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Pathology of the Intrahepatic Biliary Tree after Liver Transplantation
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
James Neuberger, Rebecca Harrison
The classical histological features of chronic rejection are seen relatively late in the natural history of chronic rejection (Fig. 2). Ductular proliferation is not a feature and progression to biliary cirrhosis is rare. Neil and colleagues8 studied sequential liver biopsies and related the histologic features to the time after the first rise in liver tests. In general, chronic rejection arose following an episode of acute rejection; in the early period, portal features of acute rejection were present and these resolved with time and after increased immunosuppression. In contrast, centrilobular necrosis, present at the time of acute rejection did not resolve. In the portal tracts, small arterial loss developed before bile duct loss. As indicated above, the foam cell arteriopathy, characteristic of chronic rejection, was rarely seen in needle biopsies of the allograft.
A Potential Role for Immunological Mechanisms in Halothane Hepatotoxicity
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Andrea K. Hubbard, Timothy P. Roth, A. Jay Gandolfi
The reservations associated with the use of the rat models were, in part, solved with a model in the guinea pig (Luman et al., 1985; Lind et al., 1987). In this model, halothane produces in both sexes of selected strains a liver lesion which develops over a 2-day period and persists for over 7 days. The injury presents itself as either confluent centrilobular necrosis or scattered foci throughout the lobules. Neither phenobarbital pretreatment nor exposures in hypoxic atmospheres are required for the production of the hepatotoxicity. The injury is more prevalent in females and in heavier, older animals. In addition, biotransformation inhibitors or administration of deuterated halothane reduces the severity of the lesion. Although this animal model is a better representation of the clinical situation, it still does not account for the latent, progressive, often terminal liver injury seen in patients.
The Pathogenesis and Pathology of the Hemorrhagic State in Viral and Rickettsial Infections
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
Laboratory data reveal evidence for hepatocellular injury with elevated concentrations of alanine aminotransferase (ALT) and asparate aminotransferase (AST), slight hyperbilirubinemia, normal prothrombin time, prolonged partial thromboplastin time, severe thrombocytopenia, proteinuria, and azotemia.48 Necropsies have documented severe hemorrhagic diathesis involving the stomach, kidneys, adrenals, and intestines. Marked centrilobular necrosis occurs in the liver, and pulmonary edema and hemorrhage may be seen.48 The pathogenic mechanism responsible for the hemorrhage is not clear, but thrombocytopenia and hepatocellular necrosis are possible explanations.
Engineering biosafe cisplatin loaded nanostructured lipid carrier: optimisation, synthesis, pharmacokinetics and biodistribution
Published in Journal of Microencapsulation, 2022
Disha Mittal, Archu Singh, Kanchan Kohli, Anita Kamra Verma
Histopathology shows normal architecture of kidney in control mice. Treatment with Cis results in tubular dilation, glomerular congestion and necrosis in the epithelial tissue. But when treated with CisNLC, reduced pathohistological changes were observed. Hence CisNLC has reduced the nephrotoxic effects of Cis. Histological sections of liver of control group displayed normal structure of the hepatic lobule with uniformly arranged central vein but Cis treated mice showed liver injury shown by dilation of the central vein, severe centrilobular necrosis and hepatic degeneration, vacuolisation and cytoplasmic disruption and also number of cells undergoing necrosis. Cis exhibits detrimental e pathological effect of Cis due to the degradation products that could react with DNA or proteins in the liver by alkylation (Palipoch and Punsawad 2013). Platinum-based drugs are known to damage hepatic sinusoids (Ghaferi et al. 2020) that leads to sinusoidal dilatation and finally results in dysfunction of hepatocytes (Bhattacharyya and Mehta 2012).
Whole-body inhalation exposure to 2-ethyltoluene for two weeks produced nasal lesions in rats and mice
Published in Inhalation Toxicology, 2021
Madelyn C. Huang, Cynthia J. Willson, Sridhar Jaligama, Gregory L. Baker, Alan W. Singer, Yu Cao, Jessica Pierfelice, Esra Mutlu, Brian Burback, Guanhua Xie, David E. Malarkey, Barney Sparrow, Kristen Ryan, Matthew Stout, Georgia K. Roberts
In our previous study, centrilobular necrosis in the liver was observed in animals exposed to 1000 and 2000 ppm 2-ET for 2 weeks (Roberts et al. 2017). Here, centrilobular liver hemorrhage and necrosis were observed only in F1 offspring rats and mice in the 600 ppm group where there was clear acute toxicity. These microscopic lesions were not observed in 150 or 300 ppm groups. The liver may be a relevant target organ as C9 alkylbenzenes are known to be metabolized by P450 enzymes in the liver. For instance, 95% of absorbed xylene is metabolized in the liver (Langman 1994). However, hepatotoxicity is varied across other C9 alkylbenzenes, where some show indications of hepatotoxicity caused by oxidative stress (ethylbenzene, Zhang et al. 2015) while others show mild, potentially adaptive, effects (xylene, ATSDR 2007; trimethyl benzenes, EPA 2016b) or none (toluene, Brautbar and Williams 2002).
Lagerstroemia speciosa (L.) Pers., ethanolic leaves extract attenuates dapsone-induced liver inflammation in rats
Published in Drug and Chemical Toxicology, 2022
Thakur Rohit Singh, Devaraj Ezhilarasan
The liver architectural distortion was investigated by H and E staining. The control liver tissue shows the normal architecture of the liver with intact central vein and radiating sinusoidal space. The liver tissue of DDS administered rats (group II) shows moderate periportal fibrosis (PPF) and peribillary fibrosis (PBF) with the proliferation of connective tissues. The liver tissue of group III rats showed centrilobular necrosis. The liver tissue of rats post-treated with EBLE at 250 mg/kg after DDS administration showed mild PBF. While DDS + EBLE 500 mg/kg and DDS + SIL treatments showed nearly normal architecture of the liver. Masson’s trichrome staining was performed to access the fibrotic changes in the liver tissue. Control rats liver tissue shows normal liver architecture with no extracellular matrix accumulation, groups II and III rats liver tissue showed mild PPF and PBF. While EBLE 250 mg/kg post-treated rat livers showed moderate PBF and PPF with infiltration of inflammatory cells, DDS + EBLE 500 mg/kg and DDS + SIL treatments showed no apparent fibrotic changes in the liver tissue. In Sudan Black staining, control liver tissue shows no appearance of black color fat droplets. Rat liver tissues in groups II and III showed black fat droplets. In DDS + EBLE and DDS + SIL treated liver tissue architecture not contains a black stain of lipid droplets (Figure 6(A)). The liver injury score was significantly (p < 0.001) increased in DDS alone administered rats (group II and III). EBLE (p < 0.01 vs 250 mg/kg and p < 0.001 vs 500 mg/kg) and SIL post-treatments (p < 0.001) significantly reduced liver injury score (Figure 6(B)).