Prevalence of occult HBV infection in haemodialysis patients with chronic HCV

AIM: To study the prevalence and clinical effects of occult HBV infection in haemodialysis patients with chronic HCV. METHODS: Fifty chronic hemodialysis patients with negative HbsAg, and positive anti-HCV were included in the study. These patients were divided into two groups: HCV-RNA positive and HCV-RNA negative, based on the results of HCV-RNA PCR. HBV-DNA was studied using the PCR method in both groups. RESULTS: None of the 22 HCV-RNA positive patients and 28 HCV-RNA negative patients revealed HBV-DNA in serum by PCR method. The average age was 47.2±17.0 in the HCV-RNA positive group and 39.6±15.6 in the HCV-RNA negative group. CONCLUSION: The prevalence of occult HBV infection is not high in haemodialysis patients with chronic HCV in our region. This result of our study has to be evaluated in consideration of the interaction between HBsAg positivity (8%-10%) and frequency of HBV mutants in our region.     

Hepatic iron, liver steatosis and viral genotypes in patients with chronic hepatitis C

Hepatic iron has been described in hepatitis C virus (HCV) infection as an important cofactor of disease outcome. The mechanisms leading to hepatic iron deposits (HIDs) in HCV patients are partially understood. We investigated HIDs in the liver biopsies of a consecutive series of 242 HCV-infected patients with well-compensated liver disease. Serum ferritin was elevated in 20.7% and transferrin saturation in 19.0%, while 38.8% had stainable HIDs indicating that serum markers of systemic iron overload have low sensitivity in predicting HIDs in hepatitis C. A cut-off value of serum ferritin (350 microg/L in females and 450 microg/L in males) had good negative predictive value in excluding presence of mild-moderate HIDs (grade II-III). Hepatic iron deposits correlated by multivariate analysis with serum ferritin [odds ratio (OR) 1.008, 95% confidence interval (CI) 1.005-1.011] and albumin (OR 1.15, 95% CI 1.02-1.297). Hepatic iron deposits were more frequent in HCV-3-infected cases than in other genotypes (P = 0.027) while raised serum iron indices were more frequent in non-HCV-3 genotypes (P = 0.02). Furthermore, advanced fibrosis (F3-F4 by METAVIR) was more frequent in non-HCV-3 genotypes (P = 0.04). In HCV-3 cases there was a close association between HIDs and severe (grade II-III) steatosis (P < 0.00001). These results indicate that in well-compensated chronic hepatitis C HIDs are strongly associated with HCV-3 and viral-induced hepatic steatosis, while in the presence of other genotypes they might merely reflect a more advanced stage of liver disease and/or a systemic iron overload. Serum ferritin could identify a subgroup of patients in which the need of venesection could be excluded without liver biopsy.     

Noninvasive assessment of liver steatosis, fibrosis and inflammation in chronic hepatitis C virus infection.

BACKGROUND: Duplex-Doppler ultrasound is a noninvasive method for the assessment of hepatic hemodynamics beyond conventional gray-scale imaging. The clinical value of the method for the grading and staging of chronic hepatitis C virus (HCV) infection and the prediction of hepatic steatosis still has to be determined. This study aimed to compare Duplex-Doppler and ultrasound with the histologic staging and the estimation of hepatic steatosis in chronic HCV infection. PATIENTS AND METHODS: One hundred and nineteen consecutive patients with chronic HCV infection underwent both liver biopsy and ultrasound with Duplex-Doppler. Maximum portal venous blood flow velocity, portal venous flow undulation, hepatic venous flow pattern and spleen size were assessed and compared with histologic findings. Histologic grading and staging was performed according to the modified HAI and hepatic steatosis was estimated. RESULTS: Doppler ultrasound was unable to discriminate between different degrees of fibrosis. Sensitivity/specificity of portal venous flow and undulations for the diagnosis of hepatic cirrhosis was 74.5%/53% and 76.5%/100%. The PPV and NPV of reduced undulations was 100% and 96.2%. Mono- or biphasic hepatic venous flow indicated advanced hepatic steatosis (sensitivity 88.2%, specificity 74.5%, PPV 36.6%, NPV 97.5%). Spleen size was significantly enlarged both in patients with cirrhosis and steatosis. CONCLUSIONS: Although Duplex-Doppler of the portal and hepatic veins is not a substitute for histologic grading and staging, portal vein undulations can predict liver cirrhosis with considerable accuracy. Moreover, triphasic patterns of hepatic venous flow virtually exclude significant fatty liver disease. Additional studies should perform intraindividual follow-up investigations to further define the role of Duplex-Doppler ultrasound in chronic HCV infection.     

High sCD36 plasma level is associated with steatosis and its severity in patients with genotype 1 chronic hepatitis C

Summary. Soluble CD36 (sCD36) plasma levels, a known marker of cardiometabolic disorders, are associated with surrogate markers of steatosis, while experimental and human studies show a link between CD36 expression in the liver and steatosis. In a cohort of patients with genotype 1 chronic hepatitis C (G1 CHC), we tested the association of sCD36 plasma levels with host and viral factors and sustained virological response (SVR). One hundred and seventy‐five consecutive biopsy‐proven patients were studied. sCD36 plasma levels were assessed by an in‐house ELISA. All biopsies were scored by one pathologist for staging and grading (Scheuer) and graded for steatosis, which was considered moderate–severe if ≥20%. Patients underwent standard of care therapy with pegylated interferon and ribavirin. The severity of steatosis progressively increased according to sCD36 quartiles (P = 0.02); total and low‐density lipoprotein (LDL) cholesterol levels were significantly higher in patients in the lower quartile compared to all the others. Gamma‐glutamyl transferase (P = 0.02), homoeostasis model assessment (HOMA) score (P = 0.002) and sCD36 (P = 0.04) were independently associated with the severity of steatosis as continuous variable. Multivariate logistic regression analysis showed that HOMA (OR 1.243, 95% CI 1.04–1.484, P = 0.01) and sCD36 (OR 1.445, 95%CI 1.135–1.839, P = 0.003) were independently linked to steatosis ≥20%. No association was found between sCD36 and SVR. CD36 is linked to steatosis and insulin resistance in patients with G1 CHC, but does not predict response to treatment. The potential of sCD36 as a surrogate marker of steatosis should be further investigated.     

Association of chronic hepatitis B virus infection with insulin resistance and hepatic steatosis

Background and Aim: Chronic viral infections such as human immunodeficiency virus and hepatitis C virus (HCV) may decrease tissue response to insulin, thereby causing insulin resistance. In addition, insulin resistance is associated with hepatic steatosis. However, whether these phenomena hold true for chronic hepatitis B virus (HBV) infection remains largely unknown. The present study therefore aimed to investigate the association of chronic HBV infection with insulin resistance and hepatic steatosis. Methods: A total of 507 subjects (243 men and 264 women; mean age 46.56 years) less than 60 years‐old attending a health examination center were enrolled in the study. All the subjects were negative for antibodies against HCV and consumed less than 140 g alcohol/week. Demographic, anthropometric, clinical, and laboratory data were obtained from each subject. Insulin resistance index was determined using homeostasis model assessment (HOMA‐IR). Hepatic steatosis was identified by ultrasound examination. Results: Of the 507 subjects, 50 (9.9%) were positive for hepatitis B surface antigen (HBsAg) and designated HBV carriers. All variables were comparable between HBV carriers and non‐HBV carriers, except that HBV carriers had significantly higher serum alanine aminotransferase and aspartate aminotransferase levels (P < 0.05). By multivariate linear regression, HBV carriers were not associated with insulin resistance. In addition, multivariate regression analyses showed that HBV carriers were not associated with the presence of ultrasonographic fatty liver. Conclusions: Chronic HBV infection seems not to be associated with insulin resistance or hepatic steatosis in HBV carriers.     

Smoking is associated with steatosis and severe fibrosis in chronic hepatitis C but not B

Objective. The results of retrospective studies suggest an association between smoking, insulin resistance, steatosis and fibrosis in patients with chronic hepatitis C (CHC); no data are available for chronic hepatitis B (CHB). The purpose of this study was to evaluate the relationship, if any, of such factors on liver fibrosis in a cohort of patients with CHB and CHC. Material and methods. The study prospectively included 271 consecutive patients with CHB (n=95) or CHC (n=176) who had undergone liver biopsies. Each patient completed a questionnaire on smoking habits; anthropometric measurements and laboratory examinations were carried out and histological lesions were recorded. Results. In CHC patients, severe fibrosis was independently associated with a higher body mass index (BMI) (OR: 1.180, 95% CI: 1.028–1.354; p=0.019), heavy smoking (OR: 3.923, 95% CI: 1.356–11.348; p=0.012), higher alanine aminotransferase (ALAT) levels (OR: 1.010, 95% CI: 1.003–1.017; p=0.005) and alkaline phosphatase (ALP) levels (OR: 1.016, 95% CI: 1.001–1.030; p=0.03) and presence of necroinflammation (OR: 11.165, 95% CI: 1.286–96.970; p=0.029). Moreover, steatosis was independently associated with high gamma-glutamyl transpeptidase (GGT) values, heavy smoking and presence of necroinflammation. In CHB patients, no association between smoking habits and fibrosis or steatosis was noted. Conclusions. Heavy smoking is associated with severe fibrosis in CHC but not CHB. Heavy smoking is also significantly associated with steatosis in CHC and this could be the link between smoking and fibrosis progression.     

Evaluation of hepatic steatosis by ultrasound in patients with chronic hepatitis C virus infection.

OBJECTIVE: To compare two alternative ultrasound parameters, hepatic vein flow (HVF) pattern and presence of focal hypoechoic areas (FHA) within the liver hilus, as non-invasive predictors of liver steatosis in patients with chronic hepatitis C virus (HCV) infection. DESIGN: In 122 consecutive patients with chronic HCV infection, the HVF pattern and presence of FHA within the liver hilus were assessed by Duplex-Doppler and B-mode sonography. All patients underwent liver biopsy and the sonographic results were compared with a histological score of steatosis used as the gold standard for this purpose. Association of fatty infiltrations with clinical and sonographic features were evaluated by a stepwise logistic regression analysis. RESULTS: Reduced HVF and FHA, but not standard clinical and laboratory parameters, strongly correlated with steatosis on histology (P<0.001). Both sonographic parameters made excellent predictions for the subgroup of patients with severe steatosis, particularly when both tests were combined [sensitivity (SE) 95%, specificity (SP) 96%, positive predictive value (pPV) 93%, negative predictive value (nPV) 97%, and accuracy 96%]. However, the sensitivity and accuracy of HVF pattern analysis were markedly reduced when all degrees of steatosis were defined as positive (SE 71%, SP 76%, pPV 81%, nPV 64%, and accuracy 73%). In contrast, the dichotomous parameter FHA remained a powerful indicator even under the latter conditions (SE 74%, SP 100%, pPV 100%, nPV 72%, and accuracy 84%). The combination of both sonographic tests resulted in improved sensitivity (82%), but significant loss of specificity (76%) and accuracy (80%) for prediction of liver steatosis. CONCLUSION: Sonographic evaluation of reduced HVF and FHA within the liver hilum is easy to perform, non-invasive, and, when present, gives a high degree of confidence in the diagnosis of liver steatosis. However, the lack of sonographic evidence of steatosis cannot definitively exclude the presence of mild steatosis, as shown on biopsy.     

Elevated serum CK18 levels in chronic hepatitis C patients are associated with advanced fibrosis but not steatosis

Summary. Cytokeratin‐18 (CK‐18) is a major intermediate filament protein in liver cells. The M30 fragment of CK‐18 has been identified as a useful marker of apoptosis associated with fibrosis and steatosis in nonalcoholic steatohepatitis (NASH). We sought to assess the relationship of this marker and steatosis in a cohort of adult patients with chronic hepatitis C. The study cohort included sera from 267 treatment‐naïve chronic hepatitis C (CHC) patients and 100 healthy controls with normal alanine aminotransferase (ALT). Biopsies from CHC patients were assessed for METAVIR fibrosis stage, Histology Activity Index (HAI) inflammation score and steatosis grade by expert histopathologists. The M30 fragment of CK‐18 was quantified by ELISA. Wilcoxon Rank Sum, Spearman Correlation and Linear Regression tests were performed for statistical analysis. Median CK‐18 levels were higher in CHC patients compared to controls (411 vs 196 U/L, P < 0.0001). Fibrosis stage was associated with increasing serum CK‐18 levels (P = 0.015) and CK‐18 levels were higher for F2–F4 vs F0–F1 (500 vs 344 U/L; P = 0.001). There was no association between CK‐18 and increasing steatosis grade 1, 2 or 3 (460.7 vs 416.8 vs 508.3 U/L; P = 0.35) and presence or absence of steatosis (445.3 vs 365.8 U/L; P = 0.075). Fibrosis stage was independently associated with serum M30 in a multivariable linear regression model (P = 0.03). CK‐18 levels were higher in CHC compared to healthy controls and associated with hepatic fibrosis. There was no difference in CK‐18 M30 levels between CHC patients with and without steatosis. Although apoptosis may still contribute to hepatitis C virus (HCV)‐mediated steatosis, our results suggest that serum CK‐18 will not be a clinically useful test for identifying significant steatosis in CHC.     

Hepatic steatosis in chronic hepatitis B patients is associated with metabolic factors more than viral factors

Background and Aims:  Hepatic steatosis is commonly seen in chronic hepatitis C (CHC) patients. It has been reported to be associated with both metabolic factors and viral factors, and affects the severity of fibrosis in CHC. However, the relationship between hepatic steatosis and chronic hepatitis B (CHB) is unclear. The aims of this study were to investigate the frequency of hepatic steatosis in CHB patients, to identify the factors associated with its presence, and assess the relationship between the stage of steatosis and the severity of fibrosis.
Methods:  Medical records of 153 adult patients with CHB who had undergone a liver biopsy within the past 4 years were included in the study.
Results:  Body mass index (BMI) and age of CHB patients with steatosis was significantly higher than the patients without steatosis ( P  < 0.05), as determined by the univariate analysis. Steatosis was found to correlate with the BMI values and alanine aminotransferase (ALT) levels, and ALT levels were associated with hepatitis B virus (HBV)–DNA levels and histology activity index (HAI) scores, stages of fibrosis were associated with the HAI score and HBV–DNA, as determined by the multivariate analysis. In contrast, there was no significant association between advanced stages of fibrosis and steatosis.
Conclusion:  Our data indicate that hepatic steatosis is more frequently present in CHB patients than in the general population. We hypothesize that steatosis in CHB patients may be due to metabolic factors and the ability of HBV to indirectly facilitate the development of steatosis. In the present study, steatosis in CHB patients was not found to be associated with the severity of fibrosis.     

The burden of HBV infection in HCV patients in Italy and the risk of reactivation under DAA therapy

Background

There is increasing awareness of HBV reactivation in HCV-RNA-positive/HBV-coinfected patients with chronic liver disease (CLD) treated with oral direct-acting antivirals (DAAs).

Hepatic steatosis in chronic hepatitis C patients infected with genotype 2 is associated with insulin resistance, hepatic fibrosis and affects cumulative positivity of serum hepatitis C virus RNA in peginterferon and ribavirin combination therapy

Aim: Hepatic steatosis is one of the factors limiting the virological response to interferon‐based antiviral therapy for chronic hepatitis C (CH‐C) patients infected with genotype 1, while contradictory results have been reported for genotype 2. We aimed to clarify the effect of hepatic steatosis on therapeutic outcome and cumulative positivity of serum HCV RNA in CH‐C patients infected with genotype 2 treated by peginterferon (PEG‐IFN)α2b and ribavirin (RBV) combination therapy. Methods: A total of 74 treatment‐naïve non‐cirrhotic CH‐C patients infected with genotype 2 who received PEG‐IFNα2b and RBV according to the standard regimen were divided into hepatic steatosis 0–10% and >10% groups. The clinical backgrounds, sustained virological response (SVR) rates and cumulative positivity of serum HCV RNA were compared between the two groups. Results: Among the 74 patients, 61 (82.4%) had hepatic steatosis 0–10% and 13 (17.6%) had hepatic steatosis >10%. Scores of homeostasis model assessment‐insulin resistance and hepatic fibrosis were higher in patients with hepatic steatosis >10% than hepatic steatosis 0–10% (P = 0.040 and 0.042, respectively). Non‐SVR was more frequent in patients with hepatic steatosis >10% than hepatic steatosis 0–10% (P = 0.003). Cumulative positivity of serum HCV RNA was significantly higher in patients with hepatic steatosis >10% than hepatic steatosis 0–10% (P = 0.004). Conclusions: In CH‐C patients infected with genotype 2 treated by PEG‐IFNα2b and RBV combination therapy, hepatic steatosis >10% was associated with increased insulin resistance, advanced hepatic fibrosis and higher cumulative positivity of serum HCV RNA, which lead to a higher risk of non‐SVR.     

Hepatic steatosis and fibrosis in young men with treatment‐naïve chronic hepatitis B

Objectives: The clinical significance of liver steatosis has been studied because steatosis plays a role in the progression of liver fibrosis. Nevertheless, the impact of steatosis in the early stage of fibrosis in non‐obese young men with chronic hepatitis B (CHB) is poorly understood. Thus, the purpose of this study was to investigate the prevalence of hepatic steatosis, assess the relationship between hepatic steatosis and fibrosis and to assess the laboratory parameters for predicting clinically significant liver fibrosis in non‐obese young men with CHB. Methods: We prospectively evaluated liver biopsies in young male patients with CHBwith a serum alanine aminotransferase level of more than two times the upper limit of normal for at least 3 months before enrollment. Patients were excluded when they had co‐infection with another virus and prior antiviral treatment. Demographical, anthropometric and laboratory parameters were analysed. Liver steatosis, necroinflammation and fibrosis were also assessed. Results: A total of 86 young male patients with CHB were included in this study. The median age was 21 years (range, 20–26 years) and the median body mass index was 23.0 kg/m² (range, 18.0–28.3 kg/m²). Steatosis was present in 44 patients (51.2%). Significant fibrosis (beyond periportal fibrosis) was present in 50 patients (58.1%). Steatosis was associated with insulin, homeostasis model for insulin resistance (HOMA‐IR), total cholesterol and triglycerides. On multiple regression analysis, steatosis was independently associated with triglyceride and HOMA‐IR. Significant fibrosis was independently associated with γ‐glutamyltransferase (GGT) and necroinflammation activity. However, there was no significant association between significant fibrosis and the presence of steatosis. Conclusions: The prevalence of hepatic steatosis is a common finding in young male patients with CHB. Hepatic steatosis in CHB patients seems to be associated with insulin resistance, but it is not associated with hepatic fibrosis. GGT levels can provide useful information on the stage of CHB.     

HIV感染献血者并发感染HBV、HCV及梅毒调查分析

目的:了解曲靖市无偿献血人群中艾滋病病毒(HIV)感染者并发感染乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)和梅毒的状况。方法:应用酶联免疫吸附试验(ELISA),对HIV感染献血者检测HBsAg、抗-HCV、抗-TP。结果:133例HIV感染献血者中,HBV感染率为1.5%,HCV感染率为10.5%,梅毒感染率为7.5%。结论:曲靖市HIV感染的献血者中,并发HCV和梅毒感染率高,而并发HBV感染率较低。     

HBV、HCV在原发性肝癌与其他恶性肿瘤患者及健康人群中的感染率调查

为了调查原发性肝癌与其他恶性肿瘤患者及健康人群中HBV、HCV感染率 ,将上述三组人群的HBV、HCV的感染情况进行分析比较。结果显示原发性肝癌组HBV感染率、HBV/HCV混合感染率均明显高于其它恶性肿瘤组和健康对照组 (P <0 0 1) ;其他恶性肿瘤组与健康对照组之间无显著差异 (P >0 0 5 ) ;单纯HCV感染率在三组之间均无显著差异 (P >0 0 5 )。由此可见HBV感染、HBV/HCV混合感染是原发性肝癌的主要致病因素     

Determinants of serum ALT normalization after phlebotomy in patients with chronic hepatitis C infection

Background Phlebotomy is performed to reduce excessive iron accumulation in hepatic tissue. We studied serum alanine aminotransferase (ALT) normalization rates and 50% reduction in initial serum ALT (ALT_50% reduction rate) in patients with hepatitis C viral (HCV) infection and investigated the factors that influenced the response to phlebotomy therapy. Methods We evaluated 23 consecutive patients with HCV infection who underwent phlebotomy. Phlebotomy was performed a few times per week, then a few times per month, and 200–400 ml of blood was removed at each session, depending on the clinical response. During the course of therapy, hemoglobin (Hb), serum ALT, and ferritin levels were assessed monthly. Results In patients with Hb of less than 11 g/dl, the ALT_50% reduction rate was 87.5%. In patients with a serum ferritin level of less than 10 g/dl the ALT_50% reduction rate was 83.3%. In patients with Hb of less than 11 g/dl, the ALT normalization rate was 50%, and in those with a serum ferritin level of less than 10 g/dl, the ALT normalization rate was 41.7%. Multivariate analysis identified ALT less than 100 IU/l at the start of phlebotomy as an independent factor associated with ALT normalization. Of the 7 patients who showed no response to phlebotomy, 85.7% were obese (body mass index ≥25 kg/m²), and 40% showed more than 30% steatosis on liver histology. The cumulative ALT normalization rate in relation to the total volume of blood loss was 43.9% with a blood less or more than 3 l, and thus was optimal above 3 l. Conclusions Although the sample number was relatively small, the results of our study suggest that phlebotomy is effective therapy for HCV patients who are nonobese, show little or no steatosis on liver histology, and have a baseline serum ALT level of less than 100 IU/l.     

2000例门诊和住院患者中HIV与HBV、HCV混合感染的血清学分析

目的分析医院对艾滋病病毒(HIV)抗体筛选结果,了解HIV感染与HBV、HCV肝炎病毒混合感染的关系.方法1998年6月～1999年6月采用ELISA法、MEIA(微粒子酶免法)对HIV、HBV、HCV检测.结果(1)抗HIV感染率为1.4%,其中男性占1.8%,女性占0.9%.民族分布维吾尔族占3.09%,汉族占0.27%,回族占0.77%;维吾尔族与汉族感染率有极显著性差异(χ2=25.34;P＜0.01).(2)在HIV阳性血清中抗HIV单一感染率14.29%;HIV、HCV双重感染率60.71%,HIV、HBV、HCV三重感染率25%;HIV、HCV与HIV、HBV、HCV混合感染率有极显著性差异(χ2=23.9;P＜0.01).结论在本组血清中HIV感染率高,HCV阳性在HIV/AIDS病人血清中混合感染率高,这与青年人静注毒品有关.HIV与HCV有共同传播途径--血液传播.     

Significance of serum leptin and adiponectin levels in Egyptian patients with chronic hepatitis C virus associated hepatic steatosis and fibrosis

AIM: To study serum levels of leptin and adiponectin in patients with chronic hepatitis C virus infection genotype-4 (HCV-4) related steatosis and fibrosis. METHODS: We prospectively studied 45 untreated men with chronic HCV-4, with proven steatosis (group I, 30 patients), and fibrosis (group II, 15 patients), on liver biopsy. In addition, 15 healthy men (group III), matched for age, and body mass index were included. However, we excluded another five patients with steatohepatitis, and six patients with cirrhosis. We measured total serum leptin and adiponectin levels, as potential predictors for liver steatosis and fibrosis. Also, a correlation between these adipokines and various clinical and laboratory data were evaluated. All subjects were selected from Tropical and Internal medicine departments, Menoufiya University Hospital, Menoufiya, Egypt, during the period from February 2010 to August 2011. RESULTS: In group I, severity of hepatic steatosis was mild, moderate, and severe, in 19 patients (63.5%), 8 patients (26.5%), and 3 patients (10%), respectively. In contrast, in group II, hepatic fibrosis was found to be in stage 1, 2, and 3, in 6 patients (40%), in 6 patients (40%), and in 3 patients (20%), respectively. On comparing group I with group II, there was a significant decrease in serum adiponectin levels (131.4 ± 7.91 pg/mL vs 436 ± 9.75 pg/mL, P < 0.001), while there was no significant difference between both groups regarding serum leptin levels (34.69 ± 7.69 ng/mL vs 35.17 ± 1.06 ng/mL, P > 0.05). However, in the same group, when compared with group III, there was a significant increase in serum leptin levels (34.69 ± 7.69 ng/mL vs 10.69 ± 0.84 ng/mL, P < 0.001), while there was a significant decrease in serum adiponectin levels (131.4 ± 7.91 pg/mL vs 342.4 ± 44.48 pg/mL, P < 0.001). In contrast, in group II, when compared with group III, there was a significant increase in serum leptin and adiponectin levels (35.17 ± 1.06 ng/mL vs 10.69 ± 0.84 ng/mL, P < 0.001, and 436 ± 9.75 pg /mL vs 342.4 ± 44.48 pg/mL, P < 0.05, respectively), while there was no significant difference between both groups regarding serum creatinine (0.83 ± 0.34 vs 0.89 ± 0.24, P > 0.05). On the other hand, serum leptin was not correlated with serum adiponectin in group I and in group II (r = 0.09, P > 0.05, and r = -0.1, P > 0.05, respectively). However, serum adiponectin was significantly negatively correlated with serum aspartate transaminase in group I, but no correlation detected in group II (r =-0.39, P > 0.05, and r = -0.03, P > 0.05). CONCLUSION: In male patients with chronic HCV-4, serum adiponectin levels are elevated in hepatic fibrosis, but decreased in steatosis. Therefore, in contrast to leptin, adiponectin may be used as a non-invasive marker.     

Fluctations in viral load (HCV RNA) are relatively insignificant in untreated patients with chronic HCV infection

SUMMARY. A recently available assay to quantify serum viral load in hepatitis C virus (HCV) infection has been used to evaluate the effects of anti-viral therapies. However, variability in HCV RNA levels in untreated patients with HCV infection has not yet been established. We therefore prospectively measured the biological fluctuations of HCV RNA in sera from untreated patients with chronic HCV infection. Sera were collected from seven patients at 8 am and 4 pm on the same day to assess the effect of diurnal variation, daily for 5 days in a further 10 patients, biweekly for 6 weeks in nine patients and monthly for 3 months in 11 patients. All patients had biopsy-proven chronic liver disease with elevated alanine aminotransferase (ALT) values and had not received anti-viral treatment. HCV RNA was measured blinded, in duplicate, using the quantitative branched (bDNA) amplification assay (Quantiplex™ HCV RNA. Chiron Co. Erneryville. CA) 36 of the 37 patients studied had measurable HCV RNA throughout the study. There was no significant correlation between HCV RNA levels and ALT values or histological activity. HCV RNA levels did not appear to vary significantly within any of the groups studied and there did not appear to be a change associated with diurnal variation. All individual patients demonstrated less than a threefold fluctuation in HCV RNA throughout the study period. Hence HCV RNA levels remain relatively stable in untreated individuals with chronic HCV infection. Changes of a magnitude of threefold (0.5 log) or greater in HCV RNA levels were not observed in untreated patients.