Concurrence of Histologic Features of Steatohepatitis
with Other Forms of Chronic Liver Disease
Elizabeth M. Brunt, MD, Sunil Ramrakhiani, MD, Barry G. Cordes, MD,
Brent A. Neuschwander-Tetri, MD, Christine G. Janney, MD, Bruce R. Bacon, MD,
Adrian M. Di Bisceglie, MD
Saint Louis University Liver Center Departments of Pathology (EMB, BGC, CGJ) and Internal Medicine
(SR, BAN-T, BRB, AMDB), and Division of Gastroenterology and Hepatology (BAN-T, BRB, AMDB), Saint
Louis University Health Sciences Center, St. Louis, Missouri
Steatohepatitis, of either alcoholic or nonalcoholic
etiologies, is ultimately diagnosed by clinical-
pathologic correlation and is characterized histo-
logically by lesions that differ from the portal-based
chronic inflammation and fibrosis of most other
forms of chronic liver disease. With the increasing
prevalence of steatohepatitis in our society, it is
likely that some patients will have coexistent clini-
cal and/or histopathologic findings of steatohepati-
tis concurrently with another form of liver disease.
The aim of this study was to document clinical and
histologic findings in biopsies in an academic refer-
ral center. Ninety-three non-allograft liver biopsies
with lesions of both steatohepatitis and another
liver disease were retrospectively identified in 85
patients. The finding of coexisting disease repre-
sented 5.5% of all hepatitis C biopsies and 4.0% of
other forms of chronic liver disease in the 34 month
time period. Clinical chart review of patients with
concurrent disease showed the following: Group 1,
patients with hepatitis C (n ? 54); Group 2, patients
than 80 g/d alcohol consumption (n ? 20); Group 3,
patients with other forms of chronic liver disease (n
? 11). Groups 1 and 3 had <10 g/d alcohol use.
Obesity (body mass index >30) was noted in 75%,
60%, and 33% respectively, while 94%, 87% and
100% of patients were considered overweight (body
mass index > 25). Diabetes was reported in 35%,
25%, and 9%. The concurrence of clinical and his-
tologic features of steatohepatitis with another
chronic liver disease may be a reflection of the fre-
quency of steatohepatitis in the population at large.
KEY WORDS: Clinical correlations, Concurrence
with chronic liver disease, Steatohepatitis.
Mod Pathol 2003;16(1):49–56
Nonalcoholic steatohepatitis is the current nomen-
clature for a chronic, progressive form of liver dis-
ease of diverse and incompletely understood etiol-
recognized with increasing frequency in adult and
pediatric populations in the western world (1–6).
The histologic features that characterize nonalco-
holic steatohepatitis were documented in the well-
known study by Ludwig et al. in 1980 (4). The con-
stellation of histologic lesions, which are similar
regardless of the etiopathogenesis (2, 4–6), are con-
sidered to be morphologic manifestations of com-
plex metabolic derangements and consequent
necroinflammatory lesions that result in hepatocel-
lular fat accumulation, liver cell injury, parenchy-
mal inflammation and perisinusoidal fibrosis that
may progress to cirrhosis. The histologic features of
steatohepatitis are commonly noted to be predom-
inantly found in zone 3 of the acinus of precirrhotic
biopsies, and are distinct from the characteristic
portal-based chronic inflammation and fibrosis,
and spotty lobular necrosis of most other forms of
chronic viral, metabolic and cholestatic liver dis-
More than one disease process may concurrently
involve the liver; the lesions may be distinguishable
by histopathologic examination. In some settings,
coexistence of more than one process may be sig-
nificant in disease progression. Some examples in-
clude hepatitis C and B (8–10), hepatitis C and
alcoholic liver disease (11, 12), hemochromatosis,
and/or HFE mutations in patients with several
other forms of viral and metabolic liver disease
(13–16). Although some of the histologic lesions
found in various entities of differing etiologies may
be similar, or may be considered “nonspecific”
necroinflammatory findings, careful microscopic
Copyright © 2003 by The United States and Canadian Academy of
VOL. 16, NO. 1, P. 49, 2003 Printed in the U.S.A.
Date of acceptance: October 7, 2002.
Address reprint requests to: Elizabeth M. Brunt, MD, Division of Surgical
Pathology, 4th Floor, St. Louis University Hospital, 3635 Vista Avenue, St.
Louis, MO 63110; e-mail: firstname.lastname@example.org; fax: 314-268-5120.
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