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      Cirrose biliar em felinos associada à ectasia do ducto cístico e desvios portossistêmicos extra-hepáticos Translated title: Biliary cirrhosis in cats associated with cystic duct ectasia and extra-hepatic portosystemic Shunts


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          Descrevem-se três casos de cirrose biliar em felinos. O quadro clínico manifestado pelos animais afetados consistia em icterícia, vômitos, emagrecimento progressivo, prostração, anorexia e aumento de volume do abdome acompanhado de dor abdominal. Os principais achados macroscópicos incluíam fígado firme e com a superfície natural e de corte irregulares e de aspecto reticulado, ducto cístico acentuadamente distendido (ectasia), desvios portossistêmicos venosos extra-hepáticos ("shunts"), efusões cavitárias e carcaças em mau estado corporal. Histologicamente, havia fibrose periportal acentuada, dissecante, associada a infiltrado inflamatório mononuclear, proliferação ductal e retenção biliar. Em um dos casos, a coloração de Brown-Hopps revelou a presença de cocos gram-positivos associada à inflamação no lúmen ductal. A presença de bactérias intralesionais é um achado histológico raramente descrita no complexo colangite/colangio-hepatite felina e não tem sido descrita na cirrose biliar. Ectasia do ducto cístico e formação de desvios portossistêmicos extra-hepáticos são complicações incomuns do estágio terminal dessa síndrome. Cirrose biliar é a forma de apresentação menos comum do complexo colangite/colangio-hepatite felina. O número reduzido de casos dessa condição se deve ao fato de que a maior parte dos animais afetados por esse complexo morrem espontaneamente ou são submetidos à eutanásia antes de a doença progredir para a sua fase terminal. Desconhece-se a prevalência dessa enfermidade nas populações felinas locais das diversas regiões do Brasil.

          Translated abstract

          Three cases of biliary cirrhosis in cats are described. Clinical signs included icterus, vomiting, weight loss, depression, anorexia and distension of the abdomen accompanied by abdominal pain. Main gross findings included firm liver with irregular capsular and cut surfaces and enhanced reticular pattern, marked distension of the cystic duct (ectasia), extrahepatic portosystemic venous shunts, cavitary effusions and thin carcasses. Microscopic lesions included severe periportal, dissecting fibrosis with lymphoplasmacytic inflammation, biliary proliferation and cholestasis. In one case, Brown-Hopps’ stained slides revealed gram-positive cocci with associated inflammation inside the ductal lumen. The histological finding of intralesional bacteria in cases of feline cholangitis/cholangiohepatis complex is reported only on rare occasions and has not been described for biliary cirrhosis. Dilation of the cystic duct and formation of portosystemic shunts are also unusual complications of this syndrome. Biliary cirrhosis is an uncommon condition since most cats die or are euthanatized before reaching the final stage of this progressive inflammatory hepatic disease. The prevalence of this entity in local feline populations remains to be determined in Brazil.

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          Most cited references17

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          Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats.

          To determine whether cats with inflammatory hepatic disease had concurrent inflammatory bowel disease (IBD), pancreatitis, or chronic interstitial nephritis.
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            Clinical features of inflammatory liver disease in cats: 41 cases (1983-1993).

            To compare the clinical and clinicopathologic findings in and prognosis for cats with lymphocytic portal hepatitis (LPH) versus cats with acute or chronic cholangiohepatitis (CH). Retrospective study. 25 cats with LPH; 16 cats with CH (7 acute, 9 chronic). Cats with LPH and CH were selected by evaluating records from liver biopsy specimens submitted to the University of Minnesota Veterinary Teaching Hospital during a 10-year period. Clinical and clinicopathologic data were retrieved. Cats with CH had higher segmented and band neutrophil counts, alanine aminotransferase activities, and total bilirubin concentrations than did cats with LPH. Cats with acute CH had higher segmented and band neutrophil counts and lower serum alkaline phosphatase activities and total bilirubin concentrations than did cats with chronic CH. Twelve of 14 cats with LPH or CH had coarse or nodular texture to the liver on ultrasonography, with loss of portal vein wall clarity noticed in 4 of 8 cats with LPH. Sixteen of 23 cats with LPH and 8 of 15 cats with CH survived > 1 year. Of those cats living < 1 year, all cats with LPH and 5 of 7 cats with CH had a serious concurrent illness that may have been responsible for their deaths. LPH and CH can be detected and tentatively differentiated through evaluation of clinical laboratory test results, but histologic evaluation of liver specimens is necessary for definitive differentiation. Survival time was good regardless of the type of inflammatory liver disease.
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              Animal models for primary sclerosing cholangitis.

              Since the aetiopathogenesis of primary sclerosing cholangitis (PSC) in humans remains undefined, investigators have studied a variety of animal models to gain insights into immunopathogenetic mechanisms associated with obliterative fibrous cholangitis of intra- and extra-hepatic bile ducts. To date, no animal model has been developed that exhibits all of the attributes of PSC. Rodent models instigated by bacterial cell components or colitis are promising because they may help to explain the strong association between PSC and inflammatory bowel disease (IBD). Other models of direct injury to biliary epithelia, peribiliary vascular endothelia or portal venous endothelia indicate that inflammation, chemokines and cytokines can produce diffuse sclerosis of bile ducts. Models of toxic, infectious or intra-luminal injury of the biliary tract also exhibit focal biliary sclerosis mediated by inflammation and cytokines. The histopathology of several models suggests a sequence of events beginning with secretion of proinflammatory cytokines by activated hepatic macrophages followed by peribiliary infiltration with CD4 and CD8 T cells with a T helper 1 phenotype. These results strongly suggest co-ordinated, pathogenetic roles for both the innate and adaptive immune responses. However, the stimuli that initiate and perpetuate peribiliary fibrosis remain unknown. Interestingly, several models are also associated with the development of anti-neutrophil cytoplasmic antibodies that react in a perinuclear and cytoplasmic pattern similar to that observed in patients with ulcerative colitis and/or PSC. Finally, models of extra-hepatic biliary obstruction continue to provide important information about the pathogenesis of portal fibrosis and secondary biliary cirrhosis that occurs in PSC and other diseases with obstruction of bile flow. Future studies in either existing or new animal models should advance our understanding of the pathogenesis of PSC, the major prerequisite for the development of effective therapies. Copyright 2001 Harcourt Publishers Ltd.

                Author and article information

                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Ciência Rural
                Cienc. Rural
                Universidade Federal de Santa Maria (Santa Maria )
                August 2004
                : 34
                : 4
                : 1147-1153
                [1 ] Universidade Federal do Rio Grande do Sul Brasil
                [2 ] Universidade Federal de Santa Maria Brazil
                [3 ] Universidade Federal de Santa Maria Brazil
                [4 ] Universidade Federal do Rio Grande do Sul



                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0103-8478&lng=en

                biliary cirrhosis,liver,cats,feline cholangitis/cholangiohepatitis complex,cirrose biliar,fígado,complexo colangite/colangio-hepatite felina


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