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References in periodicals archive ?
In our study, liver of rats treated with TAA showed degeneration of hepatocytes with vacuolar cytoplasm, and periportal inflammatory cell infiltration with intense centrilobular necrosis, and congestion of blood sinusoids and central veins that was similar to finding of Chen et al.
Conversely, the inflammation grade (G) (P < 0.001), lobulitis (P = 0.001), interface inflammation (P = 0.001), rosettes (P < 0.001), periportal lymphocytes (p < 0.001), plasma cells (P < 0.001), neutrophils (P = 0.001), monocytes (P < 0.001), eosinophils (P = 0.002), bile duct injury (P < 0.001), centrilobular necrosis (P = 0.005), lobular neutrophils (P < 0.001), monocytes (P < 0.001), eosinophils (P = 0.002), and eosinophilic bodies (P = 0.05) were all significantly different between the acute and chronic groups (see Table 3 and Figure 2).
Out of these two, the zonal hepatocellular necrosis which contains the centrilobular necrosis, random hepatocellular necrosis, focal hepatic necrosis, multifocal hepatic necrosis, and occasional hepatic necrosis was primarily observed in the liver tissue (Figure 6).
(5-7) Biopsy findings include centrilobular and sinusoidal dilation and centrilobular necrosis, depending on the severity of the cardiac disease.
Histologic analysis of liver biopsies suggests rapid development of ubiquitous centrilobular necrosis and hepatocellular apoptosis during the course of sepsis [24].
Vascular congestion was present with centrilobular necrosis, marked by pyknotic nuclei and vacuoles.
20.###1 DM-HTN-IHD- PTB MGN###(Missed) Centrilobular necrosis Liver+Massive
Grades (0-5) were as follows: 0, no lesions; 1, minimal lesions, only necrotic cells at the first cell level from the central vein; 2, mild lesions, necrotic cells extending two to three cell levels from the central vein; 3, moderate lesions, necrotic cells extending three to six cell levels within peripheral distribution; 4, marked lesions, the same as in 3 but with necrosis extruding to another central vein; and 5, lesions more severe than those in 4, with progressive centrilobular necrosis throughout the section.
On microscopically 25.87% of cases show centrilobular necrosis, sinusoidal dilatation found in 22.37%, fatty changes in 11.88%, both venous congestion, combined sinusoidal dilatation and degenerative change in 1.39% of cases, each 2.09% of cases show degenerative change, centrilobular necrosis and venous congestion, and sinusoidal dilatation and venous congestion respectively, each 3.49% show combined centrilobular necrosis and sinusoidal dilatation, fatty change and degenerative change respectively, 08.39% of cases show centrilobular necrosis and fatty change, 06.99% cases show sinusoidal dilatation and fatty change, 07.69% have no significant histopathological changes, 0.69% case show centrilobular necrosis and degenerative change (p value-0.0001)[Table-4].
Liver biopsy showed centrilobular necrosis with inflammatory cell infiltration compatible with a toxic etiology (Fig.
Histological changes are similar to those observed in the Reye's syndrome, with early production of microvesicular steatosis followed by the development of centrilobular necrosis.5,6
Liver histology can show steatosis, portal and lobular inflammation, hepatic granulomas, centrilobular necrosis, microabscesses, haemochromatosis, cholestasis, nonspecific reactive changes, and infrequent cirrhosis [4].