Serum leptin levels in patients with viral chronic hepatitis or liver cirrhosis

BACKGROUND/AIM: Serum levels of leptin, the adipocyte-derived hormone regulating food intake and energy expenditure in mammals, have been found to be increased in cirrhotic patients. The aim of the present study was to investigate leptin serum level in relation to anthropometric features and liver function in patients with viral chronic hepatitis or liver cirrhosis. METHODS: Serum leptin levels were determined by radioimmunoassay in 30 male and 10 female patients with chronic hepatitis, in 42 male and 10 female patients with liver cirrhosis, and in four respective control groups. Liver function was evaluated by the monoethylglycinexylidide formation test. Body mass index and body fat mass were estimated by weight, height and skinfold thickness measurements. RESULTS: Compared with controls, absolute serum leptin levels were significantly (p<0.01) lower in chronic hepatitis patients and similar in cirrhotic patients. Leptin serum levels were significantly (p<0.05) higher in cirrhotic than in chronic hepatitis patients. When expressed in relation to body fat mass, the above differences persisted; however, cirrhotic females showed significantly (p<0.05) higher serum leptin values than controls. Serum leptin values correlated negatively (p<0.01) with monoethylglycinexylidide serum values in all groups of patients. CONCLUSIONS: In patients with chronic viral liver disease, serum leptin levels tend to increase as liver function worsens. This may reflect a decline in the ability to downregulate energy expenditure as an adaptation to anorexia and/or to defective substrate utilisation due to liver disease and may negatively influence body weight homeostasis in these patients.     

Serum Leptin Levels in Patients with Liver Cirrhosis and Chronic Viral Hepatitis

Background: The aim of the present study was to investigate serum leptin levels in relation to anthropometric features in patients with liver cirrhosis (LC) and chronic viral hepatitis (CVH), and to determine the effect of the severity and aetiology of the LC on serum leptin levels. Methods: Forty-nine patients with LC, 32 patients with CVH and 69 control subjects were age, body mass index (BMI) and sex-matched and included in the study. Plasma glucose, serum leptin and insulin levels were determined. Insulin resistance was assessed using homoeostasis model assessment (HOMA). Body composition was estimated by skinfold thickness. Results: Female patients with Child-A LC had higher levels of leptin, and female and male patients with Child-A LC had higher absolute leptin (leptin/BFM) levels compared to patients with Child-C LC and control subjects. Serum leptin levels of the patients with alcohol LC were higher than the control subjects, but the absolute leptin levels were comparable. When alcoholic and post-viral hepatitis cirrhotic patients were compared with each other on an aetiologic basis, there was no significant difference between them in leptin and absolute leptin levels. There were significant correlations between leptin and BMI, body fat percentage (BFP), BFM (body fat mass) in all three groups in both sexes. Conclusions: These data suggest that the physiologic correlations among serum leptin level, sex, BMI and BFM were well preserved in patients with chronic liver disease. Patients with alcohol LC had higher leptin levels. In early stages of liver disease, leptin levels and absolute leptin levels are higher than in normal subjects. However, in advanced stages of the disease the significant decline in leptin levels and similar levels of leptin expressed in relation to BFM compared to control subjects predominantly represent the expression of fat mass.     

Serum leptin levels in patients with liver cirrhosis and chronic viral hepatitis

BACKGROUND: The aim of the present study was to investigate serum leptin levels in relation to anthropometric features in patients with liver cirrhosis (LC) and chronic viral hepatitis (CVH), and to determine the effect of the severity and aetiology of the LC on serum leptin levels. METHODS: Forty-nine patients with LC, 32 patients with CVH and 69 control subjects were age, body mass index (BMI) and sex-matched and included in the study. Plasma glucose, serum leptin and insulin levels were determined. Insulin resistance was assessed using homoeostasis model assessment (HOMA). Body composition was estimated by skinfold thickness. RESULTS: Female patients with Child-A LC had higher levels of leptin, and female and male patients with Child-A LC had higher absolute leptin (leptin/BFM) levels compared to patients with Child-C LC and control subjects. Serum leptin levels of the patients with alcohol LC were higher than the control subjects, but the absolute leptin levels were comparable. When alcoholic and post-viral hepatitis cirrhotic patients were compared with each other on an aetiologic basis, there was no significant difference between them in leptin and absolute leptin levels. There were significant correlations between leptin and BMI, body fat percentage (BFP), BFM (body fat mass) in all three groups in both sexes. CONCLUSIONS: These data suggest that the physiologic correlations among serum leptin level, sex, BMI and BFM were well preserved in patients with chronic liver disease. Patients with alcohol LC had higher leptin levels. In early stages of liver disease, leptin levels and absolute leptin levels are higher than in normal subjects. However, in advanced stages of the disease the significant decline in leptin levels and similar levels of leptin expressed in relation to BFM compared to control subjects predominantly represent the expression of fat mass.     

Lack of association between serum leptin levels and hepatic steatosis, fibrosis or response to antiviral therapy in Korean chronic hepatitis C patients

BACKGROUND/AIMS: Leptin has been recently implicated in the development of hepatic steatosis and fibrosis in chronic hepatitis C (CHC) infection. The serum levels of leptin are known to be strongly affected by anthropometric parameters such as body mass index (BMI) and total body fat, which show differences between races or ethnicities. In this study, we examined whether serum leptin levels are correlated with clinical, virological, and histological features, and with response to antiviral therapy in Korean CHC patients. METHODOLOGY: We evaluated correlations between serum leptin level and age, sex, BMI, fasting glucose, alanine aminotransferase, genotype, hepatitis C virus RNA titer, steatosis, fibrosis, and response to antiviral therapy after 24 weeks completing 24 weeks of interferon-alpha based therapy in 47 Korean CHC patients. RESULTS: Of the variables examined, only female sex and a BMI > 25kg/m2 were identified as independent variables related to a higher leptin level by multivariate analysis. Baseline leptin levels and leptin changes before/after antiviral therapy were not correlated with response to therapy. CONCLUSIONS: In Korean CHC patients, serum leptin levels were found to be correlated with anthropometric parameters, but not with virological or histological features. In addition, serum leptin levels did not predict response to antiviral therapy.     

Serum leptin levels in patients with nonalcoholic steatohepatitis

OBJECTIVE: Leptin is a peptide hormone that mainly regulates food intake and energy expenditure of human body. A close correlation between serum leptin levels and the percentage of body fat stores is well known. Nonalcoholic steatohepatitis (NASH) is a common disorder which causes serum liver enzyme elevation. In this study, the serum leptin levels were investigated in patients with NASH to determine a possible role in the pathogenesis and in patients with chronic viral hepatitis to ascertain the effect of hepatic inflammation on serum leptin level. METHODS: Forty-nine patients (38 men, 11 women) with NASH diagnosed by biopsy, 32 patients with biopsy-proven chronic viral hepatitis (21 men and 11 women), and 30 healthy adults (17 men, 13 women) enrolled in the study. Fasting blood samples were obtained, and serum leptin levels were measured by ELISA. Body mass index (BMI) was calculated for all subjects, and serum insulin, C-peptide, and lipoprotein levels were also detected. RESULTS: The mean serum leptin levels (+/-SEM) were 6.62 +/- 0.71, 4.24 +/- 1.0, and 4.02 +/- 0.46 ng/ml in NASH, chronic hepatitis, and the control group, respectively. Mean serum leptin level in the NASH group was significantly higher than those in the other groups tested. BMI was also slightly higher in the NASH group when compared to the other groups (26.7 +/- 0.3, 23.7 +/- 0.6, and 24.6 +/- 0.3, respectively). There was a significant correlation between BMI and serum leptin levels when all the subjects were evaluated together (NASH, hepatitis, and control groups, r = 0.337, p = 0.012) but not in the NASH group when evaluated alone (r = 0.238, p = 0.1). Of the predisposing factors for NASH, obesity was observed in 24% of patients and hyperlipidemia in 67%. Serum cholesterol and triglyceride levels were significantly higher in the NASH group than those in controls (p < 0.05). It has been detected that most of these patients consumed high amounts of fat in their dietary habits. CONCLUSIONS: The serum leptin levels were significantly higher in patients with NASH, while they were not affected by chronic hepatitis. This elevation is out of proportion to BMI of these patients and may be related to hyperlipidemia in most. Elevated serum leptin levels, therefore, may promote hepatic steatosis and steatohepatitis.     

Association between leptin, metabolic factors and liver histology in patients with chronic hepatitis C.

BACKGROUND: Steatosis is common in hepatitis C virus (HCV)-infected patients and likely accelerates fibrosis progression. Leptin, the peptide product of the obesity gene (ob), has been implicated in hepatic fibrogenesis; circulating levels of leptin correlate with body fat mass. The objective of the present study was to determine the clinical and histological correlates of serum leptin in HCV-infected patients, and to determine its utility in predicting liver histological lesions. PATIENTS AND METHODS: In 62 patients with chronic HCV, serum leptin was measured using a commercially available immunoassay. Associations between leptin, metabolic parameters, and severe hepatic fibrosis (stages 2 to 4) and steatosis (30% or greater) were determined. The utility of leptin in predicting liver histology was determined using receiver operating characteristic (ROC) curves. RESULTS: The median body mass index (BMI) was 23.2 kg/m2 (range 17.7 kg/m2 to 35.6 kg/m2); 16% of patients (n=10) had HCV genotype 3. Severe fibrosis and steatosis were present in 23% and 13% of patients, respectively. Leptin was strongly correlated with the BMI, and its levels were higher in women. BMI-corrected leptin levels were not independently associated with severe fibrosis but were significantly associated with steatosis (OR of 1.07; 95% CI 1.01 to 1.04). On it own, leptin was poorly predictive of severe steatosis (area under the ROC curve was 0.64; 95% CI 0.42 to 0.87). However, its accuracy improved with the addition of HCV genotype (area under the ROC curve was 0.86; 95% CI 0.72 to 1.00; P=0.07). CONCLUSIONS: As observed in the non-HCV setting, serum leptin correlates with BMI; higher leptin levels are found in women than men with chronic HCV. Serum leptin is a poor predictor of HCV-related fibrosis but may play a role in predicting steatosis when combined with HCV genotype.     

In overweight patients with chronic hepatitis C, circulating insulin is associated with hepatic fibrosis: implications for therapy

BACKGROUND/AIMS: Host factors such as increased body mass index (BMI) and genotype-specific viral factors contribute to the development of steatosis in patients with chronic hepatitis C (HCV). We hypothesized that host metabolic factors associated with increased BMI may play a role in disease progression. METHODS: Fasting serum was collected from 160 patients with chronic HCV at the time of liver biopsy and 45 age, gender and BMI matched controls, and assessed for levels of insulin, c-peptide and leptin. RESULTS: Patients with viral genotype 3 had more severe steatosis (P=0.0001) and developed stages 1 and 2 fibrosis at a younger age (P<0.05) than patients with genotype 1. For both genotypes, overweight patients had significantly more steatosis and increased insulin and leptin levels. In contrast to lean patients, there was a statistically significant increase in circulating insulin levels with increasing fibrosis in overweight patients with chronic HCV (P=0.03). Following multivariate analysis, insulin was independently associated with fibrosis (P=0.046) but not inflammation (P=0.83). There was no association between serum leptin levels and stage of fibrosis. CONCLUSIONS: Increasing circulating insulin levels may be a factor responsible for the association between BMI and fibrosis in patients with HCV, irrespective of viral genotype.     

Decreased plasma adiponectin concentrations are closely related to steatosis in hepatitis C virus-infected patients

OBJECTIVES: The mechanisms underlying steatosis during hepatitis C virus (HCV) infection are complex and multifactorial. Obesity is a well-recognized risk factor for the development of steatosis in chronic hepatitis C infection. The aim of our study was to investigate the role of adipocytokines in HCV-related steatosis. Therefore, we hypothesized that the endocrine function of adipose tissue could be, in part, responsible for HCV-related steatosis. Seventy-one consecutive untreated chronic hepatitis C patients were studied to assess the effects of adipocytokines, body mass index (BMI), age, and HCV genotype on steatosis. We used ELISA to determine serum adiponectin, leptin, and soluble TNF receptors I and II concentrations. RESULTS: Steatosis was observed in 42 (59.1%) patients. BMI was significantly associated with leptin (r = 0.64; P = 0.0001) and was border significantly associated with adiponectin concentrations (r = -0.22; P = 0.06). In univariate analyses, age, HCV genotype 3, BMI, increased leptin level, increased insulin level, and decreased adiponectin concentration were associated with steatosis. In multivariate analysis, steatosis was significantly associated with low adiponectin concentration, age, HCV genotype 3, and aspartate aminotransferase (ASAT) level, whereas steatosis was not associated with leptin, insulin, and BMI. CONCLUSION: In chronic HCV patients, hypoadiponectinemia is significantly associated with the development of liver steatosis. The fact that the plasma levels of adiponectin inversely correlate with steatosis in HCV-infected subjects suggests that hypoadiponectinemia may contribute to hepatic steatosis progression and liver injury in this population. One practical implication is that therapy to increase circulating adiponectin concentration, such as overweight reduction or thiazolidinediones, provides the potential to improve steatosis in chronic hepatitis C infection.     

High Ascitic Fluid Leptin Levels in Patients with Decompensated Liver Cirrhosis and Sterile Ascites: Relationship with TNF-α Levels

Leptin is an adipocyte-derived hormone involved in the homeostasis of body composition. An imbalance in leptin regulation has been observed in patients with liver cirrhosis. We aimed to assess serum and ascitic leptin levels in a group of patients with decompensated liver cirrhosis and to evaluate the relationship of these levels with tumor necrosis factor alpha (TNF-alpha). We assessed both serum and ascitic fluid leptin levels in a series of 16 consecutive patients with liver cirrhosis. We calculated the body mass index (BMI) and assessed body fat (BF) of all patients by means of bioelectric impedence analysis. Leptin levels were analyzed in relationship to biochemical indexes, TNF-alpha levels, and body composition. None of the patients had spontaneous bacterial peritonitis. Both serum and ascites leptin levels were correlated with BMI and BF. On average, ascitic fluid leptin levels (13.1 +/- 10.9 ng/ml) were twice as high as serum levels (7.0 +/- 6.4 ng/ml), and the ascitic fluid/serum ratio of leptin was > 1 in all patients. Serum and ascites leptin levels were positively correlated (rS = 0.675, P = 0.009), while no correlation was observed between leptin and TNF-alpha levels, both in serum and in ascites. Serum and ascites TNF-alpha were not correlated. The ascitic fluid leptin levels of cirrhotic patients with sterile ascites are on average two times higher than circulating levels of this hormone. Noteworthily, they correlate significantly with body composition. These findings seem to suggest that in patients with decompensated liver cirrhosis, intraabdominal production of leptin may contribute to the metabolic picture.     

Leptin levels in nonalcoholic steatohepatitis and chronic hepatitis C.

BACKGROUND/AIMS: Leptin is a peptide which regulates food intake and energy expenditure. Moreover, it is involved in the homeostasis of body composition and is linked to the regulation of insulin signaling, thus playing an important role in liver fat storage. Steatosis is a common finding in chronic hepatitis C, and both viral and metabolic factors have been suggested to explain the presence of this histological characteristic. In order to study leptin in chronic liver disease characterized by the presence of steatosis, we evaluated its serum levels in patients with nonalcoholic steatohepatitis (NASH), in chronic hepatitis C (CHC) patients with no histological findings of steatosis, and CHC patients with steatosis but no risk factors for its development. METHODOLOGY: We studied 6 male patients with NASH whose diagnosis was made on the basis of histological findings and clinical criteria. From among a cohort of 170 CHC patients we put together 2 groups of 6 male patients each (with or without steatosis at liver biopsy examination), who had no risk factors for NASH. Male patients were chosen in order to avoid gender influence on leptin levels. Further criteria for admission were similar impairment of liver metabolic function as assessed by the monoethylglycinexylidide (MEGX) test and, in patients with CHC, similar body mass index (BMI) and histological staging. Moreover, we evaluated leptin/BMI ratio, in order to rule out BMI influence on leptin levels. Leptin levels were assessed by means of radioimmunoassay. RESULTS: We found that BMI was higher in NASH compared to CHC (27.2 +/- 2.9 vs. 23.9 +/- 1.8; p = 0.01). Analysis of serum leptin levels showed an increasing trend starting from patients with CHC without steatosis (3.2 +/- 0.4 ng/ml), through CHC patients with steatosis (4.2 +/- 0.7 ng/ml) up to patients with NASH (5.7 +/- 2 ng/ml), although the differences observed were not statistically significant. Moreover, the ratio of leptin to BMI also followed the same trend showing increasing values (CHC without steatosis = 0.04 +/- 0.02; CHC patients with steatosis = 0.17 +/- 0.03; NASH = 0.203 +/- 0.07). Leptin levels and BMI showed a significant relationship (n = 18; r = 0.60; p < 0.01). CONCLUSIONS: The increasing trend observed in leptin serum levels among the different groups of patients showed that in chronic liver disease characterized by the presence of steatosis, leptin signaling is preserved. Moreover, CHC factors different from the metabolic ones should be investigated in order to explain the presence of steatosis. Further studies on broader groups of patients are needed to verify these preliminary results.     

High serum leptin is an independent risk factor for non-response patients with low viremia to antiviral treatment in chronic hepatitis C

AIM:To determine whether body weight and/or serumleptin were independent predictors of response toantiviral treatment in patients with chronic hepatitis C.METHODS:A retrospective evaluation was performedin 139 patients with chronic hepatitis C treated withinterferon(IFN)from 1996 to 2000.Sustained responsewas defined as negative by hepatitis C virus(HCV)RNAanalysis using PCR and normal transaminase at 24 wkafter cessation of IFN therapy.Patients who remainedpositive for HCV RNA at the end of IFN treatment weredefined as resistant to IFN therapy.Sex,age,body massindex(BMI)(≥25 vs<25),complication of diabetesmellitus,serum leptin level(≥8.0 μg/L vs<8.0 μg/L),and the stage of liver fibrosis by needle biopsy(F1/F2 vsF3/F4)were examined.RESULTS:Sustained response was achieved in 33patients(23.7%),while others failed to show a responseto IFN therapy.Overall,the factors associated withsustained antiviral effects were HCV-RNA load,HCVgenotype,serum leptin level,and stage of liver fibrosisevaluated by univariate analysis.BMI was not associatedwith any therapeutic effect of IFN.Multivariate analysisindicated that HCV-RNA load was a significant risk factor,but among the patients with low viremia(HCV-RNA<100 MU/L),leptin level was an independent risk factorfor IFN resistance.Namely,a high level of serum leptinattenuated the effect of IFN on both male and femalepatients with low viremia.CONCLUSION:High serum leptin level is a negative predictor of response to antiviral treatment in chronichepatitis C with low viremia.     

Lipid metabolism in children with chronic hepatitis C, A preliminary report

BACKGROUND/AIMS: The importance of lipid metabolism in the pathogenesis of chronic hepatitis C has been recognized in recent years. Bearing in mind remote sequelae of chronic hepatitis C in children, it seems reasonable to seek to determine potential risk factors for the development of cirrhosis and carcinogenesis. The aim of the study was to assess lipid metabolism in children with chronic HCV-related hepatitis. METHODOLOGY: The study comprised 16 children with chronic hepatitis C and 16 healthy controls. In all the children anthropometric data and after, overnight fasting, serum levels of total bilirubin, AST, ALT, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were investigated. In the study group biopsy specimens were assessed. RESULTS: Macrovesicular steatosis in numerous hepatocytes was found in 3 children. Total cholesterol level in children with chronic hepatitis was significantly lower than in control group (p < or = 0.05). Mean values of body mass, height, body mass index (BMI), levels of bilirubin, HDL-cholesterol, LDL-cholesterol, triglycerides and HDL/C index did not differ significantly between the two groups. No correlation between lipid parameters and histological markers, hepatic enzymes, patient age, weight, height or BMI was found. CONCLUSIONS: Neither obesity nor hyperlipidemia, which are recognized risk factors for steatosis were found in children with HCV-related hepatitis. Lower cholesterol levels in children with chronic HCV infection compared to the controls and only scarce signs of steatosis which were noted could suggest the risk, existing already in such young patients, of developing fatty liver disease with its consequences including cirrhosis and neoplastic disease.     

Evaluation of the diagnostic value of serum and tissue apoptotic cytokeratin-18 in patients with chronic hepatitis C

Background and study aimsHepatitis C virus (HCV) is considered the most common aetiology of chronic liver disease (CLD) in Egypt. The disease severity ranges from mild illness to cirrhosis and hepatocellular carcinoma. A role for apoptosis in liver damage caused by HCV chronic infection has been suggested. Cytokeratin 18 (CK-18) is the major intermediate filament protein in the liver and is a known caspase substrate in hepatocyte apoptosis. Therefore, we analysed the serum and tissue levels of CK-18 in patients with chronic HCV infection to evaluate its role in hepatocyte apoptosis. We also correlated CK-18 expression with the severity of hepatic pathology.Patients and methodsThis study examined 80 Egyptian patients with liver disease. There were 69 patients with chronic hepatitis C and 11 patients with hepatitis C-induced cirrhotic changes. Fifteen healthy controls were also included in the study. The levels of CK-18 fragment were quantified in paired serum and liver biopsy samples.ResultsThe serum and tissue CK-18 levels were reduced in chronic HCV patients compared to early cirrhosis patients. This result indicates that serum levels of CK-18 and the hepatic expression of CK-18 might play an important role in disease progression. The serum and tissue levels of CK-18 were significantly increased and directly correlated with inflammation severity, stage of fibrosis, and ALT levels in the chronic HCV group and the cirrhotic liver group. There was no significant difference in viral load between patient cohorts.ConclusionThe serum level and the hepatic expression of CK-18 are related to disease activity and are directly correlated with METAVIR scoring. This result suggests that serum CK-18 levels may be useful for monitoring disease activity in chronic HCV and liver cirrhosis patients.     

肝硬化患者血清瘦素与胰岛素抵抗的关系

目的 探讨肝硬化患者血清瘦素水平的变化情况和影响因素,及其与胰岛素抵抗的关系。方法 选择肾功能正常的43例肝硬化患者和30例与其在性别、年龄和体重指数（BMI）相匹配的时照者,应用放免法测定血清瘦素。同时测定肝肾功能、血糖、血脂、胰岛素和C-肽等指标,并测量其身高、体重,计算BMI。结果 肝硬化患者血清瘦素水平同比对照组相比差异不显著;肝硬化组与对照组血清瘦素水平女性均高于男性;肝硬化患者血清瘦素水平与BMI、胰岛素和C-肽呈正相关,与胰岛素抵抗指数呈负相关;不同肝功能分级的肝硬化患者间血清瘦素水平差异不显著。结论 肝硬化患者血清瘦素水平存在性别差异。瘦素水平不能作为评价肝硬化严重程度的指标。瘦素与肝硬化患者的胰岛素抵抗相关。     

TIPS implantation raises leptin levels in patients with liver cirrhosis.

Increased leptin levels in patients with liver cirrhosis are postulated to result in malnutrition and increased energy expenditure. Since cirrhotic patients show improved nutritional status after a transjugular intrahepatic portosystemic stent shunt (TIPS), it was the aim of this study to evaluate plasma leptin levels and their influence on nutritional status prior to and after the TIPS procedure. We evaluated plasma leptin levels, body mass index (BMI), Child-Pugh score and pertinent biochemical parameters in 31 patients (19 men and 12 women) with severe complications of liver cirrhosis (74% ethyltoxic men, 50% ethyltoxic in women), prior to and after TIPS. Nineteen cirrhotic patients without TIPS served as controls. In women ascitic-free BMI significantly increased (from 22.8 +/- 4.6 kg/m2 to 23.9 +/- 4.9; p = 0.004 three months after TIPS), whereas in men only a tendency toward higher values (26.1 +/- 4.7 vs. 26.7 +/- 4.4; p = 0.28) was found. Analysis of peripheral venous leptin concentrations before and three months after TIPS revealed a significant increase in women (11.9 +/- 8.8 ng/ml vs. 18.6 +/- 14.9; p = 0.009) and in men (7.7 +/- 6.2 ng/ml vs. 12.2 +/- 9.0; p = 0.005). In addition, the leptin-BMI ratio increase significantly in women and men three months after TIPS implantation (women 0.49 +/- 0.29 vs. 0.73 +/- 0.52; p = 0.017; men 0.28 +/- 0.22 vs. 0.43 +/- 0.28; p = 0.002). On the other hand, patients without TIPS implantation showed no significant alterations of BMI and peripheral venous leptin concentrations. After TIPS implantation in liver cirrhotic patients, leptin levels were increased and the nutritional status improved. Therefore, our analysis suggests that in patients with predominantly ethyltoxic liver cirrhosis, elevated leptin levels are not a major reason for poorer body composition.     

Leptin levels in the differential diagnosis between benign and malignant ascites

AIM： To evaluate the role of leptin levels in the differentia diagnosis of ascites.
METHODS： Ascitic leptin, TNFα and serum leptin levels were measured in 77 patients with ascites （35 with malignancies, 30 cirrhosis and 12 tuberculosis）. Control serum samples were obtained from 20 healthy subjects. Leptin and TNFα levels were measured by EUSA. Body mass index （BMI） and percentage of body fat （BFM） by skin fold measurement were calculated for all patients and control groups. Peritoneal biopsy, ascites cytology and cultures or biochemical values were used for the diagnosis of patients.
RESULTS： In patients with malignancies, the mean serum and ascites leptin levels and their ratios were significantly decreased compared to the other patient groups and controls. In tuberculosis peritonitis, ascitic fluid TNFα levels were significantly higher than malignant ascites and cirrhotic sterile ascites. BMI and BFM values did not distinguish between patients and controls. CONCLUSION： In patients with malignant ascites, levels of leptin and TNFα were significantly lower than in patients with tuberculous ascites.     

血清瘦素水平、胰岛素抵抗与慢性丙型肝炎抗病毒应答的相关性

目的探讨血清瘦素水平、胰岛素抵抗号慢性丙型肝炎抗病毒持续病毒学应答（SVR）的相关性，评价血清瘦素水平、胰岛素抵抗是否为慢性丙型肝炎抗病毒SVR的独立危险因素。方法40例慢性丙型肝炎患者，接受干扰素α-2a5MU联合利巴韦林1．0g（0．8～1．2g）抗病毒治疗24周，检测空腹血清瘦素、胰岛素、血糖、丙型肝炎病毒RNA、丙氨酸氨基转移酶、天冬氨酸氨基转移酶，计算胰岛素抵抗指数、体重指数，统计方法采用单因素相关分析和多因素逐步回归分析。结果40例丙型肝炎患者抗病毒治疗24周，随访6个月，获得SVR23例，占57．5％，部分和无病毒学应答17例，占42．5％。获得SVR的患者较未获得SVR患者有较低的血清瘦素水平，胰岛素抵抗指数和体重指数（P〈0．01）。单变量分析SVR与年龄、丙型肝炎病毒RNA含量、血清瘦素水平、胰岛素抵抗相关，与性别、血清转氨酶无相关性，多变量逐步回归分析，血清瘦素、胰岛素抵抗是慢性丙型肝炎抗病毒治疗获得持续病毒学应答的独立预测因子。结论血清瘦素水平，胰岛素抵抗与慢性丙型肝炎抗病毒SVR相关，是SVR的独立预测因子。     

Regulatory failure of serum prohepcidin levels in patients with hepatitis C

BACKGROUND/AIMS: Elevated serum ferritin and hepatic iron concentrations are frequently observed in chronic hepatitis C (CHC), which may be related to hepcidin. Because the role of hepcidin in CHC patients remains unknown, we aimed in this study to generate some information about hepcidin in CHC. METHODS: To determine whether serum hepcidin correlates with markers of iron status in patients with viral hepatitis, we measured serum prohepcidin levels in patients with hepatitis C virus (HCV) and hepatitis B virus (HBV) infection and in healthy controls. RESULTS: Serum prohepcidin and ferritin levels were negatively correlated (r=-0.182, P=0.037) in HCV patients and positively correlated in HBV patients and in healthy controls. The total iron scores in liver specimens from HCV patients were also negatively correlated (r=-0.403, P=0.013). Serum prohepcidin levels in patients with liver cirrhosis (LC) were significantly lower than in patients with chronic hepatitis (CH). In both CH and LC patients, serum prohepcidin levels were significantly lower in HCV patients than in HBV patients. CONCLUSION: Failure of homeostatic regulation of serum prohepcidin concentrations may be induced by HCV infection, resulting in elevation of serum ferritin levels, which leads to the progression of liver injury by iron overload in CHC patients.     

Mechanisms of increased insulin resistance in non-cirrhotic patients with chronic hepatitis C virus infection

Background and Aim: Evidence showing a higher prevalence of diabetes mellitus (DM) in patients with chronic hepatitis C virus (HCV) infection has been accumulating. However, the reason why chronic HCV infection promotes DM remains unknown. In the present study, the authors focused on non‐cirrhotic and non‐diabetic patients with chronic HCV infection and evaluated the factors responsible for increases in insulin resistance. Methods: Fifty‐six patients diagnosed with HCV‐related chronic liver disease were included. Biochemical information including body mass index (BMI), aspartate aminotransferase (AST), alanine aminotransferase, cholinesterase, triglyceride, total cholesterol, hemoglobin, platelet count, glycosylated hemoglobin, immunoreactive insulin (IRI), and serum levels of tumor necrosis factor (TNF)‐α and HCV‐RNA were determined using venous blood samples obtained from each patient after overnight fasting. Homeostasis model assessment of insulin resistance (HOMA‐IR), a simple and convenient measure of insulin resistance, was also calculated. The relationship between the stage of liver fibrosis and HOMA‐IR, and the clinical factors responsible for the increase in HOMA‐IR in non‐diabetic patients was investigated. Results: Homeostasis model assessment of insulin resistance and IRI levels increased parallel with the progression of fibrosis. Among the non‐diabetic patients with mild to moderate liver fibrosis, BMI, serum levels of AST and TNF‐α were related with HOMA‐IR (BMI: r = 0.395, P = 0.041; AST: r = 0.465, P = 0.014; TNF‐α: r = 0.396, P = 0.040). In contrast, HOMA‐IR related to TNF‐α (r = 0.526, P = 0.013) in non‐diabetic patients with advanced liver fibrosis. Conclusion: Collectively, hepatic fibrosis and inflammation appear to play key roles in the increase in insulin resistance in patients with chronic HCV infection.     

男性乙型肝炎肝硬化患者血清瘦素及血脂水平的研究

目的检测男性乙型肝炎肝硬化患者血清瘦素及血脂水平，探讨其异常变化的临床意义。方法男性乙型肝炎肝硬化患者64例，男性健康受试者28名，用ELISA法检测血清瘦素水平，用全自动生化分析仪检测肝功能和血脂。对血清瘦素、血脂与肝功能的关系进行分析。结果各组乙型肝炎肝硬化Child-Pugh分级患者与对照组比，血清瘦素水平无显著性差异（P〉0．05）；与正常对照组比，乙型肝炎肝硬化患者血CHO和LDL水平显著降低（P〈0．01），按Child分级由A到C级各组CHO和LDL水平逐渐降低，差异有显著性（P〈0．01）。无腹水肝硬化患者血清瘦素水平与BMI及Fat％均呈显著正相关。结论血清瘦素水平不能作为评价男性乙型肝炎肝硬化患者病情严重程度的指标，血清胆固醇、低密度脂蛋白是肝功能减退的指标。瘦素可能参与了男性乙型肝炎肝硬化患者的营养不良。