中西医结合治疗非酒精性脂肪肝60例临床观察

目的观察中西医结合治疗非酒精性脂肪肝的临床疗效。方法将60例非酒精性脂肪肝患者随机分为实验组和对照组。2组均予西医常规处理,实验组加用当飞利肝宁胶囊并配合针灸治疗,比较2组临床疗效。结果治疗后实验组患者总有效率治疗组为94.3%,对照组为80%,2组疗效有显著性差异(P<0.05)。结论中西医结合疗法与单纯西药治疗相比治疗效果明显。     

硫普罗宁治疗酒精性肝病30例疗效观察

目的探讨硫普罗宁治疗酒精性肝病的临床疗效。方法60例酒精性肝硬化患者随机分治疗组和对照组,治疗组给予硫普罗宁(凯西莱)50mL/d溶于250mL、5%GS静脉滴注;对照组给予维生素C、肌酐、护肝片、ATP、CDP等基础治疗,观察比较2组患者的临床疗效及肝功能变化情况。结果治疗组的总有效率为90.0%,明显高于对照组的总有效率(66.7%),2组总有效率比较,经统计学分析,具有统计学意义(P<0.05)。治疗组ALT、AST、DBIL水平较对照组明显降低,经统计学分析,具有统计学意义(P<0.05)。结论硫普罗宁治疗酒精性肝病疗效较好,值得临床推广和应用。     

高压氧联合银杏达莫注射液治疗脑血栓形成临床疗效分析

目的探讨提高临床脑血栓形成的疗效方法。方法以高压氧配合银杏达莫注射液治疗脑血栓形成患者56例为治疗组,另采用常规药物治疗脑血栓形成50例为对照组,在治疗前及治疗3个疗程后对患者进行神经功能缺损评分,比较2组神经功能缺损的改善率。结果临床疗效总有效率分别为94.7%和78%。结论高压氧联合银杏达莫注射液治疗组明显优于常规药物治疗对照组的疗效(P<0.05)。     

强的松联合普乐可复治疗V型狼疮性肾炎临床观察

目的对V型狼疮性肾炎的强的松联合普乐可复综合治疗进行临床分析。方法选取132例V型狼疮性肾炎患者,随机分配到对照组和实验组。每组各66例。实验组采用强的松与普乐可复的综合治疗,对照组只采用普乐可复的治疗方式。利用SPSS13.0对2组的疗效进行统计学处理。结果实验组治疗效果要明显好于对照组患者,而并发症却少于对照组患者。结论对V型狼疮性肾炎患者采用强的松联合普乐可复的综合治疗要比只单独采用普乐可复治疗更加有效,更加安全。所以研究V型狼疮性肾炎的有效治疗方式是极具临床价值的。     

阿托伐他汀治疗100例不稳定型心绞痛的临床疗效观察

目的观察阿托伐他汀治疗不稳定型心绞痛的疗效及其对血脂的影响。方法将200例病人随机分为实验组100例,对照组100例。2组均给予常规抗凝、抗血小板聚集、硝酸酯类等药物治疗;观察组加用阿托伐他汀10mg,每晚顿服。疗程均为4周。4周后2组对比疗效与血脂的变化。结果实验组总有效率分别为:94%,疗后观察组LDL-C下降,TC、HDL-C升高(P<0.05);与对照组比较,观察组治疗后LDL-C、降低,TC、HDL-C升高(P<0.05),在降低血脂方面明显高于对照组。结论阿托伐他汀治疗不稳定心绞痛,疗效显著,可通过调脂及抑制炎症反应而对不稳定型心绞痛起治疗作用值得推广使用。     

倍他乐克联合心达康治疗冠心病心绞痛的临床分析

目的观察用倍他乐克联合心达康治疗冠心病心绞痛的临床疗效。方法将确诊的冠心病心绞痛患者62例随机分为对照组和治疗组各31例,对照采用常规治疗,治疗组采用倍他乐克联合心达康治疗,两组均以30天为1个疗程。连续治疗2个疗程。疗程结束后统计疗效。结果两组患者病情都有明显改善,治疗组与对照组相比疗效更为显著(P<0.05)。结论倍他乐克联合心达康治疗冠心病心绞痛疗效显著。     

低分子肝素联合尿激酶对急性心肌梗死的疗效研究

目的探讨低分子肝素联合尿激酶对急性心肌梗死的疗效。方法抽取120例心肌梗死患者,按照住院号奇偶分成2组各60例,实验组给予低分子肝素联合尿激酶治疗,对照组给予常规治疗,对比2组治疗效果的差异。结果实验组总体有效率为91.6%,远高于对照组总体有效率80.0%(P<0.05)。实验组心率失常发生率为6.7%,出血发生率为16.7%,与对照组比较差别具有统计学意义(P<0.05)。实验组发生心脏事件21.7%,死亡8.3%,与对照组比较差别有统计学意义(P<0.05)。实验组左室射血分数明显高于对照组(P<0.05)。结论低分子肝素联合尿激酶治疗急性心肌梗死疗效较好,具有较高的临床应用价值,值得推广。     

他汀序贯疗法治疗的急性冠脉综合征临床研究

目的探讨应用他汀序贯疗法治疗急性冠脉综合征的临床疗效。方法回顾性分析收治我院的64例急性冠脉综合征患者的病例资料,所有患者随机分成2组,各32例,治疗组采用阿托伐他汀序贯的疗法进行治疗,对照组采用常规剂量的他汀类药物进行治疗。所有患者均进行随诊,随诊时间6个月以上,并对2组患者的严重心血管事件发生率进行对比分析。结果 2组进行对比显示治疗组的严重心血管事件发生率明显低于对照组,2组对比差异有统计学意义(P<0.05)。结论他汀序贯疗法治疗急性冠脉综合征可明显降低患者发生死亡、心源性休克、心力衰竭、心律失常等疾病的发生几率,值得临床推广。     

肝胆管结石的外科治疗

目的探讨不同的手术方式治疗肝胆管结石的临床效果。方法选择2009年9月至2010年11月在本院治疗的120例肝胆管结石患者,随机分为对照组60例进行采用常规开腹肝部分切除术,并进行T管引流术进行治疗;治疗组60例采用采用腹腔镜微创治疗。术后进行T管引流,观察2组患者的临床疗效。结果观察组手术时问、术中出血量、术后引流时间、术后下床时间明显低于对照组(P<0.05);术后复发率、感染率、并发症发生率治疗组明显低于对照组,P<0.05,差异均有统计学意义。结论微创下腹腔镜联合T管引流治疗肝胆管结石临床疗效好,值得临床推广应用。     

非酒精性脂肪性肝病患者药物及生活方式联合干预的效果观察

目的观察在多烯磷脂酰胆碱等药物治疗基础上对非酒精性脂肪性肝病(NAFLD)患者进行生活方式干预的治疗效果。方法将93例NAFLD患者随机分为药物治疗组(A组,47例)和生活方式干预组(B组,46例),B组在药物治疗基础上进行生活方式干预并观察6个月。比较2组治疗前后肝功能、血脂、血糖以及肝脏B超的变化。结果治疗后B组肝功能和血脂指标较A组均明显缓解(P<0.05),B组影像学(B超)也明显得到改善(P<0.05)。结论对NAFLD患者在进行多烯磷脂酰胆碱治疗的同时给予生活方式的干预,可明显改善各临床指标,其疗效优于单纯药物治疗。提示药物及生活方式干预联合应用对非酒精性脂肪肝病的治疗效果较好。     

Synergistic and Detrimental Effects of Alcohol Intake on Progression of Liver Steatosis

Nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are the most common liver disorders worldwide and the major causes of non-viral liver cirrhosis in the general population. In NAFLD, metabolic abnormalities, obesity, and metabolic syndrome are the driving factors for liver damage with no or minimal alcohol consumption. ALD refers to liver damage caused by excess alcohol intake in individuals drinking more than 5 to 10 daily units for years. Although NAFLD and ALD are nosologically considered two distinct entities, they show a continuum and exert synergistic effects on the progression toward liver cirrhosis. The current view is that low alcohol use might also increase the risk of advanced clinical liver disease in NAFLD, whereas metabolic factors increase the risk of cirrhosis among alcohol risk drinkers. Therefore, special interest is now addressed to individuals with metabolic abnormalities who consume small amounts of alcohol or who binge drink, for the role of light-to-moderate alcohol use in fibrosis progression and clinical severity of the liver disease. Evidence shows that in the presence of NAFLD, there is no liver-safe limit of alcohol intake. We discuss the epidemiological and clinical features of NAFLD/ALD, aspects of alcohol metabolism, and mechanisms of damage concerning steatosis, fibrosis, cumulative effects, and deleterious consequences which include hepatocellular carcinoma.     

益赛普治疗类风湿关节炎伴冠心病的临床疗效

目的观察TNFα拮抗剂益赛普治疗类风湿关节炎(Rheumatoid arthritis,RA)伴冠心病的临床疗效。方法选取60例确诊为活动期RA并发冠心病患者,随机分为慢作用药物组(30例,接受慢作用药物治疗,并在整个观察期内保持不变)和益赛普组(30例,在原慢作用药物治疗基础上皮下注射益赛普,每次25 mg,每周2次,持续3个月)。分别于治疗前及治疗12个月后采血,应用全自动荧光偏振免疫分析法测定血清同型半胱氨酸(Homocysteine,HCY)水平;评价临床疗效;经胸超声心动图测定冠状动脉血流储备(Coronary flow reserve,CFR);应用高分辨率B超对所有观察对象的肱动脉进行扫查,测定肱动脉内皮依赖性血管舒张率(Flow-mediated dilation rate,FMD);并记录12个月内发生的心血管疾病、不良反应以及肝肾功能的变化。结果益赛普组治疗后与治疗前比较,患者的血清HCY水平显著下降(P<0.05),CFR和FMD显著升高(P<0.05);慢作用药物组治疗后与治疗前比较,HCY、CFR和FMD均有所下降,但差异无统计学意义(P>0.05);与慢作用药物组比较,经益赛普治疗后,患者血清HCY水平显著下降(P<0.05),CFR和FMD显著升高(P<0.05);益赛普组临床症状缓解有效率明显高于慢作用药物组(P<0.05);12个月内,益赛普组主要心血管疾病发生率与慢作用药物组比较明显降低(P<0.05);两组不良反应发生率差异无统计学意义(P>0.05)。结论益赛普可以明显缓解RA患者的临床症状,延缓冠心病的进展,减少心血管危险疾病的发生。     

The Role of Gut Dysbiosis in Acute-on-Chronic Liver Failure

Acute-on-chronic liver failure (ACLF) is an important syndrome of liver failure that has a high risk of short-term mortality in patients with chronic liver disease. The development of ACLF is associated with proinflammatory precipitating events, such as infection, alcoholic hepatitis, and intense systemic inflammation. Recently, the role of the gut microbiome has increasingly emerged in human health and disease. Additionally, the gut microbiome might have a major role in the development of liver disease. In this review, we examine evidence to support the role of gut dysbiosis in cirrhosis and ACLF. Additionally, we explore the mechanism by which the gut microbiome contributes to the development of ACLF, with a focus on alcohol-induced liver disease.     

IFN-α2a对多发性硬化患者外周血中免疫抑制因子IL-10的影响

目的观察重组人干扰素α－２ａ对ＭＳ的治疗效果，探讨其治疗机理。方法采用ＥＬＩＳＡ夹心法检 测２２例ＭＳ患者治疗前后血清中ＩＬ－１０浓度，结合临床疗效进行对比分析。结果重组人干扰素α－２ａ治疗组患者 血清中ＩＬ－１０浓度明显增高，临床症状明显改善，与对照组比较差异有显著意义。结论重组人干扰素ＩＦＮ－α２ａ可 提高ＭＳ患者体内ＩＬ－１０水平，对ＭＳ有良好疗效。     

23例主动脉夹层的临床分析

目的探讨主动脉夹层的临床特征,以积累经验,提高诊治率。方法对我院收治的23例主动脉夹层患者的临床资料进行回顾性分析。结果本组23例患者中误诊11例,误诊率44.00%;16例好转出院(69.57%),7例死亡(30.43%)。结论主动脉夹层患者的症状和体征表现多样,临床较易误诊,早期正确诊断和治疗对预后很关键。     

凯西来联合阿德福韦酯治疗慢性乙型肝炎疗效观察

目的探讨凯西来联合阿德福韦酯治疗慢性乙型肝炎疗效观察。方法90例慢性乙肝患者,治疗组患者用凯西来200mg,加入5%葡萄糖注射液250 mL中静脉点滴,1次/d,疗程10～20d。对照组采用一般护肝治疗(甘利欣、门冬氨酸钾镁、肌苷等)。观察两组患者肝功能及肝纤维化指标(HA、PⅢP、LN、Ⅳ-C)等。结果治疗组疗效明显优于对照组,两组疗效差异有显著性意义。结论凯西来联合阿德福韦酯治疗慢性乙型肝炎疗效显著。     

The Purinergic P2X7 Receptor-NLRP3 Inflammasome Pathway: A New Target in Alcoholic Liver Disease?

The World Health Organization has estimated that approximately 3 million deaths are attributable to alcohol consumption each year. Alcohol consumption is notably associated with the development and/or progression of many non-communicable inflammatory diseases—particularly in the liver. Although these alcoholic liver diseases were initially thought to be caused by the toxicity of ethanol on hepatocytes, the latest research indicates Kupffer cells (the liver macrophages) are at the heart of this “inflammatory shift”. Purinergic signaling (notably through P2X7 receptors and the NLRP3 inflammasome) by Kupffer cells appears to be a decisive factor in the pathophysiology of alcoholic liver disease. Hence, the modulation of purinergic signaling might represent a new means of treating alcoholic liver disease. Here, we review current knowledge on the pathophysiology of alcoholic liver diseases and therapeutic perspectives for targeting these inflammatory pathways.     

Liver Disease: Induction,Progression, Immunological Mechanisms,and Therapeutic Interventions

The liver is an organ with impressive regenerative potential and has been shown to heal sizable portions after their removal. However, certain diseases can overstimulate its potential to self-heal and cause excessive cellular matrix and collagen buildup. Decompensation of liver fibrosis leads to cirrhosis, a buildup of fibrotic ECM that impedes the liver’s ability to efficiently exchange fluid. This review summarizes the complex immunological activities in different liver diseases, and how failure to maintain liver homeostasis leads to progressive fibrotic tissue development. We also discuss a variety of pathologies that lead to liver cirrhosis, such as alcoholic liver disease and chronic hepatitis B virus (HBV). Mesenchymal stem cells are widely studied for their potential in tissue replacement and engineering. Herein, we discuss the potential of MSCs to regulate immune response and alter the disease state. Substantial efforts have been performed in preclinical animal testing, showing promising results following inhibition of host immunity. Finally, we outline the current state of clinical trials with mesenchymal stem cells and other cellular and non-cellular therapies as they relate to the detection and treatment of liver cirrhosis.     

双侧支持钢板内固定治疗胫骨近端粉碎性骨折86例临床探讨

目的探讨采用双侧支持钢板内固定治疗胫骨近端粉碎性骨折的临床疗效。方法回顾性分析2009年3月至2011年3月我院采用双侧支持钢板内固定治疗的86例胫骨近端粉碎性骨折患者的临床疗效,并以同期采用闭合复位经皮锁定钢板内固定治疗的86例胫骨近端粉碎性骨折患者为对照组,比较2组治疗效果和安全性。结果观察组患者手术时间、术中出血量、手术并发症发生率均低于对照组,组间比较差异具有统计学意义(P<0.05);观察组优良达94.17%,略高于对照组,组间比较差异无统计学意义(P>0.05)。结论双侧钢板内固定治疗胫骨近端粉碎性骨折,安全可靠,值得临床借鉴。     

CXCL10 Decreases GP73 Expression in Hepatoma Cells at the Early Stage of Hepatitis C Virus (HCV) Infection

Golgi protein 73 (GP73), which is up-regulated in hepatocellular carcinoma (HCC), has recently been identified as a novel serum marker for HCC diagnosis. Several reports also noted the increased levels of GP73 expression in chronic liver disease in patients with acute hepatitis of various etiologies, chronic Hepatitis C virus (HCV) infection and alcoholic liver disease. The molecular mechanisms of GP73 expression in HCV related liver disease still need to be determined. In this study, we aimed to evaluate the effect of HCV infection on GP73 expression. GP73 was highly expressed in Huh7, Hep3B, 293T and HUVEC cells, and was low-expressed in HepG2 cells. HCV infection led to down-regulation of GP73 in Huh7 and HepG2/CD81 cells at the early stage of infection. CXCL10 decreased GP73 expression in Huh7 and HepG2 cells. Up-regulation of GP73 was noted in hepatocytes with cytopathic effect at advanced stage of HCV infection, and further research is needed to determine the unknown factors affecting GP73 expression. In conclusion, our study provided additional evidence for the roles of GP73 in liver disease.