12 research outputs found

    Cholelithiasis with atrophy of the right lateral hepatic lobe in a horse Colelitíase com atrofia do lobo lateral direito em um cavalo

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    A 22 year-old horse developed cholelithiasis with marked atrophy of the right lateral hepatic lobe. The horse had a history of intermittent colic since three years of age, and one of the first episodes of colic was associated with icterus. The size of the right lateral hepatic lobe was extremely reduced. There was a large choledocholith in the common hepatic duct, and several hepatoliths and choleliths in the intra- and extra-hepatic billiary ducts. Microscopically, there was severe atrophy of the right lobe with diffuse proliferation of connective tissue and billiary ducts. The left lateral lobe had peri-portal fibrosis with proliferation of billiary ducts, and billiary stasis. Chemical analysis of the calculi detected amorphous and triple phosphate, bilirubin, calcium, and iron.<br>Um cavalo de 22 anos de idade desenvolveu quadro de colelitíase severa com atrofia do lobo lateral direito. O animal tinha histórico de cólica recorrente, desde os três anos de idade, sendo que um dos primeiros episódios de cólica foi acompanhado de icterícia. O lobo hepático lateral direito estava extremamente diminuído de volume. Havia um grande coledocólito localizado no ducto hepático comum e inúmeros hepatólitos e colélitos nos ductos biliares intra e extra-hepáticos. Microscopicamente, foi observada atrofia acentuada do lobo direito, com proliferação difusa de tecido conjuntivo fibroso e de ductos biliares. O lobo lateral esquerdo apresentava fibrose periportal difusa associada à proliferação acentuada de ductos biliares e estase biliar. Análise química das concreções detectou fosfato triplo e amorfo, bilirrubina, cálcio e ferro

    Gastric mucosal inflammation and epithelial cell turnover are associated with gastric cancer in patients with Helicobacter pylori infection

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    Background—Infection with a virulent Helicobacter pylori strain is associated with gastric mucosal damage and the increased risk of gastric cancer. Aims—To examine the characteristics of host gastric mucosal responses in patients with gastric cancer, histological grade of gastritis, gastric epithelial apoptosis, and proliferation were studied. Methods—Thirty two patients with early gastric cancer and 32 sex and age matched controls were studied. All subjects were infected with a virulent H pylori strain (vacA s1/m1, cagA positive genotype). Biopsy specimens were taken from the antrum and the corpus of the stomach. The grade of gastritis was assessed according to the updated Sydney system. Apoptotic cells were detected using terminal uridine deoxynucleotidyl nick end labelling, and epithelial cell proliferation was determined by means of the Ki-67 labelling index. Results—In patients with gastric cancer, significantly higher grades were observed when glandular atrophy (p < 0.05) and intestinal metaplasia (p < 0.01) were present in the antrum, and when mononuclear cell infiltration was present in the corpus (p < 0.05). The numbers of apoptotic cells were increased in patients with cancer (p < 0.05) and the apoptotic index correlated significantly with the grade of glandular atrophy. Epithelial cell proliferation was more likely to be increased in mucosa where intestinal metaplasia was present. Conclusions—Infection with H pylori causes increased gastric epithelial apoptosis, resulting in more severe glandular atrophy in patients with gastric cancer. Increased damage of gastric epithelial DNA and the presence of more severe atrophic gastritis might contribute to the development of gastric cancer. Key Words: gastric cancer • cell proliferation • apoptosis • gastritis • Helicobacter pylor

    Hepatitis in horses

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