复发性流产伴胰岛素抵抗患者的中医体质分析

目的探讨复发性流产伴胰岛素抵抗患者的中医体质分布特征,了解此类患者血清SHBG、PAI-1水平,并探讨其与中医体质的关联性。方法采用横断面问卷调查形式,选择复发性流产伴胰岛素抵抗患者92例(观察组)和复发性流产不伴胰岛素抵抗患者92例(对照组),比较两组中医体质及血清SHBG及PAI-1水平进行统计分析。结果观察组中医体质类型以阳虚质(27.01%)、气郁质(13.79%)、痰湿质(12.07%)为主,对照组以阳虚质(34.67%)、气郁质(13.33%)、阴虚质(11.33%)为主,两组痰湿质差异有统计学意义(P<0.05)。观察组中血清SHBG的表达水平为(9.692.78)nmol/ml,对照组中血清SHBG的表达水平为(11.09±2.56)nmol/ml,观察组中血清SHBG表达水平低于对照组,差异具有统计学意义(P<0.05)。观察组中血清PAI-1的表达水平为(11,056.1±1631.8)pg/ml,对照组中血清PAI-1的表达水平为(10,302.7±1688.8)pg/ml,观察组中血清PAI-1的表达高于对照组,差异有统计学意义(P<0.05)。复发性流产伴胰岛素抵抗患者不同的中医体质类型中阳虚质的SHBG表达水平为(9.51±3.14)nmol/ml,气郁质SHBG表达水平为(9.96±2.94)nmol/ml,痰湿质SHBG表达水平为(9.94±2.50)nmol/ml,各组间比较差异无统计学意义(P>0.05)。阳虚质的PAI-1表达水平为(11,241.6±1701.7)pg/ml,气郁质PAI-1表达水平为(10,739.3±1334.6)pg/ml,痰湿质PAI-1表达水平为(11,046.7±1372.1)pg/ml,各组间比较差异无统计学意义(P>0.05)。结论复发性流产伴胰岛素抵抗患者中医体质以阳虚质、气郁质、痰湿质为主。血清SHBG水平在复发,性流产伴胰岛素抵抗患者表达偏低,血清PAI-1水平在复发性流产伴胰岛素抵抗患者表达升高。     

Postprandial coagulation activation in overweight individuals after weight loss: Acute and long-term effects of a high-monounsaturated fat diet and a low-fat diet

Diet is important in the prevention of cardiovascular disease, and it has been suggested that a high-MUFA diet is more cardioprotective than a low-fat diet. We hypothesised that the postprandial thrombotic risk profile is improved most favourably by a high-MUFA diet compared with a low-fat diet. This was tested in a parallel intervention trial on overweight individuals (aged 28.4 (SD 4.7) years) randomly assigned to a MUFA-diet (35-45% of energy as fat; > 20% as MUFA, n = 21) or a low-fat (LF) diet (20-30% of energy as fat, n = 22) for 6 months after a weight loss of ~ 10%. All foods were provided free of charge from a purpose-built supermarket. Meal tests designed after the same principles were performed before and after the dietary intervention, and blood samples were collected at 8.00 h (fasting), 12.00 h, and 18.00 h and analysed for factor VII coagulant activity (FVII:C), activated FVII, fibrinogen, prothrombin fragment 1 + 2 (F1 + 2), D-dimer, plasminogen activator inhibitor (PAI:Ag), and thrombin activatable fibrinolysis inhibitor. There were significant postprandial increases in F1 + 2 and D-dimer before and after dietary intervention, with significantly lower values after 6 months. No significant differences were observed between the postprandial changes induced by the two diets. The postprandial decrease in FVII:C and PAI:Ag did not differ before and after intervention, irrespective of the diets. Our findings suggest postprandial coagulation activation in overweight subjects with more pronounced acute than long-term effects. We observed similar effects of the MUFA diet and the LF diet on the postprandial prothrombotic risk profile.     

Role of Helicobacter pylori in patients with HCV-related chronic hepatitis and cirrhosis with or without hepatocellular carcinoma: possible association with disease progression

The discovery of Helicobacter hepaticus as a causal agent of hepatitis and hepatocellular carcinoma (HCC) in mice has stimulated interest in looking for Helicobacter species in human liver samples. In this study, we searched for association between H. pylori and HCV-related liver disease. Liver specimens were collected from eighty-five patients; they were divided into five different groups according to liver pathology (METAVIR system). Group I (the 1st control group) consisted of 16 patients with chronic hepatitis C without histological activity. Group II consisted of 25 patients with chronic active hepatitis C, Group III, 17 patients with HCV-related cirrhosis and Group IV, 16 patients with HCV-related cirrhosis and HCC. Group V (2nd control group) consisted of 11 patients suffering from gastro duodenal and gall bladder diseases but negative for HCV. All cases were tested by polymerase chain reaction on liver samples for the presence of H. pylori DNA Cag A gene. Routine biochemical, radiological and RT-PCR for HCV RNA were also performed for all cases. The positivity of H. pylori PCR CagA gene in liver tissue was directly proportional to the severity of liver pathology, this being 75%, 52.9% and 32% in groups IV, III and II, respectively, which was more significant than the 1st and 2nd control groups (P < 0.001). There was a significant difference between H. pylori PCR values when compared to METAVIR staging (F) in different groups (P = 0.001). Helicobacter pylori PCR (Cag A gene) was positive in about 28.2% cases of late fibrosis (F3 + F4) while positivity was (5.9%) in early fibrosis (F1 + F2) (P = 0.0001). There was significant difference between H. pylori PCR (Cag A gene) in liver tissue and METAVIR activity in different groups (P = 0.002) as most of H. pylori PCR-positive cases were METAVIR activity A1 and A2 (15.3% and 12.9%, respectively). There was no association between H. pylori PCR and quantitative HCV RNA (P = 0.531). Also there was no significant difference of Child-Pugh staging in the H. pylori PCR-positive group when compared to the negative group (P = 0.996). There may be an association between the presence of H. pylori (Cag A gene) in the liver and disease progression in HCV-related chronic hepatitis and cirrhosis with and without HCC.     

卡托普利对动脉损伤后内膜增生时纤溶系统的影响

目的　通过兔颈总动脉球囊损伤模型 ,观察卡托普利 (开搏通 ,captopril)对动脉球囊损伤后内膜增生时纤溶系统的影响。方法　以兔右颈总动脉内膜剥脱为实验模型 ,36只兔随机分为假手术组 (对照组 )、单纯损伤组、损伤 +药物治疗组 (简称药物治疗组 ) ,每组各 12只。药物治疗组术前1d至术后 30d给予captopril2mg·kg 1 ·d 1 ,余二组不给药 ,用ELISA法检测各组术前、术后 1、3、7、14、30d的血浆组织纤溶酶原激活剂 (t PA)、纤溶酶原激活剂抑制物 1(PAI 1)的水平 ,并于术后 30d行病理形态学观察各组血管内膜厚度及管腔狭窄度。结果　动脉球囊损伤后 ,药物治疗组PAI 1水平、内膜的厚度及管腔狭窄度均明显低于单纯损伤组。结论　血管球囊损伤术后纤溶系统作用的减弱影响动脉壁损伤再修复过程 ,captopril可使纤溶系统保持平衡 ,预防血管成形术后再狭窄。