慢性丙型肝炎后肝硬化患者心电图改变与Child-Pugh分级相关性

目的探讨慢性丙型肝炎(CHC)后肝硬化患者心电图改变与Child-Pugh分级和肝硬化性心肌病(CCM)之间的关系。方法设立健康对照组(51例)、CHC组(45例)、CHC后肝硬化组(51例)。CHC后肝硬化组按照Child-Pugh分级标准又分为Child-Pugh A级14例,Child-Pugh B级20例,Child-Pugh C级17例。所有病例使用日本光电心电图机ECG-1550P标准12导联同步心电图机记录、测量、分析心电图,比较各组心电图改变的差异及与Child-Pugh分级和CCM发病的关系。结果1心电图异常:CHC后肝硬化组心电图异常率为72.55%,总心电图异常例次112,平均每例患者有2.20次异常心电图;健康对照组、CHC组心电图异常率分别为1.96%、6.66%,均为轻微异常心电图。2CHC后肝硬化主要心电图异常种类:Q-T间期延长(28/51,54.90%),ST-T改变(27/51,52.94%),肢导低电压(17/51,33.33%),说明3种异常心电图组合较为常见。3CHC后肝硬化组患者心电图异常组合与Child-Pugh分级之间的关系:Child-Pugh A级Q-Tc间期延长0例(0/14),ST-T改变1例(1/14),肢导低电压1例(1/14);Child-Pugh B级Q-Tc间期延长13例(13/20),ST-T改变11例(11/20),肢导低电压5例(5/20);Child-Pugh C级Q-T间期延长15(15/17),ST-T改变15例(15/17),肢导低电压11例(11/17)。结论 CHC后肝硬化患者存在多种心电图异常,其中以Q-Tc间期延长、ST-T改变、肢导低电压为主,出现3种心电图异常组合且肝功能为Child-Pugh B级、ChildPugh C级,且并发CCM,对判断CHC后肝硬化预后具有重要提示作用。

实时荧光定量PCR分析慢性丙型肝炎患者胸腺近期输出功能

目的观察慢性丙型肝炎(CHC)患者外周血单个核细胞(PBMCs)中T细胞受体重排删除环(TRECs)的含量,从而推测CHC患者的胸腺近期输出功能,并且比较TRECs含量与HCV载量的关系。方法利用实时荧光定量PCR方法检测22例CHC患者及16例正常人PBMCs中TRECs含量,用RT-PCR方法结合荧光探针的检测技术检测CHC组外周血血清中的HCVRNA。结果CHC患者中TRECs含量为(5.52±1.87)copies/103PBMCs,低于正常人TRECs水平(7.19±2.42)copies/103PBMCs,P<0.05;TRECs含量与HCV载量直线相关分析r=-0.427,P<0.05。结论CHC患者TRECs水平低于正常人,显示其胸腺近期输出功能明显降低,且与HCV载量呈负相关性。

Hyperhomoysteinemia as a risk factor for coronary heart diseases in chronic hepatitis C patients

Hepatitis C virus is one of the major health problems worldwide. It affects mainly the liver but several extrahepatic manifestations are also accounted. Chronic hepatitis C patients are at an increased risk of developing hepatic steatosis, which share many clinical features with the metabolic syndrome. Hepatic steatosis has also been associated with elevated levels of markers of inflammation such as homocysteine, identified as hyperhomocysteinemia (HHC). HHC due to Methylenetetrahydrofolate Reductase (MTHFR) gene, in particular the C677T polymorphism, was recently associated with coronary heart diseases (CHD) in chronic hepatitis C (CHC) patients. Homocysteine is an intermediate in methionine metabolism, which takes place mainly in the liver metabolism. Deficiencies of micronutrients (folate, vitamin B 6 and possibly vitamin B 12) along with mild hyperhomocysteinemia, perhaps, act synergistically with other classical risk factors to further increase the risk of CHD. Clinical data indicate that HHC is associated with an increased incidence of CHD as well as with the severity of the disease in CHC patients. In conclusion, HHC might be a potential aetiological factor of CHD in CHC patients. The aim of this review is to investigate the progression of coronary heart diseases in chronic hepatitis C patients and correlate with levels of homocysteine in concurrence to genetic defects and nutrient deficiencies. However, future studies need to clarify the mechanistic role of HHC in CHD and CHC as a useful paradigm with most interesting therapeutic implications.

Causes and Stages of Hepatocellular Carcinoma at Patient Presentation at a Tertiary Medical Center in Western Saudi Arabia

Background: With 748,300 new cases diagnosed every year, hepatocellular carcinoma (HCC) is the 5th?and the 7th?most common cancer among males and females, respectively, and causes 7% of all cancer-related deaths. HCC represents more than?90% of primary liver cancers. Objective: The aim of the present study was to recognize the stages of HCC at presentation in patients who were diagnosed at King Abdul Aziz University Hospital (KAUH) and to identify the associated laboratory features of advance HCC.?Materials and Methods: A retrospective analysis of 57 HCC patients admitted to KAUH between January 2008 and December 2012 was conducted. The diagnosis was established using ultrasound (U/S), computed tomography (CT) and/or magnetic resonance imaging (MRI), with or without a liver biopsy, as well as blood testing for alpha-fetoprotein.?The following data were extracted from the medical records at KAUH: patient demographics (age, sex and nationality), laboratory results (CBC, LFT, PT, INR and alpha-fetoprotein), radiological results, biopsy results for those patients who underwent biopsy, outcomes (living, deceased or lost from the follow-up), and mortality and survival rates. Results: A total of 57 HCC patients were admitted during the study period, and 3 patients were excluded from the analysis. Of the remaining 54 patients, 44 (81.5%) were males and 10 (18.5%) were females. The mean age was 64.54 years (SD, 11.2 years;range, 31?-?86 years). The majority of patients were Saudis (19, 35.2%), non-Saudis (35, 64.8%), Egyptians (9, 16.6%) and Yemenis (7, 13%). The remaining 19 (35.2%) patients comprised other nationalities. Chronic hepatitis C virus was the most common cause for liver cirrhosis (35 patients, 64.8%). CT was the primary diagnostic method (37 patients 68.5%), while 9 (16.7%) cases were confirmed by adnominal MRI. Six patients (11.1%) were diagnosed with abdominal ultrasound examination and elevated alpha-fetoprotein levels. In 2 (3.7%) patients, HCC was confirmed by liver biopsy. The majority of the patients (37, 68.5%) had advanced disease. Only 21 (39%) patients underwent radio frequency appellation (RFA). The mean survival time from diagnosis to death was 5.9 months (SD, 5.7 months), and the longest survival time to death was 20 months. Conclusion: The majority of our patients presented at an advanced disease stage, and CHC was the most common underlying cause for liver cirrhosis in our cohort of HCC patients. The proper implementation of HCC screening programs for cirrhotic patients is expected to help detect the treatable stages of HCC in a timely manner.

丙肝患者病毒载量及危险因素与配偶感染关系

目的 研究慢性丙型肝炎(CHC)患者外周血浆病毒载体量、危险因素与其配偶感染的关系。方法 应用酶免法(EIA)及FQ -PCR法检测12 2例CHC患者的血浆、尿液、泪液和精液及其配偶血浆抗丙型肝炎病毒(抗-HCV)及HCVRNA含量。结果 CHC患者血浆、尿液、泪液和精液及其配偶血浆抗-HCV检出率分别为94 . 2 6 %(115 / 12 2 ) ,4 2. 8% (2 1/ 4 9) ,11 .19% / (5 / 4 2 ) ,4 7 .2 2 % (17/ 35 )和2 2 . 5 0 % (2 7/ 12 0 ) ;HCVRNA的检出率分别为88 .15 % (6 7/ 12 2 ) ,5 5 . 10 % (2 7/ 4 9) ,19 .0 4 % (8/ 4 2 ) ,6 6 . 6 7% (2 4 / 36 )和2 5 . 83% (31/ 12 0 ) ,对照组均无抗-HCV及HCVRNA检出。男性配偶的抗-HCV、HCVRNA的检出率分别为15 .0 6 % (11/ 73) ,78. 0 8% (5 7/ 73) ;女性配偶的抗-HCV、HCVRNA的检出率分别为2 9. 78% (14 / 4 7)、89 .36 % (42 / 4 7)。当CHC患者外周血浆HCVRNA≥10 5copies/ml时,其配偶HCVRNA的检出率为2 9. 1% (2 1/ 6 9) ;当CHC患者外周血浆HCVRNA <10 5copies/ml时,其配偶HCVRNA的检出率为19 4. 7% (11/ 5 7)。配偶婚龄<10 ,11～2 0 ,2 1～30 ,31～5 4年的4个组HCVRNA的检出率分别为13 .33% (2 / 15 )、2 2 . 2 2 % (4/ 18)、32 . 0 0 % (8/ 2 5 )和5 5. 32 % (2 7/ 4 7)。

铁过载抑制人肝癌Huh7.5细胞增殖和促进细胞凋亡的机制

目的观察铁过载对人肝癌Huh7.5细胞活性的影响及机制。方法用(50、100、200)μmol/L枸橼酸铁铵(FAC)处理Huh7.5细胞,铁离子荧光探针Phen Green FL标记结合荧光显微镜检测细胞铁载量。MTT法检测铁过载细胞的增殖活性,实时定量PCR检测铁过载细胞运铁蛋白受体1(TfR1)、TfR2、二价金属离子转运体1(DMT1)和膜铁转运蛋白1(FPN1)的mRNA水平,Western blot法检测TfR1、TfR2、DMT1和FPN 1蛋白水平,二氯二氢荧光素乙酰乙酸酯(DCFH-DA)染色结合流式细胞术检测活性氧(ROS)水平;在FAC处理细胞以及FAC联合400μmol/L N-乙酰半胱氨酸(NAC)处理后,采用异硫氰酸荧光素标记的膜联素Ⅴ/碘化丙啶(annexinⅤ-FITC/PI)双染色结合流式细胞术检测细胞凋亡。结果细胞铁载量随FAC增加呈浓度依赖性上升;FAC处理细胞TfR1、TfR2和DMT1 mRNA和蛋白水平显著下调,FPN1 mRNA和蛋白水平显著上调;ROS水平随FAC浓度增加显著升高,细胞增殖活性随FAC浓度增加显著下降;FAC处理细胞的凋亡率均显著高于对照组,而向FAC处理细胞加入抗氧化剂NAC后,细胞凋亡率显著下降。结论铁过载抑制Huh7.5细胞增殖活性并促进细胞凋亡,其作用机制可能与氧化应激途径有关。

慢性丙型肝炎合并甲状腺功能异常患者转归情况及抗病毒疗效分析

目的 探讨慢性丙型肝炎（chronic hepatitis C,CHC）合并甲状腺功能异常（thyroid dysfunction,TD）患者的抗病毒疗效及TD转归。方法 采用前瞻性研究方法,对2008年8月至2011年3月收治的符合纳入标准的CHC患者采用标准抗病毒治疗方案[聚乙二醇干扰素α-2a 180μg/周,联合利巴韦林10.6~15.0 mg/（kg·d）],疗程48周,停药后随访至24周。于基线治疗第12、24、48周及停药后24周复查丙肝病毒（HCV）RNA、甲状腺功能,分析抗病毒治疗效果及TD转归。结果 194例患者完成48周的抗病毒治疗。随访24周,TD组脱落2例,非TD组脱落1例。TD组50例患者中共17例甲状腺功能复常,占34.0%,其中基线TD、治疗中新出现TD患者分别有17.4%（4/23）与48.1%（13/27）出现甲状腺功能复常,后者明显高于前者,差异有统计学意义（掊2=5.202,P=0.037）。TD组12周早期病毒学应答（EVR）率为44.2%（23/52）,非TD组为54.2%（77/142）;TD组治疗结束时病毒学应答（ETVR）率为59.6%（31/52）,非TD组为58.5%（83/142）;TD组治疗结束后随访24周持续病毒学应答（SVR）率为60.0%（30/50）,非TD组为54.6%（77/141）。两组EVR、ETVR、SVR的差异均无统计学意义（P〉0.05）。结论 TD不影响干扰素的抗病毒治疗效果。完成治疗后随访24周,部分TD可复常,干扰素治疗后合并TD者其临床转归明显优于基线合并TD者。

Ulcerative colitis triggered by pegylated interferon alpha-2b in a patient with chronic hepatitis B: A case report and literature review

Interferon(IFN)is a multifaceted immunomodulator that is effective against many diseases,including chronic hepatitis B and chronic hepatitis C infection.IFN defends against viral infection,but may also cause various side effects,such as ulcerative colitis(UC).Herein,we present a case of UC triggered by pegylated interferon alpha-2b(PEG-IFN-α-2b)therapy in a patient with concurrent chronic hepatitis B(CHB)infection.The diagnosis was based on typical clinical symptoms,colonoscopy findings,colonic mucosal biopsy,and histopathology.Accordingly,treatment with mesalazine was initiated without stopping PEG-IFN-α-2b.Fortunately,UC relieved gradually without compromising the effects of treatment.Simultaneously,we conducted a literature review of previously published case reports on the side effect of UC in patients with underlying chronic hepatitis.Various reactions have been reported,including induction,exacerbation,and no change.This is the first report of UC triggered by PEG-IFN-α-2b in a CHB patient.We recommend that physicians pay attention to the rare side effect of UC during administration of PEG-IFN-α-2b.Mesalazine can relieve UC with sustained use of PEG-IFN-α-2b.