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Gut. 2007 August; 56(8): 1170–1171.
PMCID: PMC1955497

Non‐alcoholic fatty liver disease in patients with HCV genotype 4

Hepatitis C infection is considered the leading cause of chronic liver disease in Egypt. Hepatitis C virus (HCV) genotype 4 is the predominant genotype in the Middle East including Egypt.1

A striking feature of HCV infection is its association with fat accumulation within hepatocytes,2 which is defined by the presence of hepatic steatosis with or without steatohepatitis.3 Hepatic steatosis has been reported in 30–70% of patients with HCV infection, even when the most common causes of steatosis are excluded.4 A causal relationship between infection with HCV genotype 3 and the incidence of hepatic steatosis has been elicited.5

In Egypt the true prevalence of non‐alcoholic fatty liver disease is unknown among patients with HCV who are commonly infected with genotype 4. Our aim was to determine the prevalence of steatosis in patients infected with HCV genotype 4 and to correlate steatosis with risk factors such as obesity, type 2 diabetes mellitus, hypertriglyceridaemia and the impact of steatosis on necroinflammatory injury and fibrosis score.

The study was conducted at Cairo Liver Center and included all patients who underwent liver biopsy during the period from January 2003 to May 2005. One hundred and twenty‐four patients were diagnosed with chronic HCV genotype 4 (group 1) and 48 subjects with non‐HCV chronic liver disease matched for age and sex were included for comparison (group 2). The histopathological, clinical and biochemical features of all patients were reviewed. Associated comorbid conditions such as overweight/obesity (body mass index [gt-or-equal, slanted]25 kg/m2), type 2 diabetes mellitus and hypertriglyceridaemia were studied for their correlation with steatosis. Further assessment of the biopsy specimens with steatosis was carried out to identify steatohepatitis. The paraffin sections were retrieved and new 4 μm thick sections were obtained and immunohistochemical staining for cytokeratin 8/18 was applied to detect Mallory hyaline bodies (fig 11).).

figure gt123331.f1
Figure 1 Immunohistochemical staining for cytokeratin 8/18 and detection of Mallory hyaline bodies (peroxidase ×400).

Steatosis was mainly macrovesicular in all specimens and was detected in 50 (40.3%) patients in group 1 and 16 (33.3%) patients in group 2 (p = 0.550). Steatohepatitis was identified in four patients in group 1, which was increased to seven (5.6%) in group 1 and one (2.1%) in group 2 (p = 0.445) after applying the immunohistochemical staining for detection of Mallory hyaline bodies. Pericellular fibrosis was identified in all steatohepatitis sections, but neutrophil inflammatory reaction was only identified in three specimens. Necroinflammatory injury, as reflected by modified Histology Activity Index (HAI), was significantly higher in group 1 than in group 2 (6.7 (2.7) vs 4.8 (3.4), p = 0.01). The fibrosis score was significantly higher in group 1 than in group 2 (3.3 (1.9) vs 1.8 (1.7), p = 0.002). Overweight/obesity ([gt-or-equal, slanted]25 kg/m2) was reported in 80.6% of patients in group 1 and 62.5% in group 2 (p = 0.097), type 2 diabetes mellitus (fasting blood sugar >126 mg/dl and postprandial blood sugar 200 mg/dl on more than one occasion) was encountered in 27.4% of group 1 and 12.5% in group 2 (p = 0.038), while hypertriglyceridaemia (>200 mg/dl) was found in 6.5% of group 1 and 8.3% of group 2 (p = 0.759, table 11).

Table thumbnail
Table 1 Pathological features of the two study groups

While steatosis was not associated with HCV (p = 0.555), it was significantly correlated with overweight/obesity (p = 0.001), diabetes mellitus (p = 0.001) and hypertriglyceridaemia (p = 0.019).

By multivariate analysis, only overweight/obesity and diabetes mellitus were found to be significantly associated with steatosis. Neither necroinflammation nor fibrosis was correlated with steatosis in patients with HCV genotype 4 (p = 0.953 and 0.463). This lack of correlation may be explained by the discrepancy between a high frequency of steatosis (40%) and a low frequency of steatohepatitis (5.6%) in group 1.

We conclude that hepatic steatosis is prevalent in nearly 40% of patients infected with HCV genotype 4, which is more highly attributed to associated metabolic factors. It seems that there is no correlation between necroinflammation or fibrosis and steatosis in patients with HCV genotype 4.

Footnotes

Competing interests: None.

References

1. Nguyen M H, Keeffe E B. Prevalence and treatment of hepatitis C virus genotypes 4, 5, and 6. Clin Gastroenterol Hepatol 2005. 3S97–S101.S101 [PubMed]
2. Lonardo A, Adinolfi L E, Loria P. et al Steatosis and hepatitis C virus: mechanisms and significance for hepatic and extrahepatic disease. Gastroenterology 2004. 126586–597.597 [PubMed]
3. Contos M J, Sanyal A J. The clinicopathologic spectrum and management of nonalcoholic fatty liver disease. Adv Anat Pathol 2002. 937–51.51 [PubMed]
4. Adinolfi L E, Gambardella M, Andreana A. et al Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity. Hepatology 2001. 331358–1364.1364 [PubMed]
5. Rubbia‐Brandt L, Quadri R, Abid K. et al Hepatocyte steatosis is a cytopathic effect of hepatitis C virus genotype 3. J Hepatol 2000. 33106–115.115 [PubMed]

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