Ioanna Delladetsima1, Stratigoula Sakellariou2, Aikaterini Kokkori2,3, Dina Tiniakos4,5. 1. First Department of Pathology, Medical School, National and Kapodistrian University of Athens, Athens, Greece. jokadelladetsima@hotmail.com. 2. First Department of Pathology, Medical School, National and Kapodistrian University of Athens, Athens, Greece. 3. Institute of Pathology and Molecular Pathology, Helios Klinikum Wuppertal, Germany. 4. Institute of Cellular Medicine, Faculty of Medical Sciences, Newcastle University, UK. 5. Laboratory of Histology-Embryology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Abstract
AIM: To investigate atrophic parenchymal changes in ischemic liver conditions. DESIGN: We studied 18 cases of hepatic lesions with atrophic changes due to altered blood flow (hepatic venous congestion n=15 including 4 cases with additional nodular regenerative hyperplasia-NRH, NRH n=1, and antiphospholipid syndrome with patchy parenchymal atrophy n=2). Metaplastic hepatocellular changes, hepatocyte proliferation, hepatic stellate cell (HSC) activation, and sinusoidal capillarization were examined immunohistochemically with antibodies to keratins (K) 7 and 19, Ki67, αSMA and CD34, respectively. RESULTS: K7 was positive and K19 was negative in zone 3 atrophic hepatocytes in venous congestion and in areas of plate atrophy, as well as in congested or compressed sites in NRH. Sinusoidal CD34-positivity indicating capillarization accompanied K7 immunoexpression. Masson trichrome revealed sinusoidal fibrosis to be restricted in atrophic areas, usually mild and in 7 cases focally dense. αSMA expression expanded beyond K7-positive areas. Ki67 was negative in K7-positive hepatocytes. CONCLUSION: Ischemic parenchymal changes are characterized by hepatocyte K7 immunoexpression, sinusoidal capillarization, HSC activation and lack of cellular proliferation, indicating an early reaction of the major liver parenchyma cellular components creating a more resistant microenvironment. These phenotypic alterations may prove valuable in the discrimination of ischemic liver lesions.
AIM: To investigate atrophic parenchymal changes in ischemic liver conditions. DESIGN: We studied 18 cases of hepatic lesions with atrophic changes due to altered blood flow (hepatic venous congestion n=15 including 4 cases with additional nodular regenerative hyperplasia-NRH, NRH n=1, and antiphospholipid syndrome with patchy parenchymal atrophy n=2). Metaplastic hepatocellular changes, hepatocyte proliferation, hepatic stellate cell (HSC) activation, and sinusoidal capillarization were examined immunohistochemically with antibodies to keratins (K) 7 and 19, Ki67, αSMA and CD34, respectively. RESULTS: K7 was positive and K19 was negative in zone 3 atrophic hepatocytes in venous congestion and in areas of plate atrophy, as well as in congested or compressed sites in NRH. Sinusoidal CD34-positivity indicating capillarization accompanied K7 immunoexpression. Masson trichrome revealed sinusoidal fibrosis to be restricted in atrophic areas, usually mild and in 7 cases focally dense. αSMA expression expanded beyond K7-positive areas. Ki67 was negative in K7-positive hepatocytes. CONCLUSION: Ischemic parenchymal changes are characterized by hepatocyte K7 immunoexpression, sinusoidal capillarization, HSC activation and lack of cellular proliferation, indicating an early reaction of the major liver parenchyma cellular components creating a more resistant microenvironment. These phenotypic alterations may prove valuable in the discrimination of ischemic liver lesions.
Authors: Helmut Denk; Daniela Pabst; Peter M Abuja; Robert Reihs; Brigitte Tessaro; Kurt Zatloukal; Carolin Lackner Journal: Mod Pathol Date: 2021-10-13 Impact factor: 7.842
Authors: S Sakellariou; C Michaelides; T Voulgaris; J Vlachogiannakos; E Manesis; D G Tiniakos; I Delladetsima Journal: Virchows Arch Date: 2021-07-27 Impact factor: 4.064