Usha Dutta

Fecal lactoferrin, myeloperoxidase and serum C-reactive are effective biomarkers in the assessment of disease activity and severity in patients with idiopathic ulcerative colitis.

Background and Aim:  Disease activity and severity of ulcerative colitis (UC) is assessed using colonoscopy, which is invasive, costly and has poor patient acceptability. The role of non‐invasive biomarkers of intestinal inflammation in the evaluation of patients with UC is not known. The aim of the study was to examine the role of serum C‐reactive protein (SCRP), fecal myeloperoxidase (FMPO) and fecal lactoferrin (FLF) in assessing disease severity, activity and response to therapy.

High prevalence of human papillomavirus in esophageal squamous cell carcinoma: a study in paired samples

Esophageal squamous cell carcinoma (ESCC) is one of the common cancers with a poor prognosis. Incidences of human papillomavirus (HPV) infection range from 0 to 67% in different parts of the world. It has been frequently associated with high-risk HPV genotypes 16 and 18. The present study analyzes the prevalence of HPV infection in ESCC tumor and adjoining mucosa. Fresh tissue samples were obtained from ESCC tumor (group I) and adjoining mucosa (group II). Aliquots of DNA extracts were used. There were 23 patients with paired samples, 19 (83%) were male. HPV was positive in 20/23 (87%). Mean age of HPV positive in group I was 56.63 ± 6.96 and in group II 54.31 ± 7.13 years (P > 0.05). Majority had more than one viral type. HPV52 was the most common observed in 14 (61%) males and two (9%) females. Other common viruses were HPV55, 39, and 59. Smoking had a significant association with viral positivity. p63 and p16 oncoproteins correlated with degree of tumor differentiation but not with viral status. We documented high prevalence of high-risk HPV in ESCC. Our observations support the concept of persistent infection by an oncogenic HPV in cancer development. Our study highlights importance of documenting viral genotype in a defined geographic area.

Management of Acute Pancreatitis: "PANCREAS" Contains Eight Easy Steps to Remember the Treatment

adiology: Ultrasonography to detect gallstones, choledocholithiasis and local complications. Contrast-enhanced computed tomography (CECT) after 48-72 hours of pain onset to determine the degree and extent of necrosis. Percutaneous catheter drainage guided by ultrasound and CECT is helpful in the management of necrosis and also in bridging the time until surgery [8].

Mesenteric venous thrombosis causing jejunal stricture: secondary to hypercoagulable states and primary portal hypertension.

Ischemic stricture of the small intestine as a result of mesenteric vein thrombosis (MVT) is extremely rare (1–3). Hypercoaguable states such as mutated factor V Leiden and anti-phospholipid antibody syndrome are increasingly being recognized as causes of venous thrombosis (4–6). Portal hypertension predisposes to the development of MVT due to stasis in the mesenteric circulation. We report a patient with noncirrhotic portal fibrosis (NCPF) with portal hypertension who presented with small bowel obstruction secondary to mesenteric venous thrombosis. Interestingly, MVT in this patient was due to a combination of three predisposing factors namely: anti-phospholipid antibody syndrome, factor V Leiden mutation, and portal hypertension.

Gallbladder polyps: How to pick up the sinister ones

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Infected pancreatic pseudocyst of spleen successfully treated by combined endoscopic transpapillary stent placement and transmural aspiration

A 32-year-old man with a known case of idiopathic chronic pancreatitis for the previous 2 years presented with abdominal pain and a high-grade fever of 2 weeks’ duration. The clinical examination revealed splenomegaly, and hematologic investigations revealed neutrophilia. Contrast-enhanced CT of the abdomen showed a pseudocyst in the subcapsular region of the spleen measuring 9 5 cm (Fig. 1). The patient was given intravenous antibiotics, and endoscopic retrograde pancreatography was performed. Because of the patient’s ongoing fever, a minimal amount of contrast medium was injected, and the pancreatogram revealed disruption at the tail end of the pancreas. A 5F 12-cm stent was placed into the disruption (Figs. 2, 3). However, even after 48 hours of stenting there was no improvement in the patient’s condition, and the fever persisted. Thereafter, EUS-guided single-time aspiration of the splenic cyst was done (Fig. 4). The collection was punctured under EUS guidance with a 19-gauge needle (Echotip; Cook Endoscopy, Winston-Salem, NC) through the stomach. The cyst was completely emptied, and 200 mL of purulent material was aspirated. After this, the patient had marked improvement in his symptoms and became afebrile within 24 hours of drainage. The amylase and lipase in the aspirated fluid were very high, and the culture grew Escherichia coli. The antibiotics were continued for 2 weeks. He was thereafter discharged, and MRCP performed 6 weeks later revealed a small residual collapsed cyst in the spleen along with

Esophageal duplication cyst in an adult masquerading as submucosal tumor.

Gastrointestinal duplications usually manifest in children and may involve the esophagus in 20% cases. Esophageal duplication cysts are a rare cause of dysphagia in adults. We report the case of a 35-year-old male who presented to us with progressive dysphagia of 6 months duration. Contrast enhanced computed tomography showed a soft-tissue lesion in right lateral wall of distal thoracic esophagus. On endoscopic ultrasound, a heterogeneously echotextured lesion with anechoic component present at intramural location in the lower esophagus was noted. The patient underwent surgical excision of the lesion and histopathology confirmed the diagnosis of esophageal duplication cyst.

Embolization of Cyanoacrylate glue in systemic circulation in a case of hepatocellular carcinoma: an autopsy report

We report a case of embolism of the sclerosant dye with subsequent formation of foreign-body giant cell reaction within the veins of pulmonary and portal circulation in an autopsy case of hepatocellular carcinoma developing over an underlying primary biliary cirrhosis.

Massive lower gastrointestinal bleed due to rectal varix

IntroductionMassive lower gastrointestinal bleeding is an importantmedical emergency. Among the causes of lower gastroin-testinal bleed, variceal bleeding due to rectal varices israre. Rectal varices frequently develop in patients withportal hypertension and represent porto-systemic collater-als. We present a case of bleeding rectal varices in a patientwith extrahepatic portal vein obstruction that was managedby N-butyl-2-cyanoacrylate injection, which was obliter-ated as documented on endosonography.Case detailsA 26-year-old male patient presented with massive lowergastrointestinal bleeding. On examination, he was palewith splenomegaly, but hemodynamically stable. His hae-moglobin was 3.8 g/dL, and other blood investigationswere in the normal range. Packed red blood cells weretransfused. Abdominal imaging showed splenomegaly withportal cavernoma suggesting the aetiology of extrahepaticportal venous obstruction (EHPVO) and rectal varices(Figs. 1, 2). Colonoscopy showed rectal varices (Fig. 3a)with evidence of blood flow on endosonography (Fig. 4a).Two millilitres of N-butyl-2-cyanoacrylate was injectedinto rectal varices with no post procedural complications(Fig. 3b, c; Video 1 of Electronic supplementary material).The bleeding had stopped. Three days after injection,repeat sigmoidoscopy showed a small ulcer in the rectum atthe injected site. Repeat endorectal ultrasound showedobliteration of the varices and their feeding vessels, withevidence of glue seen in the varix (Fig. 4b). The patient isunder follow-up for 3 months without any re-bleeding. Hishypercoagulation work-up including protein C, protein Slevels, antiphospholipid antibodies, factor V Leiden levelswas negative.DiscussionRectal varices result from dilatation of submucosal veinsthat extend from the dentate line proximally into the rec-tum, and represent the porto-systemic collaterals between

Sarcoidosis presenting as acute pancreatitis

Hypercalcemic states may result in acute pancreatitis. Sarcoidosis has been rarely reported as a cause of acute pancreatitis. A 42-year-old female came with abdominal pain and was found to have acute pancreatitis. Evaluation revealed hypercalcemia and evidence of pulmonary infiltrates and mediastinal lymphadenopathy. Transbronchial lung biopsy revealed noncaseating granulomas consistent with sarcoidosis. In conclusion, sarcoidosis may result in acute pancreatitis by causing hypercalcemia.