M.A. Heilperin's Aspects of the pathology of money: monetary essays from four PDF

By M.A. Heilperin

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I(1):26 o Late stages characterized by biliary cirrhosis, bile plugs in ductules, and interlobular bile ducts without periductal fibrosis or epithelial injury o May see cholesterol clefts in bile ducts ANCILLARY TESTS Immunohistochemistry  FIC1 disease shows diffuse variable reduction in canalicular expression of CDT3, GGT, and pCEA  BSEP disease shows absent canalicular staining for BSEP but preserved staining for other canalicular enzymes such as pCEA  MDR3 disease shows absent canalicular staining for MDR3 but preserved staining for other canalicular proteins such as pCEA and BSEP Electron Microscopy  Transmission o FIC1 disease reveals coarse, granular bile, referred to as Byler bile o MDR3 disease may show cholesterol clefts in bile ducts or canaliculi DIFFERENTIAL DIAGNOSIS Bile Acid Synthesis Defect 51 Diagnostic Pathology: Hepatobiliary and Pancreatic  Also shows low GGT, but unlike PFIC, serum bile acid concentration is low Biliary Atresia  Histology shows obstructive pattern with bile duct proliferation, inspissated bile in ducts  Hepatobiliary imaging confirms atretic bile duct Other Childhood Cholestatic Disorders  Histology of many cholestatic childhood disorders is indistinguishable from PFIC, and their distinction requires wide array of serologic, biochemical, and genetic tests Primary Sclerosing Cholangitis  Histology shows periductal fibrosis  Cholangiogram shows strictures and dilatations DIAGNOSTIC CHECKLIST Clinically Relevant Pathologic Features  BRIC is characterized by cholestasis during attacks but no histologic progression  PFIC is characterized by increasing fibrosis and may show duct paucity, giant cell hepatitis, or bile ductules with bile plugging, depending on subtype  Neonatal cholestatic disorder with normal GGT and elevated serum bile acids suggests PFIC1 or PFIC2 whereas elevated GGT suggests possibility of PFIC3 Pathologic Interpretation Pearls  PFIC1 shows bland cholestasis; PFIC2 shows pattern of giant cell hepatitis; and PFIC3 shows duct proliferation with bile plugs SELECTED REFERENCES 1.

Nisa AU et al: Dubin-Johnson syndrome. J Coll Physicians Surg Pak. 18(3):188-9, 2008 2. Jedlitschky G et al: Structure and function of the MRP2 (ABCC2) protein and its role in drug disposition. Expert Opin Drug Metab Toxicol. 2(3):351-66, 2006 3. Lee JH et al: Neonatal Dubin-Johnson syndrome: long-term follow-up and MRP2 mutations study. Pediatr Res. 59(4 Pt 1):584-9, 2006 4. Rastogi A et al: Dubin-Johnson syndrome—a clinicopathologic study of twenty cases. Indian J Pathol Microbiol. 49(4):500-4, 2006 5.

Craig JM et al: The pathological changes in the liver in cystic fibrosis of the pancreas. AMA J Dis Child. 93(4):357-69, 1957 Image Gallery (Left) Hematoxylin & eosin shows irregular, confluent zones of fibrosis with proliferated, dilated bile ductules. A nodule of 61 Diagnostic Pathology: Hepatobiliary and Pancreatic liver parenchyma is seen on the right. This pattern may be referred to as multilobular biliary cirrhosis. (Center) Hematoxylin & eosin shows an expanded, irregular portal tract containing proliferating bile ductules.

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Aspects of the pathology of money: monetary essays from four decades by M.A. Heilperin


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