Host- and disease-specific factors affecting steatosis in chronic hepatitis C
Background/Aim: Steatosis is commonly present in chronic hepatitis C. Our aim was to evaluate host- and disease-specific factors associated with its occurrence. Methods: Histologic findings in 60 patients were correlated with body mass index, human leukocyte antigens, and other conventional paramete...
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Published in | Journal of hepatology Vol. 29; no. 2; pp. 198 - 206 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Elsevier B.V
01.08.1998
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Background/Aim: Steatosis is commonly present in chronic hepatitis C. Our aim was to evaluate host- and disease-specific factors associated with its occurrence.
Methods: Histologic findings in 60 patients were correlated with body mass index, human leukocyte antigens, and other conventional parameters. Comparisons were made with 41 patients who had nonalcoholic steatohepatitis and 18 patients who had chronic hepatitis B.
Results: Patients with chronic hepatitis C and steatosis had lower serum concentrations of γ-globulin (
p=0.01)_and immunoglobulin G (
p=0.05) than their counterparts without steatosis, and they had a lower frequency of antinuclear antibodies (19% versus 52%,
p=0.01). They also had a higher mean body mass index (
p=0.002) and a greater frequency of risk factors for steatosis (70% versus 34%,
p=0.009). These risk factors, however, occurred more commonly in patients with nonalcoholic steatosis (
p=0.007). Furthermore, fat deposition occurred more often in chronic hepatitis C than in chronic hepatitis B (52% versus 22%,
p=0.03), despite comparable metabolic findings. The degree of steatosis in chronic hepatitis C was not associated with individual metabolic features.
Conclusions: Steatosis in chronic hepatitis C is mainly a viral effect, and host-dependent metabolic factors may potentiate the manifestation. Fat deposition is associated with less immunoreactivity and it may connote a distinctive pathogenic mechanism. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0168-8278 1600-0641 |
DOI: | 10.1016/S0168-8278(98)80004-4 |