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In hepatic venous outflow obstruction, alcoholic liver disease, and nonalcoholic fatty liver disease, centrilobular scars, CD34+ vessels, and keratin 7+ hepatocytes are in close proximity

Authors
  • Matsukuma, Susumu1, 2
  • Takeo, Hiroaki1
  • Utsumi, Yoshitaka1
  • Sato, Kimiya1
  • 1 Japan Self-Defense Forces Central Hospital, Department of Pathology, 1-2-24 Ikejiri, Setagaya-ku, Tokyo, 154-8532, Japan , Tokyo (Japan)
  • 2 Japan Self-Defense Forces Central Hospital, Health Care Center, 1-2-24 Ikejiri, Setagaya-ku, Tokyo, 154-8532, Japan , Tokyo (Japan)
Type
Published Article
Journal
Virchows Archiv
Publisher
Springer Berlin Heidelberg
Publication Date
Jan 23, 2017
Volume
470
Issue
4
Pages
411–420
Identifiers
DOI: 10.1007/s00428-017-2074-6
Source
Springer Nature
Keywords
License
Yellow

Abstract

For hepatic venous outflow obstruction, alcoholic liver injury, and nonalcoholic fatty liver disease, the term “centrizonal injury disease” (CID) is used, because injury patterns in all three entities are similar. To elucidate CID-related CD34+ vessels (sinusoids and/or microvessels) and keratin 7+ hepatocytes (K7+ Hs), we examined a series of 41 liver tissue specimens obtained at autopsy and surgery, consisting of 32 CID cases and 9 controls. Centrizonal scars were found in 21 CID cases, and these were associated with centrizonal CD34+ vessels (P = 0.009) and centrizonal K7+ Hs (P < 0.001). Centrizonal coexistence of CD34+ vessels and K7+ Hs was observed in 22 CID cases (P = 0.057). These findings suggest close centrizonal proximity of scar, CD34+ vessels, and K7+ Hs in CID. However, centrizonal K7+ Hs without CD34+ vessels were observed in 21 CID cases. CD34+ vessels were detectable in all control samples and may represent the normal vascular bed. In 29 CID cases, centrizonal CD34+ vessel density was higher than that in controls. However, most appeared to be continuous with periportal and/or interlobular CD34+ vessels, and those CD34+ vessels restricted to centrizonal regions were focal and limited in seven CID cases. Centrizonal CD34+ vessels were associated with venoportal adhesions (P = 0.027). Our findings suggest that CID induces both venoportal adhesion-related structural distortion and expansion of normally present CD34+ vessels, which may result in increased centrizonal CD34+ vessel density.

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