Kashif Ahmed

A case of EUS-guided FNA-related pancreatic cancer metastasis to the stomach.

c a m t p p F c s EUS-guided FNA (EUS-FNA) has become a useful diagnostic and staging tool in the care of patients with pancreatic cancer. The sensitivity and specificity of EUS-FNA for pancreatic neoplasms have been reported to be 64% to 85% and 90% to 100%, respectively.1 The overall compliation rate of EUS-FNA has been reported to be 1% in arge centers.2 The risk for potential peritoneal tumor seeding appears to be much lower in EUS-FNA than with percutaneous sampling.3,4 In the English-language literaure, only 3 cases of EUS-FNA–related needle-tract seeding f tumor cells have been reported. We report a unique ase of needle-tract seeding and management in a patient ith a history of pancreatic adenocarcinoma.

Sodium taurocholate inhibits intestinal adenoma formation in APCMin/+ mice, potentially through activation of the farnesoid X receptor

In light of clinical and biological evidence that bile constituents exert preventive effects against colorectal cancer, we evaluated the influence of oral bilirubin and sodium taurocholate (NaTC) on intestinal tumor formation in APC(Min/+) mice. Mice received bilirubin and/or bovine serum albumin (BSA) and NaTC in the drinking water for 8 weeks, after which the number, size and location of intestinal adenomas were determined. Tissue specimens were analyzed by light microscopy, TUNEL staining, immunohistochemistry for beta-catenin and Ki-67 and quantitative polymerase chain reaction for farnesoid X receptor (FXR)-dependent gene expression. Colon tumor formation also was assessed in azoxymethane (AOM)-treated hyperbilirubinemic Gunn (j/j) and wild-type (+/+) rats. Compared with untreated APC(Min/+) mice, the mean number of intestinal adenomas was markedly lower in both bilirubin (10.5 +/- 0.9 versus 37.0 +/- 5.2; +/-SEM; P < 0.001) and NaTC plus BSA (14.3 +/- 5.4; P = 0.01)-treated animals. Both treatment groups exhibited reduced levels of cellular proliferation in the ileum (by Ki-67 staining), but no differences in TUNEL staining or the percentage of beta-catenin-positive crypts. Bilirubin feeding reduced intestinal inducible nitric oxide synthase expression, but did not alter adenoma multiplicity in APC(Min/+) mice or in AOM-treated j/j versus +/+ rats. Mice receiving NaTC manifested increased intestinal expression of the FXR-regulated genes, Shp, FGF15 and IBABP, and a concomitant decrease in cyclin D1 message. Administering NaTC to APC(Min/+) mice causes a marked reduction in intestinal adenomas. We postulate that this effect is mediated through activation of FXR, leading to increased Shp expression and consequent downregulation of cyclin D1.

Oxaliplatin-induced immune mediated thrombocytopenia

Oxaliplatin is a third generation platinum compound used in patients with advanced colorectal carcinoma. Recently, the mechanism of a rare drug-induced immune thrombocytopenia in patients receiving oxaliplatin has been described. This complication is caused by oxaliplatin-dependent antibodies directed against platelet surface glycoproteins, and is unrelated to myelosuppression. In this report, we describe two patients who developed thrombocytopenia immediately soon after receiving oxaliplatin. Sensitization presumably had occurred after receiving oxaliplatin during preceding courses of multiagent chemotherapy that included oxaliplatin.

Diffuse Hepatic Calcification Following Ischemic Insult in the Setting of Impaired Renal Function

t p a i s A man who had undergone liver transplantation 21 years earlier for fulminant hepatitis was admitted to he hospital for elective kidney transplantation for renal failure econdary to calcineurin inhibitor (tacrolimus) toxicity. Postperatively, the patient became profoundly hypotensive from assive intra-abdominal hemorrhage, leading to acute tubular ecrosis and failure of the transplanted kidney. Physical examnation at that point showed mild jaundice and well healed ncision from the surgery. Laboratory findings included: calium 8.1 mg/dL, phosphate 8.5 mg/dL, aspartate transaminase 1,212 U/L, alanine aminotransferase 4884 U/L, total bilirubin .9 mg/dL, direct bilirubin 4.8 mg/dL, and international noralized ratio 1.6. An abdominal computed tomography scan emonstrated focal areas of low attenuation in the liver Figure A, white arrow) consistent with ischemic injury. After resuscitation, the patient’s liver enzymes improved. A repeat computed tomography scan performed 3 weeks later revealed diffuse calcifications throughout the liver, most prominently in the areas of ischemic injury, as well as in muscle tissue (Figure B, white arrows). Liver biopsy showed marked hepatocytic and canalicular cholestasis without any calcium deposits in the endothelium (Figure C). After supportive therapy, the patient’s clinical condition stabilized, and he was discharged to a rehabilitation center. Hepatic calcifications can be grossly characterized as vascular, parenchymal, and capsular.1 While various infections (eg, hisoplasmosis, brucellosis, coccidioidomycosis, and tuberculosis) r neoplastic conditions (eg, primary hepatoma, cholangioma, nd hemangioma) can result in focal calcium deposits in the iver, diffuse hepatic calcification is quite rare.2 Scant case reports have described this condition secondary to dystrophic calcification and calciphylaxis. The term calciphylaxis (calcific uremic arteriolopathy) has been coined to describe the condition where calcium phosphate deposits in the skin and in the intima of medium to small size arterioles of hemodialysis patients. Calciphylaxis has occasionally been described in other organs, such as the lungs, stomach, and heart. Liver calciphylaxis has only been described when hepatic ischemia occurs in the setting of renal failure and a high calcium-phosphorous product.1 Dystrophic calcification, on the other hand, occurs at he site of tissue injury due to ischemia or trauma, and calcium hosphorous product can either be normal or high. In the bsence of any pathologic evidence of hepatocytic or intimal nvolvement of the liver in the above case, we will attribute this triking radiological finding to dystrophic calcification.

Protein-Losing Enteropathy in a Post-partum Female Secondary to Metastatic Melanoma of the Gut: Report of a Case

Malignant melanoma (MM) is a common metastatic tumor of the gastrointestinal (GI) tract. Although 60% of malignant melanoma patients will have post-mortem evidence of gastrointestinal involvement, only limited numbers (1–4%) of patients will actually be diagnosed with it [1]. Clinical presentation varies depending upon the site involved. We report a rare case of metastatic GI melanoma manifesting as protein-losing enteropathy.