Congenital hepatic fibrosis in Holando Argentino calf: first report in Argentina

A case of congenital hepatic fibrosis in a 10-month-old calf is described. The calf had been raised in a feed lot for the past 173 days and exhibited loss of body condition and depression, followed by death. The most remarkable macroscopic lesions observed during necropsy were: jaundice, hepatomegaly with a multilobulated liver surface and diffuse pale brown colour of the parenchyma. Microscopically, the portal tracts were thickened and connected to each other by abundant fibrous tissue, delimiting irregular lobules of hepatocytes and occasional fibrosis of the central veins (perisinusoidal scars) and hyperplasia of embryonal bile ducts. Immunohistochemistry staining of the cytoplasm of the bile ducts was positive to AE1/AE3 and cell proliferation nuclear antigen (PCNA). The findings at necropsy, together with the results of the histopathological and immunohistochemistry studies, confirmed the diagnosis of congenital hepatic fibrosis.

Congenital hepatic fibrosis in Holando Argentino calf: first report in Argentina

A case of congenital hepatic fibrosis in a 10-month-old calf is described. The calf had been raised in a feed lot for the past 173 days and exhibited loss of body condition and depression, followed by death. The most remarkable macroscopic lesions observed during necropsy were: jaundice, hepatomegaly with a multilobulated liver surface and diffuse pale brown colour of the parenchyma. Microscopically, the portal tracts were thickened and connected to each other by abundant fibrous tissue, delimiting irregular lobules of hepatocytes and occasional fibrosis of the central veins (perisinusoidal scars) and hyperplasia of embryonal bile ducts. Immunohistochemistry staining of the cytoplasm of the bile ducts was positive to AE1/AE3 and cell proliferation nuclear antigen (PCNA). The findings at necropsy, together with the results of the histopathological and immunohistochemistry studies, confirmed the diagnosis of congenital hepatic fibrosis.(AU)

Diabetes mellitus triggers oxidative stress in the liver of alloxan-treated rats: a mechanism for diabetic chronic liver disease

PURPOSE: To investigate whether Diabetes mellitus chemically induced by alloxan is capable of changing, in the long term, the oxidative balance in the liver tissue of rats. METHODS: Sixty male Wistar rats, weighing 250-280g, were randomly distributed into two experimental groups: NG - 30 non-diabetic control rats; DG - 30 alloxan- induced diabetic rats without any treatment for the disease. Each group was further divided into three subgroups containing ten rats each, which were sacrificed after one, three and six months of follow-up, respectively. Blood glucose, urinary glucose, glycosylated hemoglobin and insulin were determined in the plasma of all animals at the beginning of the experiment and prior to all sacrifice periods. The concentrations of lipid hydroperoxides (HP) and the activity of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were also measured in the liver tissue of all animals. RESULTS: Rats from the DG group showed high levels of blood glucose, urinary glucose, and glycosylated hemoglobin, with significantly lower plasma insulin levels than those observed in NG rats (p<0.001). Diabetic animals also showed increased concentration of HP free radicals in the liver tissue as compared to those shown by NG animals after one, three and six months of follow-up. In contrast, the antioxidant activity of the enzymes SOD, CAT and GSH-Px was significantly reduced in all follow-up periods (p<0.01). CONCLUSIONS: Diabetes determines oxidative stress in the liver, which is characterized by increased concentration of reactive oxygen species (ROS) in tissue and significant reduction in their antioxidant defenses. Such oxidative unbalance in the liver cells may play a relevant role in the genesis of the diabetic chronic liver disease, including the non-alcoholic fatty liver disease and its occasional progression to steatohepatitis and cirrhosis.(AU)

Liver cirrhosis on the colonic anastomotic healing in rats / Cirrose hepática na cicatrização de anastomose intestinal em ratos

PURPOSE: To investigate the effects of cirrhosis on colonic anastomosis healing in rats. METHODS: Fifty five Wistar male rats were used (23 in the control group and 32 in the cirrhosis group). On the first day of the procedure, the rats in the cirrhosis group underwent double ligation and folding of the common bile duct to induce liver cirrhosis, and the control rats underwent a laparotomy and intestinal manipulation. On the fourteenth and thirty-fifth days, all of the animals were biochemically assessed for serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, bilirubin, total protein, and albumin and for liver histopathology. On the thirty-fifth day, cirrhosis was confirmed. On the twenty-eighth day, all of the animals were subjected to left colon transection and anastomosis. On the seventh day after the colonic anastomosis, the rats were sacrificed and macroscopically evaluated for dehiscence. The region of the colonic anastomosis was removed and subjected to hydroxyproline content measurement, conventional histology, and the immunohistochemical determination of vascular endothelial growth factor (VEGF) and matrix metalloproteinase type 1 (MMP 1). RESULTS: The biochemical and histopathological examinations confirmed cirrhosis in all of the animals in the cirrhosis group. More deaths occurred after anastomosis in the cirrhosis group (5/25) than in the control group (0/21), and anastomotic dehiscence was more frequent in the cirrhosis group (8/25) than in the control group (0/21). The average hydroxyproline concentration was lower in the cirrhosis group than in the control group. The immunohistochemical studies showed that the average VEGF expression in the cirrhosis group was lower than in the control group, and the average MMP1 expression was higher in the cirrhosis group.(AU)

OBJETIVO: Investigar os efeitos da cirrose hepática na cicatrização de anastomose intestinal em ratos. MÉTODOS: Este estudo avaliou o efeito da cirrose hepática na cicatrização de anastomoses em ratos. 55 ratos Wistar machos foram utilizados (23 controles e 32 no grupo cirrose). No primeiro dia os ratos do grupo cirrose for submetidos à dupla ligadura e enovelamento do ducto hepático comum para indução de cirrose e os ratos controles foram submetidos à laparotomia e manipulação das alças intestinais. No dia 14 e 35, todos os animais foram avaliados bioquimicamente para dosagem sérica da alanina aminotransferase (AST), alanina aminotransferase (ALT), fosfatase alcalina, bilurrubinas, proteínas totais, albumina e histologia do fígado. No dia 35 a cirrose foi confirmada. No dia 28 todos os animais foram submetidos à colectomia esquerda e anastomose. 70 dias após anastomose os ratos foram submetidos à eutanásia e foram avaliados macroscopicamente a procura de deiscência. A região da anastomose colônica foi removida para dosagem de hidroxiprolina, histologia convencional e imunohistoquímica para determinação do fator de crescimento endotelial vascular (VEGF) e metaloproteinase tipo 1 (MMP 1). RESULTADOS: A análise bioquímica e histológica confirmou a cirrose em todos os animais do grupo cirrose. Óbito ocorreu em maior freqüência após a anastomose no grupo cirrose (5/25) se comparado com grupo controle (0/21), e a deiscência da anastomose foi mais freqüente no grupo cirrose (8/25) se comparado com controle (0/21). A concentração média de hidroxiprolina foi menor no grupo cirrose se comparado com grupo controle. A análise imonuhistoquímica mostrou que a expressão VEGF no grupo cirrose foi menor que no grupo controle e a expressão média da MMP1 foi maior no grupo cirrose.(AU)