肝硬化患者血清瘦素水平测定及其临床意义的探讨

为了解肝硬化患者血清，腹水中瘦素水平情况，探讨其可能的临床意义。选择肝硬化组，对照组各21例，分别测定受试者的血脂，肝功，血糖，胰岛素，血清纱及部分腹水瘦素水平，测量其身高，体重，计算体重拽数，体脂肪含量。瘦素，胰岛素分别采酶联免疫吸附试验，放射性免疫试验方法测定，胰岛素抵抗用HOMA模式估算。结果显示：肝硬化，对照组的血清瘦素水平差异不显著，且肝硬化组无性别差异。肝硬化患者的血清瘦素水平与体重指数（BMI），总蛋白，总胆固醇，空腹胰岛素相关，与胰岛素抵抗素（IR）无关。腹水中的瘦素水平与腹水的性质有关，渗出液高于漏出液。上述结果说明肝硬化患者血清瘦素水平表现异常，与疾病本身相关。     

非酒精性脂肪性肝病患者血清瘦素与胰岛素抵抗的关系

目的通过检测非酒精性脂肪性肝病(NAFLD)患者血清瘦素(Lp)的水平,探讨血清瘦素与胰岛素抵抗的关系。方法应用RIA检测30例NAFLD患者及30例对照者血清Lp水平,并检测空腹血糖、总胆固醇、甘油三酯、C-肽、胰岛素、体质指数等临床指标,分析Lp与胰岛素抵抗、血脂及非酒精性脂肪性肝病的关系。结果 NAFLD患者的Lp、BMI、胰岛素及胰岛素抵抗指数(HOMAIR)均显著高于对照组(P0.05)。男、女NAFLD患者Lp水平均高于男、女对照组(P0.05)。以HOMAIR为因变量,Lp、BMI、C-肽、总胆固醇及甘油三酯作为自变量,进行多元逐步回归分析,瘦素为影响IR的主要因素。结论 Lp可促进胰岛素抵抗,提示Lp与NAFLD有密切的关系。     

肝硬化患者血清脂联素与瘦素的相关性

目的测定肝硬化患者血清脂联素与瘦素的水平并探讨二者的相关性。方法测定73例肝硬化患者和30例健康对照的血清脂联素和瘦素及相关的临床生化参数,计算血清脂联素/瘦素比值。结果肝硬化患者血清脂联素、瘦素水平明显高于正常对照组(P<0.05);脂联素/瘦素比值>1;血清脂联素与瘦素水平呈正相关。血清脂联系、瘦素水平与胰岛素、胰岛素抵抗指数呈正相关,与胰岛素敏感指数呈负相关。结论肝硬化患者血清脂联素、瘦素水平和脂联素/瘦素比值明显升高,可能与肝硬化患者胰岛素抵抗有关。     

肝炎后肝硬化患者血清瘦素测定的临床意义

目的　检测肝炎肝硬化患者血清瘦素水平 ,并探讨瘦素与肝硬化患者肝功能、胰岛素抵抗及其营养参数之间的关系。方法　 2 0 0 2 - 0 3～ 2 0 0 3- 0 1河北医科大学第二医院 32例男性肝炎肝硬化患者及 14名男性健康受试者均测定空腹血糖 (FPG)、空腹胰岛素 (FINS)和瘦素 ,同时测量肝硬化患者的营养参数 ,并对肝硬化患者进行Child -pugh分级。结果　肝硬化患者血清瘦素水平显著高于正常对照组 (P <0 . 0 5 ) ;但依据Child -pugh分级后的 3组肝硬化患者间的血清瘦素水平差异无显著性 (P >0 . 0 5 ) ;血清瘦素水平与体重指数 (BMI)、三头肌皮褶厚度 (TSF)及FINS均呈显著性正相关 (r值分别为 0 . 343、0 .340和 0 . 35 2 ,P值均 <0 . 0 5 ) ,而与肌酐身高指数 (CHI)及胰岛素敏感指数 (ISI)均呈负相关 (r值分别为 - 0 .36 0和 - 0 . 4 16 ,P值均 <0 . 0 5 )。结论　肝炎肝硬化患者血清瘦素水平的改变可能与肝功能无关 ,但参与了肝硬化的营养不良和胰岛素抵抗。     

肝硬化患者血清瘦素水平变化及相关因素分析

目的 探讨瘦素在肝硬化发生、发展中的作用.方法 对44例肝硬化患者(肝硬化组)和17例健康查体者(正常对照组)进行血清瘦素、空腹血糖(FPG)、胰岛素(FINS)水平测定并分析相关因素.结果 肝硬化组血清瘦素水平显著高于对照组(P<0.01),肝功能Child-pugh B、C级者显著多于A级(P<0.05);血清瘦素水平与FINS、FPG、胰岛素敏感指数(ISI)呈显著正相关,FINS是瘦素的显著预测因子.结论 肝硬化患者瘦素水平显著升高;其可能通过胰岛素抵抗诱发肝性糖尿病.     

原发性高血压患者血清瘦素水平与血脂的相关性研究

目的探讨原发性高血压患者血清瘦素(Leptin)与血脂的相关性。方法原发性高血压患者86例,对照组87名,测定其空腹血清瘦素、血糖、胰岛素、胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A-1(ApoA-1)、载脂蛋白B(ApoB)、体重指数(BMI)、腰臂比(WHR),计算胰岛素抵抗指数(HOMA-IR),分析原发性高血压患者血清瘦素水平与血脂的关系。结果高血压组的BMI、WHR、TC、TG、LDL-C、ApoB、HOMA-IR、Leptin显著高于对照组,差异有统计学意义(P<0.05),多元逐步回归分析显示瘦素与甘油三酯(TG)正相关。结论原发性高血压患者血清瘦素水平与血脂有相关性。     

肝硬化患者肿瘤坏死因子与胰岛素抵抗的相关性

目的探讨肝硬化患者肿瘤坏死因子水平与胰岛素抵抗的关系。方法测定73例肝硬化患者及30例健康人血清肿瘤坏死因子水平及相关临床生化参数,并计算胰岛素敏感指数和体重指数。结果肝硬化组肿瘤坏死因子水平明显高于正常对照组,肿瘤坏死因子与胰岛素水平呈负相关,而与胰岛素敏感指数呈正相关。结论肝硬化患者血清肿瘤坏死因子水平明显升高,其可能作为肝功能的评价指标;肿瘤坏死因子水平与肝硬化患者胰岛素抵抗密切相关。     

慢性肝病血清瘦素水平测定

为了解慢性肝炎、脂肪肝、肝硬化患者血清瘦素水平情况，选择慢性肝炎17例，脂肪肝、肝硬化、正常对照各21例，分别测量受试者的身高、体重，计算体重指数(BMI)、体脂肪含量(％Fat)，血清瘦素水平采用酶联免疫吸附试验(BLISA)的方法测定，并进行结果分析。结果显示：肝炎组、脂肪肝组瘦素水平明显高于对照组；肝硬化组与对照组无差异，血清瘦素水平与肝功能分级无关；丙型肝炎病毒所致的肝病血清瘦素水平与对照组相比差异不显著。上述说明瘦素与多数慢性肝病有关。     

伴有代谢综合征的2型糖尿病患者血清瘦素水平及相关因素分析

选取伴有代谢综合征的2型糖尿病患者38人,正常对照组32人,测定患者身高、体重、腰围、臀围、血压、空腹血糖、空腹胰岛素、胆固醇、空腹瘦素等。结果病例组空腹瘦素HOMA-IR均显著高于对照组;在控制年龄、性别等因素后,空腹瘦素仅与BMI、HOMA-IR相关。结论伴有代谢综合征的2型糖尿病患者血清瘦素水平显著升高,瘦素水平升高与肥胖及胰岛素抵抗有关。     

妊娠中期胰岛素抵抗相关因素的研究

门诊常规测定妊娠中期妇女的身高、体重,计算体重指数(BMI);生化比色法测定妊娠中期妇女血清游离脂肪酸(FFA);化学发光法测定妊娠中期妇女血清胰岛素(Ins)、瘦素(LEP)水平.结果妊娠中期妇女出现胰岛素敏感指数(ISI)、BMI、Ins、FFA、瘦素水平的明显变化,与对照组比较,分别为P＜0.05和P＜0.01;以评价机体胰岛素敏感性的指标ISl为对象.分析发现ISl与BMI、FFA、瘦素呈显著正相关,而与基础胰岛素水平、体重也具有相关性,而与年龄、身高、血糖水平相关性不显著.结论妊娠妇女于妊娠中期即已出现IR,机体FFA、瘦素水平与IR的发生密切相关.     

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。     

Ghrelin/Leptin-imbalance in patients with primary biliary cirrhosis.

BACKGROUND: The recently discovered peptide hormone ghrelin mainly produced in gastric oxyntic cells may act as a counterpart to leptin in the regulation of food intake and fat utilization. Leptin, involved in the stimulation of proinflammatory cytokines and catabolic energy balance, is elevated in patients with liver cirrhosis. In the present study, we evaluated serum ghrelin and bound leptin levels in patients with primary biliary cirrhosis (PBC) in relation to C-peptide and glucose concentration. METHODS: In 22 female patients with PBC (Child-Pugh stage A) and in 36 female controls we measured serum ghrelin, bound leptin, and C-peptide levels using specific immunoassays. RESULTS: In comparison to controls serum bound leptin levels were significantly higher in patients with PBC ( p < 0.01) whereas serum ghrelin levels were decreased compared to the control group ( p < 0.01). In parallel, C-peptide concentrations were increased ( p < 0.01) with no significant change in circulating glucose levels. CONCLUSION: Our data confirm in PBC patients that serum bound leptin levels are increased and clearly show a parallel decrease in serum ghrelin concentrations acting as a physiological counterpart to leptin. Furthermore, we suggest that these changes are linked to the insulin resistance observed in our patients.     

Correlation of serum leptin levels with anthropometric and metabolic parameters and biochemical liver function in Chinese patients with chronic hepatitis C virus infection

AIM: To determine serum leptin levels and investigate their correlations with anthropometric and metabolic parameters and biochemical liver function in patients with chronic hepatitis C virus (HCV) infection and their potential clinical implications. METHODS: Forty-two chronic HCV-infected patients without anti-viral treatment were enrolled in this study, 30 patients had chronic hepatitis C, 10 had cirrhosis, and 2 had hepatocellular carcinoma (HCC). Thirty age- and sex-matched healthy individuals served as controls. Serum leptin levels were determined by ELISA. The biochemical liver function and serum lipids were determined at the same time. The height and body weight of patients and controls were measured, and body mass index (BMI) and body fat were calculated simultaneously. The correlations of serum leptin levels with anthropometric and metabolic parameters and biochemical liver function were assessed statistically. RESULTS: The mean of serum leptin levels in patients with chronic hepatitis C, HCV-associated cirrhosis, HCV-associated HCC and control groups was (6.13±3.94), (5.25±4.21), (4.17±0.28), and (3.59±3.44) ng/mL, respectively. The serum leptin level in patients with chronic hepatitis C was significantly higher than that in controls. The serum leptin levels between cirrhotic patients and controls and between male and female cirrhotic patients had no significant difference. Serum leptin levels were positively-correlated with body fat, BMI, and apolipoprotein B (Apo B) in patients with chronic HCV infection. The serum alanine aminotransferase (ALT) levels were closely-correlated with BMI in patients with chronic hepatitis C. CONCLUSION: HCV infection interferes with fat and lipid metabolism in patients with chronic HCV infection and leptin may play a role in hepatosteatosis.     

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.     

Gender-Specific Leptinemia and Its Relationship with Some Components of the Metabolic Syndrome in Moroccans

The levels of the liporegulatory hormone leptin are increased in obesity, which contributes to the metabolic syndrome; the latter is associated with elevated cardiovascular risk and morbidity. Leptin may play a role in the metabolic syndrome since correlations have been observed between serum leptin levels and several components of the metabolic syndrome. The association of leptinemia and hypertension or diabetes is inconsistent. Leptin levels are higher in females versus males and obese versus lean individuals. We investigated if correlations exist between leptin levels and several indices of the metabolic syndrome in obese and lean Moroccan subjects with (63 males, 129 females) and without (123 males, 234 females) diabetes and/or hypertension. Plasma glucose and insulin and systolic and diastolic blood pressures were higher in obese versus lean individuals. Obesity had no effect on lipid profile, plasma IGF-1, or C-peptide levels. Leptin levels were higher in females versus males and in obese versus lean individuals. The levels correlated significantly with body mass index. Serum leptin concentration did not correlate with either systolic or diastolic blood pressure, although there was a trend for higher blood pressure with increased leptin levels in females. There was no significant difference in leptin levels between NIDDM patients and healthy controls. However, in hypertensive patients, leptin levels were significantly higher in both lean males and females with diabetes as compared to those without diabetes. Similarly, the higher leptin levels paralleled elevated insulin levels in obese nondiabetic males and females, and in male and female diabetics with hypertension. Correlations were observed between leptin levels and C-peptide (an estimate of endogenous insulin secretion), but not with serum IGF-1. The calculated values of HOMA-IR, a marker of insulin resistance, were somewhat higher, parallel with elevated leptin levels, in obese male and female individuals compared to their lean counterparts. There was no relationship between leptin levels and serum lipids. There was a trend for increased serum uric acid levels with higherleptin concentrations. Thus, leptinemia is related to some components of metabolic syndrome, and in turn, it may contribute to the syndrome. This study is novel in that relationships were determined between leptin levels and various indices of metabolic syndrome in a large population of the same ethnic/regional background.     

Gender-specific leptinemia and its relationship with some components of the metabolic syndrome in Moroccans

The levels of the liporegulatory hormone leptin are increased in obesity, which contributes to the metabolic syndrome; the latter is associated with elevated cardiovascular risk and morbidity. Leptin may play a role in the metabolic syndrome since correlations have been observed between serum leptin levels and several components of the metabolic syndrome. The association of leptinemia and hypertension or diabetes is inconsistent. Leptin levels are higher in females versus males and obese versus lean individuals. We investigated if correlations exist between leptin levels and several indices of the metabolic syndrome in obese and lean Moroccan subjects with (63 males, 129 females) and without (123 males, 234 females) diabetes and/or hypertension. Plasma glucose and insulin and systolic and diastolic blood pressures were higher in obese versus lean individuals. Obesity had no effect on lipid profile, plasma IGF-1, or C-peptide levels. Leptin levels were higher in females versus males and in obese versus lean individuals. The levels correlated significantly with body mass index. Serum leptin concentration did not correlate with either systolic or diastolic blood pressure, although there was a trend for higher blood pressure with increased leptin levels in females. There was no significant difference in leptin levels between NIDDM patients and healthy controls. However, in hypertensive patients, leptin levels were significantly higher in both lean males and females with diabetes as compared to those without diabetes. Similarly, the higher leptin levels paralleled elevated insulin levels in obese nondiabetic males and females, and in male and female diabetics with hypertension. Correlations were observed between leptin levels and C-peptide (an estimate of endogenous insulin secretion), but not with serum IGF-1. The calculated values of HOMA-IR, a marker of insulin resistance, were somewhat higher, parallel with elevated leptin levels, in obese male and female individuals compared to their lean counterparts. There was no relationship between leptin levels and serum lipids. There was a trend for increased serum uric acid levels with higher leptin concentrations. Thus, leptinemia is related to some components of metabolic syndrome, and in turn, it may contribute to the syndrome. This study is novel in that relationships were determined between leptin levels and various indices of metaboli syndrome in a large population of the same ethnic/regional background.     

Severe hypoleptinaemia associated with insulin resistance in patients with common variable immunodeficiency

Objective Common variable immunodeficiency (CVI) is a primary immunodeficiency syndrome characterized by impaired production of antibodies and recurrent infections. Delay in diagnosis leads to metabolic wastage and low body weight. Leptin, a hormone produced by white adipose tissue, modulates insulin action by signal transduction cross‐talk and by direct action on pancreatic beta‐cells. We hypothesized that patients with CVI might present a defective regulation of leptin production and insulin resistance. Patients Thirteen CVI patients (39 ± 11 years) under gammaglobulin replacement were evaluated in parallel with 13 gender‐, age‐, body weight‐ and body mass index (BMI)‐matched healthy voluntaries, and with data from two large population series, the Bruneck and the Hoorn Studies. Measurements Serum leptin and insulin levels, homeostasis model assessment – insulin resistance (HOMA‐IR), body composition, haematological, biochemical and immunoglobulin measurements were obtained. Data were analysed by a one‐way analysis of variance (anova ) and by Pearson's rank analysis. The institutional ethics committee approved the study, and informed consent was obtained from patients and controls. Results No differences were found between CVI and the control group when comparing gender distribution, age, body weight, BMI, waist/hip ratio, relative body fat and fasting glucose levels. Leptin levels were lower (P < 0·05) in CVI patients than in controls and lower than fasting leptin levels detected in a large population study. CVI patients’ serum leptin levels did not correlate with BMI (r = 0·074, P = 0·8) and their high HOMA‐IR indicated insulin resistance. Conclusions CVI patients are relatively hypoleptinaemic and insulin resistant, and their serum leptin levels are not correlated to their BMI.     

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.