with biliary strictures died. Biliary calculi developed late in the follow-up period and had the appearance of biliary casts in five and sludge in three patients. Eleven (27.5%) patients with biliary disease died compared with 35 (19.4%) patients without biliary disease. Conclusions: Biliary complications occurred in 18.2% of patients after liver transplantation and included biliary leak and biliary strictures with or without calculi. Management involved a combination of endoscopic, radiologic and operative procedures. Biliary complications caused considerable morbidity and mortality in liver transplant patients. © 2004 Blackwell Publishing Asia Pty Ltd

Guidelines for treatment of patients infected with hepatitis C virus genotype 4 are not available.To perform a meta-analysis of randomized controlled trials comparing peginterferon plus ribavirin with interferon plus ribavirin treatment in treatment-naive patients infected with chronic hepatitis C virus genotype 4.The outcome measure was sustained virologic response. The measure of association employed was relative risk calculated by the random-effect model, with heterogeneity, sensitivity and subgroup analyses.Of the 565 studies screened, six randomized controlled trials including 424 patients (peginterferon plus ribavirin 219, interferon plus ribavirin 205) were analysed. Duration of therapy was 1 year in all trials. Sustained virological response obtained with peginterferon plus ribavirin (55%) was significantly higher than with interferon plus ribavirin (30%) [relative risk, 1.71 (95% confidence interval, 1.15-2.56); P = 0.0088]. In the subgroup analyses, sustained virological response in trials using standard-dose ribavirin (1000 or 1200 mg/day) was 72% as against 45.8% in trials using low-dose ribavirin (800 mg/day) (P = 0.01). Further sub-group analyses for treatment duration, body weight, viral load and cirrhosis could not be performed because of lack of relevant data.Treatment-naive patients infected with hepatitis C virus genotype 4 should be treated with peginterferon plus standard-dose ribavirin for 1 year, with an expected sustained virological response rate of 72%.

The early prognostic indicators for acute liver failure in endemic zones for hepatitis E virus have not been determined. All consecutive patients with acute liver failure from a geographically defined region endemic for hepatitis E virus were studied over the period April 1989-April 1996. Demographic, clinical and biochemical parameters were recorded at presentation and serum samples were analysed for known viral hepatitis (A-E) markers. Multiple parameters were compared in survivors and non-survivors in a univariate analysis. All significant factors on univariate analysis were entered into a stepwise logistic regression analysis to identify independent variables of prognosis. The sensitivity and specificity of significant prognostic factors was then assessed. A total of 180 [69 males and 111 females: age (mean +/- SD) 31.1 +/- 14.7 years] with acute liver failure were studied. Of these, 131 (72.8%) patients died. Hepatitis E virus was the aetiological cause in 79 (43.9%) patients, while hepatitis A virus, hepatitis B virus, hepatitis C virus and non-A, non-E agent/'s could be incriminated in four (2.1%), 25 (13.9%), 13 (7.2%) and 56 (31.1%) patients respectively. Of 83 women in childbearing age, 49 (59.0%) were pregnant, 33 (67.3%) of these were in the third trimester. Forty-seven (95.8%) pregnant women had HEV infection. Nine variables differed significantly between survivors and non-survivors on univariate analysis. Of these, four variables which predicted the adverse outcome on multivariate analysis were non-hepatitis-E aetiology, prothrombin time >30 s, grade of coma >2 and age >40 years in that order of significance. Pregnancy per se or duration of gestation did not adversely affect the prognosis. In endemic areas, hepatitis E virus is the commonest cause of acute liver failure. Acute liver failure occurs in a high proportion of pregnant women, mostly in third trimester. Early predictors of a poor outcome are non-E aetiology, prothrombin time >30 s, grade of coma >2 and age >40 years.

Ascariasis is a helminthic infection of global distribution with more than 1.4 billion persons infected throughout the world. The majority of infections occur in the developing countries of Asia and Latin America. Of 4 million people infected in the United States, a large percentage are immigrants from developing countries. Ascaris-related clinical disease is restricted to subjects with heavy worm load, and an estimated 1.2 to 2 million such cases, with 20,000 deaths, occur in endemic areas per year. More often, recurring moderate infections cause stunting of linear growth, cause reduced cognitive function, and contribute to existing malnutrition in children in endemic areas. Ascaris infection is acquired by the ingestion of the embryonated eggs. The larvae, while passing through the pulmonary migration phase for maturation, cause ascaris pneumonia. Intestinal ascaris is usually detected as an incidental finding. Ascaris-induced intestinal obstruction is a frequent complication in children with heavy worm loads. It can be complicated by intussusception, perforation, and gangrene of the bowel. Acute appendicitis and appendicular perforation can occur as a result of worms entering the appendix. HPA is a frequent cause of biliary and pancreatic disease in endemic areas. It occurs in adult women and can cause biliary colic, acute cholecystitis, acute cholangitis, acute pancreatitis, and hepatic abscess. RPC causing hepatic duct calculi is possibly an aftermath of recurrent biliary invasion in such areas. Ultrasonography can detect worms in the biliary tract and pancreas and is a useful noninvasive technique for diagnosis and follow-up of such patients. ERCP can help diagnose biliary and pancreatic ascariasis, including ascaris in the duodenum. Also, ERCP can be used to extract worms from the biliary and pancreatic ducts when indicated. Pyrantel pomoate, mebendazole, albendazole, and levamisole are effective drugs and can be used for mass therapy to control ascariasis in endemic areas.

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).

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.

The incidence, clinical disease and outcome of acute pancreatitis caused by ascariasis in an endemic area of Kashmir, India, was studied prospectively. Ascariasis was an aetiological factor in 59 of 256 patients (23.0 per cent) with acute pancreatitis. Worms had invaded the bile duct in 51 patients, the pancreatic duct in four and both ducts in four. Pancreatitis was mild in 46 patients and severe in 13. Associated pyogenic cholangitis was present in eight. Acute complications occurred in 11 patients. Endoscopic retrograde cholangiopancreatography (ERCP) was performed in all cases within 72 h of admission and delineated ascarides in the duodenum invading the ampullary orifice (44 patients), in the bile duct (55) and in the pancreatic duct (eight). At ERCP, worms were extracted from the ampullary orifice and removed via the mouth of 33 patients with intractable epigastric pain, leading to rapid relief of symptoms. The eight patients with pyogenic cholangitis underwent endoscopic nasobiliary drainage to decompress the bile ducts; worms were extracted from the bile duct of three of these patients using a Dormia basket. A total of 56 patients recovered from acute illness with a combination of conservative and endoscopic treatment; the other three required emergency surgery. At a mean(s.d.) follow-up of 19(7) months, ten patients showed symptomatic worm reinvasion of the biliary tree. The overall mortality rate was 3 per cent.

Antihelmintic treatment with piperazine (1,4-diazacyclohexane) for microfilarie parasitism results in the endogenous formation of piperazine-derived N-nitrosamines. The urinary excretion of these N-nitrosamines was determined by biochemical monitoring of 14 patients receiving 2 g piperazine citrate. The urinary excretion (mean +/- SD) of N-mononitrosopiperazine (MNPz) was 27.0 +/- 26.7 micrograms/day (range 0.6-96.0 micrograms/day). Trace levels of 0.73 +/- 0.92 micrograms/day N,N'-dinitrosopiperazine (DNPz) (range ND-2.8 micrograms/day) were also found in 7 of 14 urine samples. N-Nitroso-3-hydroxypyrrolidine (NHPYR), a metabolite of both MNPz and DNPz, was detected in 11 of 14 urine samples at a mean concentration of 1.74 +/- 1.72 micrograms/day (range ND-5.7 micrograms/day) and traces of N-nitrosodiethanolamine in two samples at levels of 0.3 and less than 0.1 micrograms/day. The results show that biochemical monitoring of urinary NHPYR may be a good indicator of endogenous MNPz formation. While DNPz was also detected in urine, conclusive validation for its endogenous formation could not be provided because no evidence was found for the presence of its major metabolite, N-nitroso-(2-hydroxyethyl)glycine in urine.

Twenty-one hepatic Echinococcus granulosus cysts (maximal diameter, 7.5 cm +/- 4.0) in 12 patients were aspirated and irrigated with hypertonic (20%) saline under sonographic guidance. All patients had signs and symptoms of a hepatic mass caused by the cysts, which had a prominent fluid component that appeared anechoic or hypoechoic, with marked enhancement of back wall echoes. The amounts of cyst fluid aspirated and of hypertonic saline used were 190 mL +/- 240 and 120 mL +/- 90, respectively. Separation of the endocyst from the pericyst and nonviability of scoleces were observed in all cysts. Mean hospital stay was 4.0 days +/- 3.4. Serial sonographic examinations revealed high-level echoes in the cyst cavity (heterogeneous echo pattern), which ultimately became uniformly echogenic (pseudotumor). After follow-up of 14.0 months +/- 5.5, maximal cyst diameter decreased to 4.1 cm +/- 3.1 (P less than .001). One patient died of unrelated causes; the remaining 11 patients experienced relief of symptoms and a decrease in liver span.

The conservative treatment of solitary rectal ulcer is generally unsatisfactory. Six patients, aged 27-54 years, with recurrent solitary rectal ulcer were treated with topical administration of sucralfate in a daily dose of 2 g twice a day for 6 weeks. Four patients experienced complete relief of symptoms and the remaining two patients had marked improvement. Although macroscopic healing of the ulcer was apparent in all, histologic improvement was not appreciable. Five of the six patients remain in remission during a follow-up period of 4-14 months (mean, 8 +/- 1.5 months). Recurrence was observed in one patient at 5 months, which satisfactorily resolved with sucralfate enemas. From these preliminary observations we infer that solitary rectal ulcer can be effectively treated with topical application of sucralfate.

Twenty-five patients (16 males and 9 females; mean age 24.7 +/- 8.4 years) with acute colitis caused by Shigella dysenteriae I were studied, a total of 115 colonoscopic examinations being performed. Twenty-two patients had weekly colonoscopic examinations until the last procedure revealed normal colonic mucosa. Six abnormal colonoscopic appearances were documented, namely mucosal edema, ulcers, friability, punctate spots, erythematous areas and luminal exudate. Mucosal edema was the dominant finding in the first week of the disease. Star-shaped mucosal ulcers and friability were observed in the 2nd and 3rd weeks of the disease. Punctate hemorrhagic spots with normal intervening mucosa in patients with minimal constitutional and colonic symptoms were the hallmark of the disease from the 4th week onwards. None of the patients revealed granularity, cobblestoning, linear fissures, pseudopolyps, pseudomembrane or anal lesions. The colonic involvement was subtotal in 20 patients and total in 5 patients. The mucosal disease was continuous in the initial stage and became patchy during the later stage of recovery. The mucosal disease lasted for 38.8 +/- 12.1 (10-65 days). All the patients followed-up by serial colonoscopy examinations eventually had normal colonic mucosa.

A total of 293 sporadic cases of acute viral hepatitis were identified in Kashmir, India, from April 1979 to December 1981; 44 (15%) were found serologically to be hepatitis A, 94 (32%) hepatitis B, and 155 (53%) non-A, non-B type. The non-A, non-B hepatitis observed was a disease of young adults (29.8 +/- 15 years) with slight male predominance (1.4:1). Six of the 155 non-A, non-B cases had history of prior parenteral exposure, while 51 (33%) had a recent contact with another case of jaundice, suggesting that this form of hepatitis was spread by person-to-person contact. Fulminant hepatic failure occurred in 19 cases, and six (31.5%) of the 19 cases occurred in pregnant women. None of 90 non-A, non-B cases followed up six months later had developed chronic hepatitis. The acute sporadic non-A, non-B hepatitis described in Kashmir resembles epidemic non-A, non-B hepatitis epidemiologically and seems to be distinct from the non-A, non-B hepatitis described in the West.

We have identified hepatitis D as an etiologic cause of an outbreak of 'hepatitis' in an endemic area for hepatitis B in South Kashmir, India. Thirty-five of the 51 patients with jaundice were hepatitis B virus carriers. Twenty-two of the 24 such patients tested had hepatitis D (hepatitis D virus superinfection). Two of the 3 patients with acute hepatitis B were coinfected with hepatitis D virus (HDV). Thirty-six asymptomatic household contacts of hepatitis D patients were assessed. Six were hepatitis B virus carriers, 3 of whom had HDV superinfection. Two contacts had acute hepatitis B, one with HDV coinfection. The disease occurred in adults with a mean age of 28.2 +/- 10.5 years (range 10-56 years) and was equally distributed between the sexes. Three patients with HDV superinfection presented with fulminant hepatic failure with a fatal outcome. All the patients with non-fulminant hepatitis D showed apparent clinical recovery. However, in the subsequent follow-up at 4 years, 7 patients with HDV superinfection had evidence of chronic hepatitis. One of these 7 patients died due to progressive chronic liver disease.

A prospective field study was carried out during an epidemic of non-A non-B hepatitis for determining the incidence and severity of hepatitis in pregnant women, nonpregnant women of child bearing age and men (15 to 45 years old). In 36 (17.3 percent) of 208 pregnant women viral hepatitis developed, as compared to 71 (2.1 percent) of 3,350 nonpregnant women and 107 (2.8 percent) of 3,822 men. The incidence of disease in pregnant women was higher than in the two control groups. The incidence of viral hepatitis in the first, second and third trimesters was 8.8 percent, 19.4 percent, and 18.6 percent, respectively. The incidence in all three trimesters was higher, when compared to that in nonpregnant women. In eight pregnant women (22.2 percent) with viral hepatitis, fulminant hepatic failure developed, as compared to its occurrence in three men (2.8 percent) and in no nonpregnant women. This significantly increased incidence of fulminant hepatitis in pregnancy was indicative of a greater severity of hepatitis during pregnancy. Increased susceptibility to fulminant hepatitis was observed exclusively in the last trimester. Nonfulminant viral hepatitis did not influence the course of pregnancy or fetal well-being. Fetal loss in fatal fulminant hepatitis was a consequence of maternal death and could not be ascribed to direct effect on the fetus or pregnancy.

Sonography was used to investigate the prevalence of symptomatic and silent biliary tract disease, in free living urban population in Kashmir. A randomly drawn sample of 1695 subjects aged 15 years or above was interviewed by a questionnaire. Twenty six had previous cholecystectomies, all for gall stones. Ultrasonography was carried out on 1104 (65.1%). The responder rates for ultrasonography in men (64.3%) and in women (66.0%) were similar (p greater than 0.2). Gall stones were detected in 49 adults. Three of these had previous biliary symptoms. The prevalence of gall stones in adult population was 6.12% (men 3.07% and women 9.6%). The prevalence of gall stones rose with age in both sexes to a peak in the sixth decade prevalence of gall stones was significantly higher in age adjusted parous women than in nullipara. There was no correlation with obesity, diet, or socioeconomic status. Five subjects had sonographic appearances of the worm Ascaris lumbricodis in the bile ducts: and had previous biliary symptoms.

Biliary ascariasis is as frequent a cause of adult biliary disease as gallstones in Kashmir Valley, India. In the present study, we prospectively evaluated the role of sonography in the diagnosis of biliary ascariasis and its utility in monitoring the exit of worms from the bile duct. Sonography was performed on 28 patients with biliary ascariasis proven by endoscopic retrograde cholangiopancreatography. The bile ducts were dilated on sonography in 26 patients. The characteristic sonographic features of worms in the bile duct were as follows: (a) a single, long, linear or curved echogenic structure without acoustic shadowing (2 patients); (b) multiple, long, linear, parallel echogenic strips, usually without acoustic shadowing (15 patients); (c) a thick, long, linear or curved, nonshadowing echogenic strip containing a central, longitudinal anechoic tube, probably representing the digestive tract of the worm (7 patients); and (d) characteristic movement of these long echogenic structures within the bile duct (8 patients). One patient with pancreatic ascariasis exhibited long, linear, nonshadowing echogenic strips in a dilated pancreatic duct. Other sonographic changes observed in these patients were (a) gallbladder distention (10 patients), edema of the gallbladder wall (8 patients), sludge within the gallbladder (11 patients), a coiled echogenic structure within the gallbladder (1 patient); (b) multiple liver abscesses (1 patient); and (c) edematous pancreatitis (4 patients). Sonography detected worms in the biliary tree in 24 of 28 patients (85.7%). Serial sonograms accurately demonstrated the spontaneous exit of worms in 18 patients and the persistence of worms in 3 patients. Sonography is a simple, rapid, and noninvasive method for diagnosis and follow-up of patients with biliary ascariasis.

Little is known about vertical transmission of hepatitis E virus from infected mothers to their infants. We studied eight babies born to mothers infected with hepatitis E in third trimester. One baby was icteric at birth with elevated transaminases and four babies had anicteric hepatitis. Two babies were born with hypothermia and hypoglycaemia and died within 24 h; one had massive hepatic necrosis. Hepatitis E virus RNA was detected by PCR in cord or birth blood samples of five infants. Six infants had evidence of hepatitis E infection. We conclude that hepatitis E virus is commonly transmitted from infected mothers to their babies with significant perinatal morbidity and mortality.

Over a three year period (1 July 1986 to 30 June 1989) all newly diagnosed and histologically proved cases of oesophageal and gastric cancer were recorded prospectively. Some 1515 cases of oesophageal cancer (1050 men and 465 women) and 966 cases of gastric cancer (789 men and 177 women) were registered. Seven patients had simultaneous oesophageal and gastric cancer. Age standardised incidence rates for oesophageal cancer were: men 43.6/100,000 per year; women 27.9/100,000 per year. The rates for gastric cancer were: men 36.7/100,000 per year, women 9.9/100,000 per annum. These figures were three to six times higher than those recorded by cancer registries in Banglore, Madras, and Bombay. The incidence rates for oesophageal and gastric cancer in Islamabad (southern district of Kashmir) were 4.1 to 5.4 times higher in men and 1.5 to 2.0 times higher in women than those for Kupwara (northern district of Kashmir). The incidence rates for oesophageal and gastric cancer in Muslims, Hindus, and Sikhs were different. The epidemiology of oesophageal cancer in Kashmir was similar to that found in the 'Asian oesophageal cancer belt'. At the same time Kashmir also had an unprecedented high incidence of gastric cancer. Kashmiries have special personal and dietary habits. Further studies are needed to define the relation between these habits and the occurrence of oesophageal and gastric cancer.

1. Twenty-eight patients who fulfilled entry criteria for sphincter of Oddi dysfunction were randomly allocated to receive nifedipine and placebo in a cross over design with 12 week treatment periods separated by a 2 week wash-out. 2. All patients had episodic pain resembling biliary pain, had previously undergone cholecystectomy, had elevated alkaline phosphatase during episodes of pain and had elevated basal pressure on sphincter of Oddi manometry. 3. Compared with placebo, significant decreases in cumulative pain score, number of pain episodes, oral analgesic tablets consumed and emergency room visits were observed during nifedipine treatment. 4. Overall 21 patients improved during nifedipine therapy while seven patients did not. None of the following predicted response to nifedipine therapy: enzyme levels, morphine-Prostigmine test, fatty meal sonography, common duct diameter and pressure, sphincter of Oddi phasic pressure, frequency and duration of phasic waves and maximal fall in the basal pressure at sphincter of Oddi manometry after sublingual administration of nifedipine. However patients with predominant antegrade propagation of phasic contractions of sphincter of Oddi did significantly better on nifedipine than those with abnormal propagation of phasic contractions. 5. Nifedipine therapy orally in maximal tolerated doses relieves pain in patients with sphincter of Oddi dysfunction who have elevated basal pressure and sphincter of Oddi phasic contractions of predominantly antegrade nature.

Background Nodular lymphoid hyperplasia of gastrointestinal tract is a rare disorder, often associated with immunodeficiency syndromes. There are no published reports of its association with Helicobacter pylori infection. Methods From March 2005 till February 2010, we prospectively followed all patients with diffuse duodenal nodular lymphoid hyperplasia (DDNLH). Patients underwent esophagogastroduodenoscopy with targeted biopsies, colonoscopy, and small bowel video capsule endoscopy. Duodenal nodular lesions were graded from 0 to 4 based on their size and density. Patients were screened for celiac sprue (IgA endomysial antibody), immunoglobulin abnormalities (immunoglobulin levels & serum protein electrophoresis), small intestine bacterial overgrowth (lactulose hydrogen breath test), and Helicobacter pylori infection (rapid urease test, and histological examination of gastric biopsies). Patients infected with Helicobacter pylori received sequential antibiotic therapy and eradication of infection was evaluated by 14C urea breath test. Follow up duodenoscopies with biopsies were performed to ascertain resolution of nodular lesions. Results Forty patients (Males 23, females 17; mean age ± 1SD 35.6 ± 14.6 years) with DDNLH were studied. Patients presented with epigastric pain, vomiting, and weight loss. Esophagogastroduodenoscopy showed diffuse nodular lesions (size varying from 2 to 5 mm or more) of varying grades (mean score ± 1SD 2.70 ± 0.84) involving postbulbar duodenum. Video capsule endoscopies revealed nodular disease exclusively limited to duodenum. None of the patients had immunoglobulin deficiency or small intestine bacterial overgrowth or positive IgA endomysial antibodies. All patients were infected with Helicobacter pylori infection. Sequential antibiotic therapy eradicated Helicobacter pylori infection in 26 patients. Follow up duodenoscopies in these patients showed significant reduction of duodenal nodular lesions score (2.69 ± 0.79 to 1.50 ± 1.10; p < 0.001). Nodular lesions showed complete resolution in 5 patients and significant resolution in remaining 21 patients. Patients with resistant Helicobacter pylori infection showed no significant reduction of nodular lesions score (2.71 ± 0.96 to 2.64 ± 1.15; p = 0.58). Nodules partially regressed in score in 2 patients, showed no interval change in 10 patients and progressed in 2 patients. Conclusions We report on a large cohort of patients with DDNLH, etiologically related to Helicobacter pylori infection.