A review of hepatic fibrosis‐associated histopathology in aged cadavers

Abstract

This article reviews hepatic fibrosis-associated histopathology of aged cadavers (mean age 82 years). A study of 68 livers identified steatosis in 35.5%, central vein fibrosis in 49.2%, perisinusoidal fibrosis in 63.2%, portal tract fibrosis in 47.7%, septa formation in 44.1%, bridging fibrosis in 30.8%, and cirrhosis in 4.4% of the samples as well as one hepatocellular carcinoma and six metastatic tumors. Other studies have revealed that collagens I, III, IV, V, and VI and fibronectin constitute the matrices of fibrous central veins, perisinusoidal space, portal tracts, and septa. Elastin is rich in portal tracts and fibrous septa but absent from the perisinusoidal space. Hepatic stellate cells are ubiquitous in the liver parenchyma while myofibroblasts localize in fibrotic foci. Factor VIII-related antigen expression signals sinusoidal to systemic vascular endothelium transformation while collagen IV and laminin codistribution indicates formation of perisinusoidal membranes. Their coincidence reflects focalized capillarization of sinusoids in the aged liver. In response to fibrogenesis, hepatic progenitor cells residing in the canal of Hering in the periportal parenchyma undergo expansion and migration deep into the lobule. Concomitantly, intermediate hepatocyte-like cells increase in advanced fibrosis stages, which is possibly related to hepatic regeneration. Metabolic zonation of glutamine synthetase expands from the perivenous to non-perivenous parenchyma in fibrosis progression but its expression is lost in cirrhosis, while cytochrome P-4502E1 expression is maintained in centrilobular and midlobular zones in fibrosis progression and expressed in cirrhosis. Hence, cadaveric livers provide a platform for further investigation of hepatic histopathologies associated with the aging liver.

Histological and Immunohistochemical Assays of <i>Trypanosoma evansi</i> Infected Camel Hepatic Tissues

“…Between the hepatocyte cords and the sinusoid wall is the Disse space. This integrated cellular contact network gains from the sinusoids' extraordinarily low blood pressure because of their advantageous position, which influences the liver's biochemical and immunological functions [34][35][36]. The liver's primary metabolic functions are well understood, but it also contributes significantly to the local and systemic immune response [22].…”

From anatomy to immunity in the gastrointestinal system

“…Another contribution by Mak, Kee, and Cheng (2022) makes a histological assessment of the prevalence of fibrosis‐related histopathologies in liver samples from 68 cadavers with a group median age at death of 82 years. It reveals a high prevalence of liver steatosis and fibrosis among the samples, even in subjects without documented liver disease as the cause of death.…”