TNF-α和IL-6在非酒精性脂肪性肝病患者血清中的水平及意义

目的:探讨肿瘤坏死因子-α(TNF-α)和白介素-6(IL-6)在非酒精性脂肪性肝病(NAFLD)患者血清中的水平及意义.方法:收集NAFLD组患者57例[包括单纯性脂肪肝21例、非酒精性脂肪性肝炎(NASH)29例肝硬化7例和正常对照组22例.采用ELISA法检测受试者血清TNF-α仅和IL-6水平.同时检查受试者体质量指数、血压、空腹血糖、空腹胰岛素、血脂,用以计算胰岛素抵抗指数(HOMA-IR)和了解合并代谢综合征情况.比较各组间血清TNF-α和IL-6水平的变化,并分析TNF-α、IL-6水平与胰岛素抵抗指数和代谢综合征发生的关系.结果:单纯性脂肪肝、NASH和肝硬化组患者血清TNF-α、IL-6水平均显著高于对照组(P<0.05),其中以NASH组水平最高,且显著高于单纯性脂肪肝和肝硬化组(P<0.05).受试者血清TNF-α、IL-6水平与HOMA-IR均呈显著性正相关(r=608,0.709,均P=0.000).合并代谢综合征的NAFLD患者血清TNF-α、IL-6水平均显著高于不合并代谢综合征的患者(P<0.05).患者血清TNF-α、IL-6水平与是否合并代谢综合征呈显著性相关(r=0.409,P=0.002;r=0.552,P:0.000).结论:TNF-α、IL-6通过诱导胰岛素抵抗对NAFLD疾病的发生发展起重要作用,并有助于NAFLD患者代谢综合征的形成.     

恶性消化道肿瘤晚期患者血TNF-α与胰岛素抵抗和胰岛素分泌的功能关系

目的:证明恶性消化道肿瘤晚期患者血浆肿瘤坏死因子α(TNF-α)与胰岛素抵抗和胰岛素分泌功能相关性,阐明恶性消化道肿瘤晚期患者糖代谢障碍机制.方法:测定40例恶性消化道肿瘤晚期患者和40例正常人员血浆TNF-α和空腹血糖、胰岛素、乳酸含量,并计算稳态模式评估法胰岛素抵抗指数(HOMA-IR)和胰岛素分泌指数(HOMA-β).结果:恶性消化道肿瘤晚期患者血浆TNFα、空腹血糖、空腹胰岛素、空腹乳酸、HOMA-IR和HOMA-β均明显高于正常对照组(3.27±0.92vs1.23±0.36,P＜0.01;5.19±0.75vs4.05±0.28,P＜0.01;14.24±6.52vs8.27±4.84,P＜0.01;7.11±0.69vs3.27±0.41,P＜0.01;3.48±0.85vs1.55±0.77,P＜0.01;181±39vs326±47,P＜0.01),但空腹血糖仍在正常参考范围内.恶性消化道肿瘤晚期患者血TNFα与空腹血糖、空腹胰岛素、空腹乳酸明显正相关(r=0.4352,P＜0.05;r=0.3136,P＜0.05;r=0.7893,P＜0.01),与HOMA-IR明显正相关(r=0.6531,P＜0.01),与HOMA-β明显负相关(r=-0.5874,P＜0.01).结论:恶性消化道肿瘤晚期患者血浆TNFα在胰岛素抵抗和胰岛素分泌功能下降及糖代谢障碍中发挥重要作用.     

肝硬化患者血清肝纤维化指标与糖代谢异常的关系

目的探讨肝硬化患者血清肝纤维化指标与糖代谢异常的关系。方法将91例肝硬化患者按口服葡萄糖耐量试验(OGTT)分为糖代谢正常组和异常组;用放射免疫法测定血浆胰岛素以及血清透明质酸()HA)、层黏蛋白(LN)、Ⅳ型胶原(4C)、Ⅲ型胶原氨端肽(PCⅢ);同步检测肝功能、凝血酶原活动度(PTA);计算胰岛素敏感性指数(ISI)。结果糖代谢异常组空腹及糖负荷后0.5～2h血糖明显升高(P值均<0.05),空腹及糖负荷后2～3h胰岛素显著增高(P<0.05);肝硬化糖代谢异常组肝纤维化四项指标升高均较糖代谢正常组更为明显,其中HA及PCⅢ水平两组的差异有统计学意义(均P<0.05);两组患者肝功能指标及ISI均有明显差异(P<0.05),肝硬化糖代谢异常组肝功能降低,组织胰岛素敏感性下降。结论肝硬化患者反复肝炎活动,肝功能进行性损害,可促进肝纤维化的进展,并导致糖代谢异常和胰岛素抵抗。     

胰岛素泵皮下输注治疗初诊T2DM患者的临床疗效及对IL-6和TNF-α的影响

目的探讨胰岛素泵皮下输注治疗初诊T2DM患者的临床疗效及对白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的影响。方法选取138例新诊断的2型糖尿病患者为研究对象,随机分成胰岛素泵组(A组)69例和多次皮下输注组(B组)69例,两组患者均治疗14 d。观察比较两组患者治疗前后IL-6、TNF-α水平的变化及空腹、餐后2 h、睡前的血糖水平,血糖达标所需时间(T)、胰岛素用量(ID)、低血糖发生率(HGR)、胰岛素抵抗指数(HOMA-IR)及胰岛素分泌指数(HOME-β)的变化。结果治疗后,两组患者餐后2h的血糖水平均得到良好控制,A组控制效果明显优于B组,差异有统计学意义(P0.05);两组患者IL-6、TNF-α水平和HOMA-IR均显著低于治疗前,HOME-β高于治疗前,差异具有统计学意义(P0.05);A组患者的血糖达标时间、胰岛素用量以及低血糖发生率均低于B组,治疗费用则高于B组,差异具有统计学意义(P0.05)。结论与多次皮下输注治疗比较,胰岛素泵皮下输注治疗可以明显地改善初诊2型糖尿病患者的β细胞功能,减轻胰岛素抵抗和降低炎症因子的水平,临床治疗效果更好。     

初诊糖尿病患者白介素-1β与胰岛素抵抗的关系探讨

目的探讨初诊糖尿病患者胰岛分泌功能及白介素-1β(IL-1β)变化与胰岛素抵抗的关系。方法选择初诊糖尿病患者80例(糖尿病组)和健康体检者50例(对照组),检测其IL-1β、空腹血糖(FBG)等指标并同期进行OGTT试验,以胰岛素抵抗指数(HOMA-IR)评价胰岛素抵抗程度。结果两组间HbA1C、FBG、TG、IL-1β、HOMA-IR比较有统计学差异(P均<0.01)。与对照组相比,糖尿病组空腹胰岛素(FIns)水平偏高,分泌峰下降延迟,峰值倍数偏低(P均<0.01)。相关分析显示,IL-1β与HOMA-IR、HbA1C、FBG、FIns呈正相关(r分别为0.314、0.347、0.241、0.237,P均<0.05),与峰值倍数呈负相关(r=-0.253,P<0.05)。IL-1β、HOMA-IR是糖尿病的独立危险因素。结论 IL-1β是初诊糖尿病患者的独立危险因素,IL-1β与胰岛β细胞分泌功能减退密切相关。     

新诊断2型糖尿病患者葡萄糖耐量试验与糖化血红蛋白水平的相关分析

目的 对比分析新诊断2型糖尿病及糖尿病前期患者口服葡萄糖耐量试验(OGTT)与糖化血红蛋白(HbAIc)水平变化的特点及影响因素. 方法 按照OGTT结果将受检者分为糖耐量正常组(正常组):31例,年龄29～75岁,平均(48.4±15.3)岁;空腹血糖受损组(血糖受损组):33例.年龄38～72岁,平均(50.8±9.8)岁;糖耐量受损组:34例,年龄33～74岁,平均(54.5±11.4)岁;2型糖尿病组(T2DM组):117例,年龄29～75岁,平均(54.3±14.1)岁.采用OGTT试验、HbAlc结果评价糖代谢状态,胰岛β细胞功能指数(HOMA-E)、OGTT 30 min胰岛素分泌增值与血糖增值比值(△I30/△G330)、胰岛素分泌曲线下面积(AUCINS)及胰岛素抵抗指数(HOMA-IR)分别反映胰岛β细胞分泌功能和胰岛素抵抗情况. 结果 (1)T2DM、糖耐量受损组和正常组HbAlc分别为7.41%、5.85%和5.21%,差异有统计学意义(P<0.01),T2DM、糖耐量受损组和血糖受损组HOMA-β指数与正常组比较,分别下降了53.1%(P<0.01)、29.3%(P<0.01)和23.4%(P<0.05),T2DM组HOMA-IR分别是正常组的1.66倍(P<0.01)、血糖受损组的1.29倍(P<0.001)和糖耐量受损组的1.44倍(P<0.05);(2)HbAIc与糖负荷后3 h血糖水平相关性最高(r=0.71,P<0.01),且独立相关;△I30/△G330与糖负荷后1 h和2 h血糖水平独立负相关(P<0.01);AUCINS只与糖负荷后3 h血糖水平独立负相关(P<0.01);HOMA-β与2 h以外的其他各点血糖独立负相关(P<0.01);HOMA-IR与OGTT各点血糖水平均呈正相关(P<0.01或P<0.05);三酰甘油与空腹血糖独立正相关(P<0.05),腰围与1/2 h血糖独立正相关(P<0.01).OGTT试验血糖水平变化的独立相关因素依次为△I30/△G330、AUCINS、HOMA-β、HOMA-IR和腰围.HbAlc水平的独立相关因素是OGTT 3 h血糖变化. 结论 在2型糖尿病、糖耐量低减及正常等不同糖代谢状态人群中,HbAlc水平存在差异,当HbAlc>8.0%时,OGTT试验、血糖、胰岛素水平或曲线下面积均不能反映出病情差别和变化的显著性.     

乙型肝炎肝硬化合并糖尿病的临床特点

目的研究乙型肝炎肝硬化合并糖尿病不同于2型糖尿病的临床特点。方法分别对乙型肝炎肝硬化合并糖尿病(肝糖组)112例和2型糖尿病(糖尿病组)106例患者进行口服葡萄糖耐量试验(OGTT)、胰岛素释放试验(IRT)、C肽释放试验(CRT),同时检测胰高血糖素(Glu),并分别计算胰岛素抵抗指数HOMA-IR、β细胞功能指数(HOMA-β,MBCI)等,分析比较两组之间的差异。结果在OGTT各时间点(0、30、60、120、180 min),肝糖组的血糖均显著低于糖尿病组(P<0.001)。两组空腹时胰岛素含量无明显差异,而肝糖组在餐后30、60、120、180 min的胰岛素含量均显著高于糖尿病组(P<0.001)。在餐后60、120、180 min,肝糖组C肽值明显高于糖尿病组(P<0.01、P<0.01和P<0.05)。与糖尿病组相比,肝糖组的Glu水平明显升高(P<0.05),异常升高人数显著增多(P<0.001)。两组间发生血糖低于正常情况有明显差异(P<0.01)。肝糖组的HOMA-IR指数较糖尿病组显著低下(P<0.01)。结论乙型肝炎肝硬化合并糖尿病具有与2型糖尿病不同的疾病特点。胰岛素抵抗和Glu异常升高可能是造成肝硬化患者发生糖代谢异常的重要原因之一。     

HBeAg阴性慢性乙型肝炎患者胰岛素抵抗指数与Fibroscan弹性值的相关性

目的探讨HBeAg阴性乙型肝炎后肝硬化患者胰岛素抵抗指数与Fibroscan弹性值相关性及临床意义。方法我院131例慢性乙型肝炎患者分为慢性乙型肝炎组、乙型肝炎肝硬化组,分别测定患者Fibroscan弹性值(LSM)与胰岛素抵抗指数(HOMA-IR)等并对比分析。结果 HBeAg阴性乙型肝炎肝硬化组患者TBIL、HA、LN、IV-C、PC-III、FPG、FINS、HOMA-IR、LSM均显著高于慢性乙型肝炎组,(P0.01或0.05),IAI显著低于慢性乙型肝炎组组患者(P0.05)。Child-Pugh B/C组FINS、HOMA-IR、LSM均显著高于Child-Pugh A组(P0.01),IAI显著低于Child-Pugh A组患者(P0.01)。HOMA-IR与LSM值呈正相关,IAI与LSM值呈负相关性。结论有机结合Fibroscan、HOMA-IR和IAI检测,进行肝硬度和胰岛素抵抗的定量研究,更精确评估HBeAg阴性慢性乙型肝炎肝病进程,进而指导临床以取得较好的治疗效果。     

酒精性肝硬化患者糖脂代谢与肝功能Child-Pugh分级关系的研究

目的分析酒精性肝硬化患者的糖脂代谢与肝功能Child-Pugh分级的关系。方法 49例酒精性肝硬化患者作为试验组,根据肝功能Child-Pugh分级将其分为A级组、B级组和C级组,另选25例无肝脏病史、无糖脂代谢异常的健康男性作为对照组,对比分析各组间糖脂代谢指标的差异。结果试验组空腹血糖、餐后2h血糖、餐后2h胰岛素、胰岛素释放指数、糖化血红蛋白显著高于对照组,胰岛素敏感指数显著低于对照组(P均0.05),A组、B组和C组间空腹血糖、空腹胰岛素、餐后2h血糖、餐后2h胰岛素、胰岛素释放指数、胰岛素敏感指数和糖化血红蛋白组间存在差异(P均0.05)。试验组低密度脂蛋白胆固醇较对照组低(P0.05),A组、B组和C组间总胆固醇和低密度脂蛋白胆固醇存在差异(P均0.05)。结论酒精性肝硬化患者存在糖脂代谢异常,随着肝功能Child-Pugh分级增高而更加突出。     

乙型肝炎病毒相关的肝源性糖尿病糖代谢异常的临床分析

目的 探讨HBV相关的肝源性糖尿病糖代谢的临床特点及其发生机制.方法 患者分为2型糖尿病组、慢性乙型肝炎合并肝源性糖尿病组(简称慢肝组)及乙型肝炎肝硬化合并肝源性糖尿病组(简称肝硬化组),所有研究对象均行口服葡萄糖耐量试验(OGTT)联合胰岛素、C肽释放试验,并测定糖化血红蛋白(HbAlc)水平.结果 肝硬化组空腹血糖、30min、60min血糖分别为(6.98±2.75)mmol/L、(11.93±2.98)mmol/L、(15.37±3.67)mmol/L,均明显低于慢肝组、糖尿病组(P＜0.01),后两组间差异无统计学意义;肝硬化组120min血糖低于糖尿病组(P＜0.01).各时间点三组之间C-肽水平差异无统计学意义,峰值出现的时间基本一致(120min),均呈低峰延迟曲线.各时间点肝硬化组和慢肝组胰岛素水平的对数值均与糖尿病组存在统计学差异(P＜0.01),前两组水平高于糖尿病组,但两组间差异无统计学意义.峰值出现的时间基本一致(120min).三组之间HbAlc差异有统计学意义(P＜0.05),肝硬化组最低,糖尿病组最高.结论 HBV相关的肝硬化患者推荐行OGTT作为糖尿病筛查指标.     

Degradation and secretion of insulin in hepatic cirrhosis.

To clarify the mechanism of hyperinsulinism of hepatic cirrhosis, plasma insulin and C-peptide levels before and after oral glucose loads were measured in 34 patients with cirrhosis, 15 patients with chronic hepatitis, and 25 normal subjects. While plasma immunoreactive insulin (IRI) levels during oral glucose tolerance testing (OGTT) were significantly increased in cirrhotics, plasma immunoreactive C-peptide (CPR) levels were elevated slightly. The C-peptide to insulin ratio throughout OGTT was significantly smaller in cirrhotics than in normal subjects (P less than 0.01). A decreased hepatic insulin degradation rate has been suggested to one of the main causes of hyperinsulinism in hepatic cirrhosis. The ratio of the difference between basal and 30-min CPR values and basal and 30-min OGTT blood glucose values [delta CPR: delta BS(30)'] as well as the delta IRI: delta BS(30') ratio was significantly decreased in cirrhotics (P less than 0.01). These results indicate that insulin secretion in response to a glycemic stimulus is reduced in cirrhotics. Both the ratios of the sums of six IRS and CPR values of OGTT (sigma CPR: sigma IRI) and delta CPR: delta BS(30') and sigma CPR: sigma BS(30') were found in inverse relationship with indocyanine green retention rate in cirrhotics.     

Chronic hepatitis C virus infection without cirrhosis induces insulin resistance in patients with alpha-thalassaemia major.

AIM: The aim of this study was to investigate the cause of increased incidence of impaired glucose tolerance and diabetes mellitus in patients with alpha-thalassaemia major and chronic hepatitis C virus (HCV) infection without cirrhosis of the liver. PATIENTS AND METHODS: The study included 28 alpha-thalassaemic multi-transfused patients (14 females and 14 males; age, 25.7 +/- 6.3 years) with normal fasting glucose levels. Sixteen were seropositive for HCV and they had biopsy proven chronic hepatitis C without cirrhosis. An oral glucose tolerance test (OGTT) was performed. Glucose, insulin and C-peptide levels were measured every 30 min for 2 h. Fasting insulin resistance index (FIRI) was calculated according to the formula: FIRI = (fasting glucose x fasting insulin)/25. RESULTS: All patients had a normal OGTT except for two HCV positive and two HCV negative patients who had impaired glucose tolerance. HCV positive patients had higher fasting insulin levels (P = 0.02), higher fasting insulin/fasting glucose ratio (P = 0.017) and higher FIRI (P = 0.016) than HCV negative patients. During the OGTT, peak insulin levels occurred at 30 min in HCV negative patients but at 60 min in HCV positive. HCV infected patients had higher mean value of insulin at 60 (P = 0.017), 90 (P = 0.04), and 120 min (P = 0.04), and higher mean increment above basal at 60 (P = 0.015), 90 (P = 0.018) and 120 min (P = 0.05). The area under the curve (AUC) of insulin was also greater in HCV positive patients as compared to HCV negative (P = 0.04), although the AUC of glucose and the glucose levels at all time points of the OGTT were similar in both groups. CONCLUSIONS: The findings of this study show that alpha-thalassaemic patients with HCV infection without liver cirrhosis are more insulin resistant and have delayed insulin secretion compared to HCV negative alpha-thalassaemic patients. These changes in insulin action and secretion are evident before the development of impaired glucose tolerance and may explain the higher prevalence of diabetes mellitus in this group.     

Insulin,C-peptide and glucagon levels during ogtt in hepatic cirrhosis and in patients with prehepatic block

Summary In order to investigate pancreatic B-cell function in hepatic cirrhosis and to elucidate the role of porto-caval shunt-circulation in the development of hyperinsulinism and hyperglucagonemia in cirrhotic patients, blood glucose, plasma insulin and glucagon, and serum C-peptide concentrations were measured during OGTT in 11 control and 16 cirrhotic subjects as well as in 7 patients with prehepatic block secondary to thrombosis of the portal vein. Insulin and glucagon levels were significantly higher in the cirrhotic than in the control group (for insulin: p<0.01, <0.001, <0.01 and <0.05 at 0, 60, 90 and 120 min, respectively; for glucagon: p<0.01, <0.01, and <0.05 at 0, 30 and 60 min, respectively). Serum C-peptide levels were, however, similar in the two groups with the exception of the 30-min value, which was significantly lower in the cirrhotic group (p<0.05). Plasma insulin and glucagon concentrations in patients with prehepatic block were similar to those of the controls but significantly lower than the values found in cirrhotic patients (for insulin: p<0.05 and <0.01 at 30 and 60 min, respectively; for glucagon: p<0.01, <0.01 and <0.05 at 0, 30, 60 min, respectively). Serum C-peptide levels of these patients were not significantly different either from the control values or from those obtained in the cirrhotic group. Accordingly, pancreatic B-cell secretion is not increased in hepatic cirrhosis. Hence, the hyperinsulinism is due to decreased hepatic degradation of the hormone. Decreased degradation of both insulin and glucagon should be attributed mainly to parenchymal liver damage, rather than porto-systemic shunting.     

炎性因子和胰岛素抵抗指数与脑卒中合并H型高血压患者的关系研究

背景近年来我国脑卒中合并H型高血压临床发病率不断升高,而有研究表明炎性反应和胰岛素抵抗可影响脑卒中疾病进程。目的探讨炎性因子和胰岛素抵抗指数(HOMA-IR)与脑卒中合并H型高血压患者的关系。方法选取2016年1月-2019年11月中国人民解放军海军安庆医院心内科及神经内科诊治的脑卒中患者136例,根据同型半胱氨酸和血压,单纯性脑卒中患者33例作为A组,单纯性高血压患者38例作为B组,单纯性高同型半胱氨酸患者23例作为C组,H型高血压患者42例作为D组。比较四组患者一般资料、同型半胱氨酸、空腹血糖(FPG)、空腹胰岛素(FINS)、HOMA-IR及炎性因子〔包括肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β)和超敏C反应蛋白(hs-CRP)〕;脑卒中合并H型高血压患者炎性因子与HOMA-IR相关性分析采用Pearson相关分析及多因素线性回归分析。采用受试者工作特征曲线(ROC曲线)评价炎性因子、HOMA-IR对脑卒中合并H型高血压患者的诊断价值。结果C组、D组患者同型半胱氨酸高于A组、B组(P<0.05),B组、D组患者收缩压、舒张压高于A组、C组(P<0.05)。B组、C组、D组患者FPG、FINS和HOMA-IR高于A组(P<0.05),D组患者FPG、FINS和HOMA-IR高于B组、C组(P<0.05)。B组、C组、D组患者TNF-α、IL-1β、hs-CRP水平高于A组(P<0.05),D组患者TNF-α、IL-1β、hs-CRP水平高于B组、C组(P<0.05)。Pearson相关分析结果显示,脑卒中合并H型高血压患者TNF-α、hs-CRP与HOMA-IR均呈正相关(r值分别为0.329、0.296,P值分别为<0.001、0.001);多因素线性回归分析结果显示,TNF-α(β=0.614)、hs-CRP(β=0.983)是脑卒中合并H型高血压患者HOMA-IR的独立影响因素(P<0.05)。ROC曲线分析显示,TNF-α、IL-1β、hs-CRP和HOMA-IR对脑卒中合并H型高血压患者诊断价值的ROC曲线下面积分别为0.700〔95%CI(0.601,0.799)〕、0.967〔95%CI(0.936,0.998)〕、0.983〔95%CI(0.964,1.000)〕和0.989〔95%CI(0.977,1.000)〕,最佳临界值分别为18.1 ng/L、15.4μg/L、11.4 mg/L和2.49。结论脑卒中合并H型高血压患者TNF-α、IL-1β、hs-CRP及HOMA-IR较高,其对脑卒中合并H型高血压有一定诊断价值,且TNF-α、hs-CRP与HOMA-IR呈正相关。     

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。     

无创心脏血流动力检测对乙型肝炎肝硬化预后的评价价值

目的无创血流动力检测法研究不同阶段乙型肝炎肝硬化患者心脏血流动力学变化,探讨心脏泵功能与肝硬化预后的关系。方法 20例慢性乙型肝炎患者作为对照,以45例乙型肝炎肝硬化患者为研究对象,根据Child-Pugh分级分为A级组(12例)、B级组(17例)和C级组(16例),根据食管静脉曲张程度分为轻度组(10例)、中度组(17例)和重度组(18例),根据病毒载量分为高病毒载量组(105拷贝/ml)(19例)和低病毒载量组(≤105拷贝/ml)(26例),采用无创血流动力检测仪测定心脏血流动力学参数。结果随着肝功能恶化,平均动脉压(MAP)、每搏出量(SV)、每搏指数(SI)、心输出量(CO)、心脏指数(CI)、左心作功(LCW)和左心作功指数(LCWI)呈降低趋势,其中C级组明显低于A级组(P<0.05)。随着食管静脉曲张程度的加重,MAP、SV、SI、CO、CI、LCW和LCWI呈降低趋势,其中重度组明显低于轻度组(P<0.05)。不同病毒载量组间MAP、SV、SI、CO、CI、LCW和LCWI差异无统计学意义(P>0.05)。结论心脏血流动力学参数可有效判断乙型肝炎肝硬化病变进展程度,心脏泵功能随肝硬化Child-Pugh分级升高及食管静脉曲张程度加重呈进行性减退。     

Pancreatic beta-cell function in cirrhotic patients with and without overt diabetes. C-peptide response to glucagon and to meal

To study the role of pancreatic beta-cell function in glucose intolerance and frank diabetes that sometimes develops in cirrhosis, the C-peptide response to a bolus IV injection of 1 mg of glucagon was measured in nine controls and in two groups of patients with cirrhosis. The first group comprised nine subjects with normal or high-normal fasting plasma glucose and no glycosuria; five of them had impaired glucose tolerance. The second group consisted of eight cirrhotics in whom frank diabetes had developed six to 48 months after the diagnosis of cirrhosis. They were characterized by fasting plasma glucose greater than 140 mg/dL and permanent glycosuria. No differences in the degree of liver impairment or portal-systemic shunting were observed between the two groups. Plasma glucose response to glucagon was similarly reduced in cirrhotic subjects. Basal C-peptide was high normal in patients with cirrhosis, and significantly increased in nondiabetic subjects. By contrast peak C-peptide levels and total C-peptide responses to glucagon were low normal in cirrhotics and significantly reduced in patients with cirrhosis and diabetes. In 14 patients the C-peptide response to a standard meal was also measured. It was significantly reduced in patients with cirrhosis and diabetes (six cases), as compared to cirrhotic subjects without diabetes. Peak C-peptide after IV glucagon significantly correlated with peak C-peptide after the meal (r = .927), or total C-peptide response to meal (r = .871). Impaired insulin secretion may add to insulin resistance in patients with liver cirrhosis, leading to the development of frank diabetes, characterized by fasting hyperglycemia and glycosuria.     

Association of nonalcoholic fatty liver disease with abnormal aminotransferase and postprandial hyperglycemia

GOALS: This study was conducted to explore the association between nonalcoholic fatty liver disease and glucose metabolism as well as insulin resistance using the homeostasis model assessment method (HOMA). STUDY: From July 2003 to June 2004, 23 patients with ultrasound-proved fatty liver and either normal (10 patients) or abnormal (13 patients) serum aminotransferase levels were enrolled. Blood tests included a routine biochemistry, a 75-g glucose oral glucose tolerance test (OGTT) with blood sampled at 30-minute intervals during a 120-minute period. Fasting and 120-minute serum leptin, insulin, and C-peptide concentrations were also measured. RESULTS: Using the Mann-Whitney U test, significant differences were found in gamma glutamyl transpeptidase (28.6+/-7.9 vs. 65.1+/-65.9 U/L, P=0.008), fasting insulin (FI) (13.11+/-7.53 vs. 31.76+/-42.95 muU/mL, P=0.02), fasting C-peptide (3.82+/-3.00 vs. 2.17+/-0.43 ng/mL, P=0.01), fasting leptin (10.34+/-4.05 vs. 24.27+/-24.97 ng/mL, P=0.01), HOMA-IR (3.34+/-1.06 vs. 8.81+/-13.18, P=0.02), and HOMA beta-cell function (120.32+/-52.50 vs. 242.20+/-247.29, P=0.02) between normal and abnormal ALT/AST function groups. From the 75-g OGTT, no significant difference of plasma glucose was noted at 0, 30, 60, and 90 minutes but significant change was noted in 120-minute plasma glucose (99.3+/-21.5 vs. 131.4+/-27.3 mg/dL, P=0.004) of 2 groups. CONCLUSIONS: In conclusion, patients with fatty liver proved by ultrasound sonography might be at high risk of developing type 2 diabetes, especially when they had elevated liver enzymes. OGTT is warranted for the early diagnosis of these high risk patients.