The Progression of Liver Damage in Chronic Hepatosis

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1 Steatosis Accelerates the Progression of Liver Damage of Chronic Hepatitis C Patients and Correlates With Specific HCV Genotype and Visceral Obesity LUIGI E. ADINOLFI, MICHELE GAMBARDELLA, AUGUSTO ANDREANA, MARIE-FRANÇOISE TRIPODI, RICCARDO UTILI, AND GIUSEPPE RUGGIERO The role of steatosis in the progression of liver damage in chronic hepatitis C (CHC) was studied. Enrolled were 180 consecutive liver biopsy-proven CHC patients and 41 additional subjects with a known duration of infection. We evaluated the histological activity index (HAI), grade of fibrosis and steatosis, body mass index (BMI; kg/m 2 ), distribution of body fat, HCV genotype, and levels of HCV RNA. Eighty six (48%) patients showed steatosis, and a higher prevalence was observed in genotype 3a infection (P <.01). A correlation between the grade of steatosis and fibrosis was observed (P <.001). Fibrosis was also associated with age (P <.001). After adjusting for age, the association between steatosis and fibrosis remained significant. The grade of steatosis also correlated with the HAI (P <.007) with a significant increase in periportal necrosis. No relation was found between steatosis and age, gender, iron storage, or levels of HCV RNA. Patients with a high grade of steatosis (>30%) showed higher serum levels of -GT and ALT (P <.001). Overall, steatosis was not significantly associated to BMI. Analysis by single genotype showed a significant association between the grade of steatosis and BMI in type 1 infection r.689; P <.001) and with levels of HCV RNA in type 3a infection r.786; P <.001). Visceral fat distribution rather than BMI proved to be associated with steatosis (P <.001). Data obtained from patients with a known date of infection confirmed that steatosis grades 3-4 were associated with a higher annual rate of fibrosis progression, and showed that alcohol and steatosis act together in increasing fibrosis (P <.05). Our data indicate that steatosis is an important cofactor in increasing liver necroinflammatory activity and in accelerating fibrosis in CHC. Visceral obesity and genotype 3a play a role in the development of steatosis. (HEPATOLOGY 2001;33: ) Abbreviations: HCV, hepatitis C virus; CHC, chronic hepatitis C; HAI, histological activity index; BMI, body mass index; HCV RNA; hepatitis C virus RNA; ALT, alanine transaminase; PCR, polymerase chain reaction. From Internal Medicine & Hepatology, Second University of Naples, Naples, Italy. Received October 4, 2000; accepted March 5, Address reprint requests to: Professor Luigi E. Adinolfi, M.D., Istituto di Terapia Medica Facoltà di Medicina, Seconda Università di Napoli, Via Cotugno, 1 (c/o Ospedale Gesù e Maria), Napoli, Italy. luigielio.adinolfi@unina2.it; fax: (39) Copyright 2001 by the American Association for the Study of Liver Diseases /01/ $35.00/0 doi: /jhep Chronic hepatitis C virus infection may result in a wide clinical and prognostic spectrum of severity and progression rate of liver disease, ranging from minimal to severe chronic hepatitis to cirrhosis and hepatocellular carcinoma. The factors implicated in the progression of disease are not well known and may be virus- and/or host-related. The knowledge of such factors is of clinical, prognostic, and therapeutic importance. The HCV genotypes do not seem to be directly implicated in the progression of liver disease, although specific genotypes are associated to distinct histopathological manifestations. 1,2 A direct correlation between HCV RNA levels and the liver histological grading and staging is reported. 3,4 Some data suggest that liver injury in chronic HCV patients may be immunologically mediated, but definitive conclusions cannot yet be drawn. 5 Other host cofactors in addition or in alternative to viral factors or host immune response to the virus may play a role. Among these, excessive alcohol intake proves to be an important factor in the progression of chronic hepatitis C. 6 The role of other factors, like hepatic steatosis or an excess of iron deposition, have not been thoroughly investigated. Hepatic steatosis is a frequent histopathological feature of chronic hepatitis C. Liver fatty changes have been reported in approximately 30% to 70% of patients. 7-9 Steatosis is associated with obesity, diabetes type 2, and dyslipemia and may induce hepatic fibrosis and cirrhosis It has not been ascertained whether steatosis may have a role in the development of fibrosis in chronic hepatitis C patients. In addition, it is not known whether steatosis may be a direct consequence of HCV infection or secondary to host factors or both. Recent evidence suggests that HCV through its core protein may directly cause steatosis 13,14 and that hepatic steatosis may be associated with body mass index and with liver fibrosis in chronic hepatitis C patients. 15 Accordingly, the aim of this study was to evaluate the role of steatosis in the progression of liver injury in a large cohort of CHC patients and its relationship with viral and host factors like HCV genotype, levels of viremia, hepatic iron deposits, body mass index, and body fat distribution. PATIENTS AND METHODS Patients. Enrolled in the study were 180 consecutive CHC patients admitted to our institution. All were of Italian birth and came from southern Italy. Inclusion criteria were increased serum aminotransferase levels for at least 6 months, serum anti-hcv (ELISA; third generation), and HCV RNA (PCR) positivity, liver-biopsy-proven chronic hepatitis, serum HBsAg, and HIV negativity, no other cause of liver disease such as alcohol intake greater than 30 g/d or autoim-

2 HEPATOLOGY Vol. 33, No. 6, 2001 ADINOLFI ET AL mune or metabolic disorders (genetic hemochromatosis, Wilson s disease), and a relatively stable weight ( 5% variation) during the last 5 years. Excluded were patients who had diabetes or dyslipemia, those who had received previous treatment with interferon or immunosuppressive agents, and those who showed a focal pattern of steatosis by ultrasound or CT scan. We also evaluated an additional subgroup of 41 patients with CHC (26 with genotype 1b, 9 with genotype 3a, and 6 with type 1a), for whom the date of infection could be ascertained and who fulfilled the above-mentioned selection criteria. The patients in this subgroup were chosen from our database of 102 subjects with an established date of infection based on blood transfusion or drug use or an acute episode of non-a non-b hepatitis, mainly postsurgery. 2 Epidemiological data were obtained from all patients. Biochemical liver function tests and liver ultrasound scan were routinely performed at the time of the liver biopsy. For all patients, the body mass index (BMI; kg/m 2 ) was calculated. Patients with a BMI of 18.5 to 24.9 were classified as normal, those with a BMI of 25.0 to 29.9 as over-weight, those with a BMI of 30.0 to 34.9 as having moderate obesity, and those with a BMI of 35.0 to 39.9 as having severe obesity. Obese patients were also evaluated for the distribution of body fat by means of the measurement of waist circumference. This measurement has a high predictive value in assessing abdominal fat mass, and it has recently been proposed to identify subjects with visceral obesity. 16 The waist was measured as the narrowest circumference between the lower costal margin and the iliac crest in the standing position. According to Lean et al., 16 patients were considered as having visceral obesity if the waist circumference was 102 cm in males and 88 cm in females. Histological Evaluation. A pathological assessment was made on sections from formalin-fixed and paraffin-embedded liver biopsy stained with hematoxylin-eosin, trichrome, and Prussian blue reaction. According to Desmet et al., 17 we considered the scores for necroinflammatory changes and architectural alterations separately. The necroinflammatory activity was scored according to the Histology Activity Index (HAI) by Knodell et al. 18 The HAI was determined by combining the scores for portal inflammation (0-4), lobular degeneration and necrosis (0-4), and periportal necrosis (0-10). The stage was defined according to the Scheuer 19 fibrosis score: 0, absence; 1, enlarged, fibrotic portal tracts; 2, periportal or portoportal septa but intact architecture; 3, fibrosis with architectural distortion but not obvious cirrhosis; 4, probable or definite cirrhosis. Steatosis was graded as follows: 0, absent; 1, 1% to 10% of hepatocytes affected; 2, 11% to 30% of hepatocytes affected; 3, 31% to 60% of hepatocytes affected, and 4, 60% of hepatocytes affected. The hepatic iron deposits were evaluated by Perls stain and were graded from 0 to 4 according to Brissot. 20 A single pathologist with no knowledge of the patient s clinical or laboratory data performed the histopathological diagnosis and all grading. Serum HCV RNA Detection, Quantitation, and Genotyping. All sera were collected at the time of the liver biopsy and stored at 60 C within 2 hours. HCV RNA was extracted from serum using the Triiso RNA extraction system (ViennaLab, Vienna, Austria) and sought by a commercial PCR (Hepatest C TM, Vienna Lab, Vienna, Austria). The cut-off of the PCR assay was about 1,000 copies/ml. Serum HCV RNA levels were assessed by the bdna assay (Quantiplex TM, version 2.0, Chiron Co, Emeryville, CA) according to the manufacturer s instructions. The detection limit of the assay was 200,000 genome equivalents/ml. HCV genotyping was done using the reverse hybridization line-probe assay (INNO LiPA HCV assay, second generation; Innogenetics, Zwijnaarde, Belgium) following the manufacturer s protocol. Hepatitis B markers and antibody to HIV were sought using commercially available ELISA assays. Statistical Analysis. Absolute frequencies were compared using the 2 test. When appropriate, demographic and laboratory data were compared using Student s t test or the Kruskal-Wallis test. The mann-whitney U Test was used to compare the group differences in the serum HCV RNA levels. The linear regression analysis was used to analyze the relation of BMI, levels of HCV RNA, age, and laboratory data with hepatic steatosis and fibrosis. The independent effects of variables on steatosis and fibrosis were evaluated using logistic regression analysis. One-way ANOVA was used to analyze the mean differences in age, BMI, levels of HCV RNA across the grades of steatosis, and fibrosis. Data analysis was performed with the computer program SPSS (SPSS for Window). Data are presented as mean SE. A 5% level was assumed to denote significance. RESULTS General Characteristics of the Patients Studied. The characteristics of the CHC patients studied are reported in Table 1. The possible source of infection was posttransfusion in 37 (21%), previous intravenous drug use in 23 (13%), and unknown in 120 (66%). Patients with genotype 1a and 3a were younger than those with genotype 1b, 2a/c, and mixed (median age: 40 and 30 years vs. 52, 50 and 54 years, respectively; P.001). The mean BMI was kg/m 2 with a range of 19.6 to Eighty (44%) patients had a BMI greater than 25, of whom 56 (70%) were over-weight, 20 (25%) showed moderate obesity, and 4 (5%) severe obesity. The mean BMI was similar in the different HCV genotypes (1a: 24.4; 1b: 24.6; 2a/c: 24.5; 3a: 23.4; mixed 25.7). At the time of the liver biopsy, the geometrical median of serum HCV RNA was (Eq/mL). There were no significant differences in the levels of serum HCV RNA among the HCV genotypes (data not shown). The histological findings of the patients are reported in Table 1. Overall, the mean values of the HAI and fibrosis scores were similar for the different HCV genotypes (data not shown). Twenty-seven (15%) patients had cirrhosis. Steatosis was present in 86 (48%) patients, and the grade distribution is reported in Table 1. Among the steatosis patients there were no cases that could be classified as having a clear histological picture of nonalcoholic steatohepatitis. Relationship Between Steatosis, Histological Features, and Liver Function Tests. Table 2 shows the HAI score for the different grades of steatosis. On the whole, the mean HAI score was Patients with steatosis grade 3-4 showed a higher HAI than those without steatosis (HAI: vs TABLE 1. Demographic, Virologic, and Histological Characteristics of Chronic Hepatitis C Patients Studied Number of patients 180 Male/female 106/74 (59%/41%) Median age yrs (range) 49 (20-66) BMI, mean SE (range) ( ) Number of patients with BMI (44%) Number of patients with visceral obesity 57 (31%) Serum HCV RNA levels (median, Eq/ml) (range: ) HCV genotype: 1a 12 (7%) 1b 88 (49%) 2a/c 44 (24%) 3a 26 (14%) Mixed 10 (6%) Chronic hepatitis 153 (85%) Cirrhosis 27 (15%) HAI score (mean SE) Fibrosis score (mean SE) Number of patients with steatosis 86 (48%) Distribution of grade of steatosis: 1 14 (16%) 2 30 (35%) 3 31 (36%) 4 11 (13%)

3 1360 ADINOLFI ET AL. HEPATOLOGY June 2001 TABLE 2. Demographic, Laboratory, and Histological Characteristics of the 180 Patients According to the Grade of Steatosis Grade of Steatosis Number of patients Median age, yrs (range) 48 (21-66) 50 (22-66) 47 (20-64) Male/female 53/41 18/21 35/12* HCV RNA serum levels (Eq/ml 10 6 ) GT: Patients with abnormal value 12% 28% 69% Mean of abnormal value SE (U/l) ALT (U/l; mean SE) HAI total score (mean SE) Portal inflammation Lobular necrosis Periportal necrosis Fibrosis score # ** *P.02. P.005. P.01 vs. grade 0. P.001 vs. grade 0 and P.005 vs. grade 1-2. P.004 vs. grade 0 and P.02 vs. grade 1-2. P.007 vs. grade 0 and P.05 vs. grade 1-2. #P.004 vs. grade 0. **P.0001 vs. grade 0 and P.04 vs. grade ; respectively, P.005). An analysis of the different components of HAI showed that the presence of steatosis grade 3-4 significantly increases periportal necrosis, but not portal inflammation or lobular degeneration (Table 2). To exclude the possible role of liver fibrosis, we evaluated periportal necrosis in the 94 patients without steatosis in relation to the different grades of fibrosis. In this subgroup, there was no difference in periportal necrosis between patients with grade 3-4 of fibrosis and those with grade 0-2 ( vs , respectively). The steatosis-hai association was independent of serum levels of viremia. A significant relationship between the grade of steatosis and the levels of fibrosis was also observed (r.486; P.001). Gender, iron stores, and levels of viremia did not correlate with either steatosis or fibrosis. No correlation was found between age and steatosis, whereas a relationship between the age of patients and grade of fibrosis was observed (r.374; P.001; data not shown). To avoid the confounding factor of age on the correlation between the grade of steatosis and fibrosis, an age-adjustment of the data was done. After adjustment for age, the grade of steatosis was still associated with the grade of liver fibrosis (P.001). A correlation between the grade of steatosis and serum levels of aminotransferases (r.40; P.001) and of -glutamyl transferase (r.385; P.001) was also observed. In particular, patients with steatosis greater than 30% showed higher levels of -GT than those with less than 30% ( vs , UI/L, P.005; Table 2) or those without steatosis ( UI/L; P.0001; Table 2). A similar trend was observed for the ALT values (Table 2). Correlation Between Steatosis and Viral and Host Factors. The effects of age, sex, genotype, viral load, BMI, and body fat distribution on both the prevalence and grade of steatosis were assessed. Patients infected with genotype 3a showed a higher prevalence of steatosis than those infected with the other genotypes (genotype 3a, 77% vs. type 1, 36%; P.001, and vs. type 2a/c, 57%, P.03). Patients infected with type 2a/c also showed a higher prevalence of steatosis than those infected with genotype 1 (P.04). The different prevalences of steatosis among the HCV genotypes were independent of age, gender, BMI, levels of viremia, grade of hepatic iron deposition, and history of drug abuse (data not shown). Overall, there was no association between serum HCV RNA levels and the grade of steatosis. The analysis by single genotype showed that in genotype 3a infection there was a correlation between the level of viremia and grade of steatosis r.786; P.001; Fig. 1), whereas, no association was observed with the other genotypes. The analysis of variance of the mean differences in the serum viral load in the different grades of steatosis also confirmed the relation between HCV genotype 3a and HCV RNA levels. There was no statistically significant association between age and prevalence or grade of steatosis (data not shown). The FIG. 1. Correlation between serum HCV RNA levels and the hepatic steatosis grade in chronic hepatitis C patients infected with genotype 3a.

4 HEPATOLOGY Vol. 33, No. 6, 2001 ADINOLFI ET AL overall prevalence of steatosis was not significantly different between males and females (51% vs. 43%). However, when the severity of steatosis between the 2 genders was evaluated, the males showed a higher prevalence of steatosis grade 3-4 than the females (33% vs. 16%; P.02). The correlation between BMI and the grade of steatosis did not reach statistical significance (r.183; P.068) when all patients were included in the evaluation (data not shown). When the analysis was done for each genotype, the grade of steatosis in genotype 1 infection correlated with the BMI (r.689; P.001; Fig. 2), and a value close to statistical significance was found in patients infected with genotype 2a/c (P.078), whereas no correlation was observed in those with 3a infection (data not shown). The analysis of variance confirmed the association between HCV genotype 1 and BMI. Of the 80 over-weight or obese patients (BMI 25), 63 (81%) showed steatosis, whereas 93% of those with visceral obesity and 43% of patients with peripheral obesity had steatosis (53/57 vs. 10/23, respectively; P.001). Overall, steatosis was associated to visceral obesity in 62% of cases (53 of 86 cases). In particular, patients infected with genotypes 1, 2a/c or a mixed genotype showed steatosis associated with visceral obesity in 76% of cases. Whereas, of the 20 patients with steatosis and genotype 3a infection, 70% had a normal weight, 25% were over-weight, and 5% were moderately obese. Grade of Steatosis and Hepatic Fibrosis in the Subgroups With a Known Time of Infection. To corroborate the data obtained from the prospective study, we also evaluated a subgroup of patients with a known time of infection, most of whom were selected from our database. 2 As patients infected with genotype 1b showed a wide range (from 5 to 42 years) of duration of infection and because duration of disease may be correlated with the severity of hepatic fibrosis, we analyzed, among patients with genotype 1b, only those with a comparable limited duration of the disease to minimize this possible confounding factor. The selected patients were grouped according to duration of infection (5-9 years, years, years, etc.). We chose those with an infection of 10 to 14 years because this was the largest group, and the duration of infection was relatively long. The total number of patients with a presumable date of infection was 31 for genotype 1b, 25 for genotype 3a, and 15 for genotype 1a. In the selected group of 31 patients with genotype 1b and a duration of disease of 10 to 14 years, steatosis was found in 14 FIG. 2. Correlation between BMI and the hepatic steatosis grade in chronic hepatitis C patients infected with genotype 1. (45%), of whom 8 (26%) with grade 3-4, and 6 (19%) with grade 1-2. The patients with steatosis of grade 3-4 showed a higher hepatic fibrosis score ( ) than those with steatosis grade 1-2 ( ) and significantly higher than those without steatosis ( ; P.001). In patients with steatosis grade 3-4, the yearly rate of fibrosis progression, calculated by dividing the score of fibrosis by the duration of infection, was significantly higher than that found in patients with steatosis grade 1-2 (fibrosis rate: vs ; respectively; P.03) or than in patients without steatosis ( , respectively; P.001). The levels of viremia and hepatic iron deposition were similar in the 3 groups of patients (high grade, low grade, and no steatosis). The median duration of disease was no different in the 3 groups (11.5 vs. 12 vs. 12 yrs). We also evaluated the progression of liver fibrosis in the subgroup of 25 patients infected with genotype 3a, who showed a high prevalence of steatosis (75%) compared with 15 patients infected with genotype 1a, who had a lower prevalence of steatosis (22%). The 2 groups were chosen as they were comparable for the prevalence of drug abuse (85% in genotype 3a vs. 73% in genotype 1a). Patients infected with genotype 3a were younger than those infected with genotype 1a (median age: 29 yrs, range vs. 41 yrs, range 24-56, respectively). The presumed duration of infection in subjects with genotype 3a was shorter than that estimated in patients infected with genotype 1a (median duration 9 yrs, range 3-18 vs. 15 yrs, range 6-24, respectively; P.003). Despite the difference in the duration of disease, no significant difference in the fibrosis score was observed between patients infected with genotype 3a and 1a (fibrosis score: vs , respectively) or in the yearly rate of fibrosis progression ( for genotype 3a and for genotype 1a). However, a higher progression rate of fibrosis was observed for 19 patients infected with genotype 3a who showed steatosis than for 12 infected with genotype 1a without steatosis (yearly rate: vs , respectively; P.004). In the subgroup of patients with genotype 1b infection, we also evaluated the impact of their low alcohol intake on the progression of hepatic fibrosis in relation to the presence or absence of steatosis. Six patients of the group of 14 with steatosis and 7 of the 17 without steatosis had been drinking alcohol at the time of the liver biopsy for a period of over 5 years. The average alcohol intake in both groups was not significantly different and was of 15 to 20 g/d. The fibrosis score in the subgroup with steatosis and alcohol intake was significantly higher than that observed in patients with steatosis and no alcohol intake ( vs , respectively; P.02). No difference was found in patients without steatosis in relation to alcohol intake or no alcohol intake ( vs , respectively). DISCUSSION The results of our study indicate that steatosis, and particularly the higher grades, is of clinical relevance because it plays an important role in accelerating the progression of chronic hepatitis C infection. Indeed, patients with significant steatosis, i.e., greater than 30%, showed a higher hepatic fibrosis score than those with a lower grade ( 30%) or without steatosis. In addition, higher necroinflammatory activity and higher serum levels of aminotransferases and -GT were observed in patients with steatosis. These findings were inde-

5 1362 ADINOLFI ET AL. HEPATOLOGY June 2001 pendent of age, gender, viral factors, and iron deposition. Thus, chronic hepatitis C patients with a high grade of steatosis may represent a group at risk for a more rapid progression to cirrhosis. Indeed, the fact that steatosis and fibrosis do occur together could also promote an alternative hypothesis that both of these histologic features follow protracted injury, i.e., without influencing each other, they may both be secondary to another independent variable. However, our data showed that steatosis is independent of age, whereas liver fibrosis is correlated with age, and most likely with the duration of the disease. The data seem to indicate that steatosis precedes the development of liver fibrosis. In addition, a greater degree of periportal necrosis is observed in patients with higher steatosis and fibrosis scores, but not in patients with only a higher fibrosis score. Thus, steatosis, by promoting greater hepatic necrosis, may accelerate fibrosis deposition. Furthermore, the data obtained in the subgroup of patients with genotype 1b and an established time of infection seem to corroborate the important role played by steatosis in the progression of liver disease. In fact, patients with grade 3 and 4 steatosis showed a significantly higher amount of fibrosis and a progression rate of fibrosis twice as high as those with grade 0-2 steatosis. Similarly, patients infected with genotype 3a, who showed the highest prevalence of steatosis, presented a degree of liver fibrosis comparable with those infected with genotype 1a despite a significantly shorter duration of the disease. It has also been reported that chronic hepatitis C patients with moderate steatosis have higher necroinflammatory activity and fibrosis than those with mild steatosis. 21 Recently, it has been shown that steatosis is an independent risk factor associated with fibrosis. 15 A correlation between fibrosis and steatosis has also been shown using a statistical model. 22 Our data also showed that males have a higher prevalence of steatosis grade 3-4 than females. This may in part explain the greater progression of liver disease reported in the male sex. 6 Hourigan et al., 15 have shown a relationship between BMI, steatosis, and fibrosis in chronic hepatitis C patients and have suggested that obesity has a role in the pathogenesis of steatosis and that the findings have important prognostic and therapeutic implications. Indeed, visceral fat, but not total fat mass, has been shown to be a predictor of steatosis. 23,24 Accordingly, in our study we evaluated not only total fat mass, but also the distribution of fat. We also assessed the role of HCV genotype in inducing steatosis, which was evaluated only in a small number of patients in the Hourigan study. Our results are somewhat different from those reported by Hourigan et al., 15 in that we did not find a direct correlation between BMI and steatosis in all the chronic hepatitis C patients studied, but we did find a relation between BMI and grade of steatosis in genotype 1 infection, a value approaching statistical significance in genotype 2, and no correlation in genotype 3 infection. These data indicate that, besides the total fat mass, other factors are implicated in the pathogenesis of steatosis. Our data show that steatosis is strictly correlated with the abdominal fat mass. Visceral obesity, therefore, rather than total fat mass, seems to play an important role in the pathogenesis of steatosis. It has been reported that visceral obesity is a predictor not only of steatosis, but also of hyperinsulinemia and peripheral insulin resistance. 25 In addition, visceral lipolysis is resistant to insulin suppression and is the source of liver fatty acids in hyperinsulinemic states such as liver disease. 26 Similar mechanisms may also be implicated in the pathogenesis of steatosis in chronic hepatitis C patients. We also showed that, in addition to visceral obesity, viral factors play an important role in the development of steatosis. In concordance with our previous results 2 and with the results of others, 27,28 the prevalences of steatosis among the HCV genotypes were significantly different, patients infected with genotype 3a showing the highest prevalence followed by type 2a/c infection and lastly type 1 infection. In addition, in type 3a infection, steatosis was closely associated with the levels of viremia, which reflect intrahepatic viral replication, 29 and was independent of age, obesity, iron deposition, alcohol intake, and of drug use. In particular, there was no difference in the hepatic iron storage and alcohol intake between patients infected with type 3a and 1a, who were comparable for age and history of drug abuse. Recently, it has been reported that the degree of liver steatosis in chronic hepatitis C patients infected with genotype 3a correlates with the levels of intrahepatic HCV replication. 30 On the whole, the data suggest that steatosis in patients with genotype 3a, and perhaps in those with type 2a/c, is in part related to HCV. Recently, Poupon et al., 31 presented a study whose aim was to evaluate the role of viral, host, and environmental factors on liver fibrosis. The results, obtained on a wide population of CHC patients for whom the date of infection was known, are in concert with the data of our study. In fact, BMI and genotype 3 were associated with steatosis, and the latter was the major determinant of fibrosis progression in CHC patients. The mechanisms underlying the development of parenchymal steatosis in HCV infection are not known. In transgenic mice, it has been shown that the HCV core protein, which can also be detected in the liver of HCV patients, induces hepatic steatosis. 13 The core protein expression within the mitochondria alters the double membrane structure and causes an impairment of lipid oxidation, which produces steatosis. 14 Influenza B virus may also induce steatosis by altering mitochondrial enzyme activity. 32 Steatosis may be a result of alterations in the lipid metabolism. It is well known that steatosis can be associated with hepatic inflammatory changes and fibrosis by causing oxidative stress and mitochondrial dysfunction. 33 Viruses, alcohol abuse and high liver-tissue iron concentration may interfere with lipid peroxidation and glutathione turnover in hepatic steatosis. 34 Lipid peroxidation is associated with stellate-cell activation and synthesis of collagen type In chronic hepatitis C infection, steatosis correlates with lipid peroxidation 34 and active fibrogenesis, 36 but the link has not been sufficiently evaluated. The results of our study seem to suggest that alcohol exerts a synergistic effect with steatosis in accelerating the progression of hepatic disease, even at a low intake (from 10 to 30 g/d), whereas in the absence of steatosis it does not aggravate the liver damage. Because of the small number of patients studied, further investigations are necessary to confirm these results. However, Poupon et al., 31 have recently reported similar results indicating that the combination of steatosis and alcohol intake, even at a low consumption, was an independent factor associated to the severity of hepatic fibrosis. Figure 3 shows our hypothesis on the events associated with steatosis and the possible mechanisms involved in the progression of fibrosis in chronic hepatitis C infection. The hypothesis is based on the data of this study and those reported by others. 2,27,28,30,31 It has also been

6 HEPATOLOGY Vol. 33, No. 6, 2001 ADINOLFI ET AL FIG. 3. Host and viral factors implicated in the pathogenesis of hepatic steatosis in chronic hepatitis C patients and possible mechanisms involved in accelerating hepatic fibrosis progression. suggested that hepatic iron may be a cofactor in inducing fibrosis in chronic hepatitis C patients. We conclude that in chronic HCV infection, steatosis is an important cofactor in accelerating the development of hepatic fibrosis and in increasing necroinflammatory activity, and that both host and viral factors play a role in the pathogenesis of steatosis in chronic hepatitis C patients. A correct therapeutic approach to steatosis would slow down the evolution of chronic hepatitis, which would be of particular importance for patients who are nonresponders to current antiviral therapies. Host (obesity, diet, diabetes, hyperinsulinemia, alcohol) and HCV virus factors play a role in the development of steatosis; in particular visceral obesity and HCV type 3a seem to be the major determinants of steatosis in this subset of patients. It is important to underscore that genotype 3a has only recently been introduced to our country and affects young people, mainly drug users, and that the progression of fibrosis is time-related. We can therefore expect in the future an increasing number of cirrhotics among these patients. The different causes of steatosis should be sought in each single patient because treatment may differ according to the factor(s) involved in the process. However, we share the belief of others 15 that the restoration of a normal weight in subjects with visceral obesity may be of clinical importance in chronic hepatitis C patients. REFERENCES 1. Benvegnù L, Pontisso P, Cavalletto D, Noventa F, Chemello L, Alberti A. 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