By M.A. Heilperin
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Aujeszky's affliction (AD) is expanding in Europe and it has develop into a significant challenge in a few of the nations of the ecu groups (EC). The keep watch over and eradication of the ailment is particularly tricky on the grounds that advert virus (ADV) inspires a persistant latent an infection in its major host, the pig. Such latent an infection may also take place whilst vaccinated pigs are uncovered to the virus.
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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.
Aspects of the pathology of money: monetary essays from four decades by M.A. Heilperin