Samir Mohindra

Small intestinal bacterial overgrowth is common both among patients with alcoholic and idiopathic chronic pancreatitis

BACKGROUND Small intestinal bacterial overgrowth (SIBO) is known to occur in patients with chronic pancreatitis, particularly of alcoholic etiology. There are, however, scanty data on frequency of SIBO in patients with chronic idiopathic pancreatitis and factors associated with its occurrence. METHODS 68 patients with chronic pancreatitis and 74 age and gender-matched healthy subjects (HS) were evaluated for SIBO using glucose hydrogen breath test (GHBT). Persistent rise in breath hydrogen 12 ppm above basal (at least two recordings) was diagnostic of SIBO. RESULT SIBO was diagnosed more often among patients with chronic pancreatitis than controls (10/68 [14.7%] vs. 1/74 controls [1.3%]; p = 0.003). Of 68 patients, 22 (32.3%) had alcoholic and 46 (67.6%) had idiopathic chronic pancreatitis. SIBO was as commonly detected among patients with alcoholic as idiopathic pancreatitis (3/22 [13.6%] vs. 7/46 [15.2%]; p = 0.86). Age, gender, body mass index (BMI), steatorrhoea, pain, analgesic use, pancreatic calcifications and use of pancreatic enzyme supplements had no relationship with the presence of SIBO. Diabetes mellitus tended to be commoner among patients with chronic pancreatitis with than without SIBO (6/10 [60%] vs. 18/58 [31%]; p = 0.07). CONCLUSION SIBO was commoner among patients with chronic pancreatitis, both alcoholic and idiopathic, than HS. Though presence of SIBO among patients with chronic pancreatitis tended to be commoner among those with diabetes mellitus, there was no relationship with age, gender, BMI, steatorrhoea, pain, analgesic use, pancreatic calcifications and use of pancreatic enzyme supplements.

Endoscopic Management of Portal Cavernoma Cholangiopathy: Practice, Principles and Strategy

Portal cavernoma cholangiopathy (PCC) is the presence of typical cholangiographic changes in patients with a portal cavernoma due to chronic portal vein thrombosis, in the absence of other biliary tract diseases. Probably due to biliary stasis related to the cavernoma, there is a high incidence of biliary sludge and calculi in PCC, which trigger symptoms that resolve with appropriate interventions. Persistent and troublesome symptoms are usually due to biliary stenoses or strictures, which may occur with or without biliary calculi and may be short or long, solitary or multifocal, extrahepatic or intrahepatic. Experience with endoscopic interventions in PCC over the last twenty years has shown that it is the procedure of choice for bile duct calculi. Plastic stenting with repeated, timely, stent exchanges is the first line intervention for jaundice or cholangitis due to biliary strictures. If biliary obstruction does not resolve, portosystemic shunt surgery (PSS) or transjugular intrahepatic portosystemic stent shunt (TIPS) is performed to decompress the portal cavernoma. However, for patients with non-shuntable veins or blocked shunts, repeated plastic stent exchanges are the only option though there are reports of the use of biliary self-expandable metal stents in this situation. If symptomatic biliary obstruction persists after successful PSS or TIPS, second stage biliary surgery may be necessary. Recent experience suggests that treating biliary strictures in PCC on the lines of postoperative benign biliary strictures with balloon dilatation and repeated exchanges of plastic stent bundles may be effective therapy. Endoscopic management appears to be associated with an increased frequency of hemobilia, which usually responds to standard management. Recurrent cholangitis with formation of sludge and concretions may be a problem with repeated stent exchanges, especially if patient compliance is poor. In conclusion, the current understanding is that symptomatic PCC is best managed jointly by the endoscopist and surgeon with sequential interventions designed initially to establish and maintain biliary drainage, then to decompress the portal cavernoma and, finally, if required, second stage biliary surgery or endotherapy for biliary strictures. Endoscopic therapy occupies a central role in management before, during and after surgical therapy. Paradigms of endoscopic therapy continue to evolve as knowledge of pathogenesis and natural history improves and newer approaches and techniques are applied.

CAPSULE ENDOSCOPY FOR OBSCURE GASTROINTESTINAL BLEEDING IN THE TROPICS: REPORT FROM INDIA

Background:  Capsule endoscopy (CE) is useful in patients with obscure gastrointestinal bleeding (OGIB). Experience in CE in OGIB in the tropics is limited.

Common Variants in CLDN2 and MORC4 Genes Confer Disease Susceptibility in Patients with Chronic Pancreatitis.

A recent genome-wide association study (GWAS) identified association with variants in X-linked CLDN2 and MORC4, and PRSS1-PRSS2 loci with chronic pancreatitis (CP) in North American patients of European ancestry. We selected 9 variants from the reported GWAS and replicated the association with CP in Indian patients by genotyping 1807 unrelated Indians of Indo-European ethnicity, including 519 patients with CP and 1288 controls. The etiology of CP was idiopathic in 83.62% and alcoholic in 16.38% of 519 patients. Our study confirmed a significant association of 2 variants in CLDN2 gene (rs4409525—OR 1.71, P = 1.38 x 10-09; rs12008279—OR 1.56, P = 1.53 x 10-04) and 2 variants in MORC4 gene (rs12688220—OR 1.72, P = 9.20 x 10-09; rs6622126—OR 1.75, P = 4.04x10-05) in Indian patients with CP. We also found significant association at PRSS1-PRSS2 locus (OR 0.60; P = 9.92 x 10-06) and SAMD12-TNFRSF11B (OR 0.49, 95% CI [0.31–0.78], P = 0.0027). A variant in the gene MORC4 (rs12688220) showed significant interaction with alcohol (OR for homozygous and heterozygous risk allele -14.62 and 1.51 respectively, P = 0.0068) suggesting gene-environment interaction. A combined analysis of the genes CLDN2 and MORC4 based on an effective risk allele score revealed a higher percentage of individuals homozygous for the risk allele in CP cases with 5.09 fold enhanced risk in individuals with 7 or more effective risk alleles compared with individuals with 3 or less risk alleles (P = 1.88 x 10-14). Genetic variants in CLDN2 and MORC4 genes were associated with CP in Indian patients.

Association between pro-(IL-8) and anti-inflammatory (IL-10) cytokine variants and their serum levels and H. pylori-related gastric carcinogenesis in northern India.

Background Interleukin (IL)-8 -251 T/A and IL-10 (-1082 G/A and -819/592 C/T) polymorphisms and their expression may influence gastritis, atrophy, intestinal metaplasia (IM) and gastric cancer (GC) following H. pylori infection. Methods Genotyping of these genes was performed (ASO-PCR) in 200, 182 and 250 with GC, functional dyspepsia (FD) and healthy controls (HC), respectively. Anti-H. pylori IgG-antibody was tested in all and serums IL-8 and IL-10 were measured randomly in 60 subjects of each group by ELISA. Results Pro-(IL-8)-251 AA and anti-inflammatory (IL-10)-819 TT genotypes were commoner among GC than HC (p = 0.023, OR 1.86 [1.09–3.2] and p = 0.020, OR 2.0 [1.11–3.5]) but comparable with FD. IL-8 AA and IL-10-819 T allele carriage was also commoner in H. pylori-infected GC than HC (p = 0.011, OR 2.47 [1.23–5.0], and p = 0.018, OR 2.3 (1.16–4.59). IL-10-1082 G/A genotype and haplotypes (ACC, GCC, ATA and GTA) were comparable in all groups. Circulating levels of IL-8 and IL-10 were higher among GC than HC but comparable to FD (IL-8; 57.64 [6.44–319.46] vs. 54.35 [4.24–318.96] and 26.33 [4.67–304.54] pg/ml, p < 0.001 and IL-10; 15.47 [1.01–270.87] vs. 12.28 [0.96–64.88] and 3.79 [1.24–56.65], p < 0.001 for GC vs. HC). IL-8/IL-10 ratio was lower among GC than HC but higher than FD (3.7 [0.18–38.41] vs. 6.59 [0.98–130.2], p < 0.001 and 4.22 [0.15–61.4], p < 0.01). Circulating levels of IL-8, IL-10 and IL-8/lL-10 ratios were different among H. pylori-infected and non-infected GC than HC (p < 0.001, p < 0.001 and p < 0.01). Conclusions Pro-(IL-8)-251 T/A and anti-inflammatory (IL-10)-819 C/T gene polymorphisms and their circulating levels may play a role in H. pylori-associated gastric carcinogenesis in northern India.

Early prognostic markers for fatal fulminant hepatic failure cases with viral hepatitis: Proton nuclear magnetic resonance spectroscopic studies of serum

BACKGROUND Fulminant hepatic failure is associated with liver metabolic derangements which could have fatal consequences. The aim of the present study is to identify serum markers for early prediction of the outcome. METHODS Proton nuclear magnetic resonance spectroscopic studies of serum of fulminant hepatic failure patients due to viral hepatitis with grade II/III of encephalopathy (twenty-four: ten prospective and fourteen retrospective) and twenty-five controls were undertaken. Of the twenty-four patients, fifteen survived with medical management alone while nine had fatal outcome. RESULTS The results demonstrated significantly elevated indices of amino acids (alanine, lysine, glutamine, histidine, tyrosine, phenylalanine and 1,2-propanediol) in fatal cases compared to survivors and controls. Principal component analysis showed clear separation of fatal and surviving cases. Liver function parameters were significantly deranged in patients but they failed to provide early significant differences between surviving and fatal cases. Compared to model for end-stage liver disease scores, principal component analysis appear to be better as an early prognostic indicator. Biochemical mapping of pathways suggested interruptions in amino acid metabolism and urea cycle. CONCLUSIONS Proton nuclear magnetic resonance studies of serum have the potential of rapidly identifying patients with irreversible fulminant hepatic failure requiring liver transplantation as life saving option.

Acute Pancreatitis-Induced Thrombotic Thrombocytopenic Purpura

CONTEXT Acute pancreatitis due to thrombotic thrombocytopenic purpura is a well recognized condition. Here, we are reporting a rare converse phenomenon, in which thrombocytopenic purpura occurred secondary to acute pancreatitis. CASE REPORT A 19-year-old male referred to our intensive care unit with diagnosis of acute pancreatitis with multi-organ dysfunction. He had history of severe abdominal pain and recurrent vomiting about one month ago, requiring hospital admission. There, on diagnostic work-up at admission, abdominal ultrasonography was suggestive of pancreatitis. His serum amylase and lipase were 1,900 and 1,582 U/L, respectively. Other laboratory parameters were within normal limits. He was managed conservatively with intravenous fluids, antibiotics and analgesics; and discharged after about 2 weeks One week after discharge he was readmitted in same hospital with abdominal pain, multiple episodes of bilious vomiting and abdominal distention. Later on he was referred to our intensive care unit; having classical pentad of thrombocytopenic purpura, i.e., thrombocytopenia, micro-angiopathic hemolytic anemia, renal failure, encephalopathy, and fever. His condition improved with plasma exchange therapy and transferred out from our ICU to ward after 10 days of stay. CONCLUSION Thrombocytopenic purpura may be precipitate by acute pancreatitis due to multiple mechanisms. A high clinical suspicion is required to make an early diagnosis and allow early initiation of plasma exchange therapy, resulting in a good prognosis.

Acute Hepatitis E-Associated Acute Pancreatitis: A Single Center Experience and Literature Review.

Objective Because acute pancreatitis (AP) associated with acute hepatitis E is rarely reported, we present such a case series. Methods Records of patients admitted with AP to our institution between May 2007 and December 2013 were reviewed. Diagnosis of AP and acute hepatitis E was based on high serum amylase and/or lipase (>3 times the upper normal limit) and abdominal imaging and presence of serum IgM antibodies against hepatitis E virus, respectively. Other causes of AP were excluded by appropriate evaluation. Results Of 790 patients with AP, 16 (2.1%; median [range] age, 25 [16–54] years; 15 males) had hepatitis E and no other cause of AP; coexistent hepatitis A and B were present in two and one of them, respectively. Acute pancreatitis began (median [range], 8 [0–35] days) after acute hepatitis and was mild in 10 and severe in 6. Complications included intra-abdominal collections (5), acute renal failure (4), and acute lung injury (2). Median (range) bilirubin, alanine aminotransferase, and prothrombin time were 9.8 (0.4–25) mg/dL, 822 (54–4009) IU/L, 14.6 (9.7–27.4) seconds, respectively. Acute liver failure occurred in 1 patient only. No patient needed surgical, endoscopic, or percutaneous intervention. Conclusions Acute pancreatitis associated with hepatitis E is not uncommon and usually has good prognosis.

Upper Gastrointestinal Bleed Following Percutaneous Liver Abscess Drainage

© 2015 Upper Gastrointestinal Bleed Following Percutaneous Liver Abscess Drainage Hemanta K. Nayak , Vivek A. Saraswat , Samir Mohindra , Raghunandan Prasad y, Arun Karyampudi * Department of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India and yDepartment of Radiodiagnosis, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India

Successful combined transpapillary and transmural management of a large biloma and bile duct injury: A case report and review of literature

Here, we report a patient with bile duct injury (BDI) following open cholecystectomy, who developed a very large biloma, causing duodenal and biliary obstruction, and also had a biliary stricture at the site of BDI. We successfully managed the patient by endoscopic biloma-gastrostomy with biliary stenting that resulted in resolution of the biloma and aggressive endoscopic management of the biliary stricture with stent bundles till resolution. Pertaining this case to be the one with largest biloma in the literature (approximately 6.5 L), which developed following open cholecystectomy that resulted in biliary stricture following injury to BD. We successfully managed the patient by endoscopic biloma-gastric stenting and an aggressive endoscopic management of biliary stricture.