复方牛胎肝提取物联合恩替卡韦治疗慢性乙型肝炎疗效分析

目的：探讨复方牛胎肝提取物片联合恩替卡韦片治疗慢性乙型肝炎患者的临床疗效。方法将48例慢性乙型肝炎患者随机分为治疗组24例,给予口服复方牛胎肝提取物片及恩替卡韦片;给予对照组24例口服恩替卡韦片,疗程均为48w。观察两组患者治疗前后肝功能、血清肝纤维化指标及肝穿刺活检组织病理学的变化情况。结果在治疗48w时,治疗组血清白蛋白水平为（41.0±2.9） g/L,显著高于对照组（36.2±2.2） g/L,P＜0.01;治疗组血清透明质酸（HA）、层粘蛋白（LN）和IV型胶原（IV-C）水平分别为（158.0±70.3） ng/ml、（83.6±29.9） ng/ml和（90.3±41.2） ng/ml,显著低于对照组（170.6±71.1） ng/ml、（107.5±33.7） ng/ml和（113.5±52.4） ng/ml,P均＜0.05;肝组织病理学检查显示治疗组患者肝脏炎症活动度及纤维化程度改善均优于对照组（P=0.041和P=0.044）。结论复方牛胎肝提取物片联合恩替卡韦片能显著改善慢性乙型肝炎患者肝脏炎症活动度及纤维化程度,促进白蛋白合成,疗效优于单用恩替卡韦治疗。     

聚乙二醇干扰素α-2b治疗慢性乙型肝炎患者外周血T淋巴细胞亚群和血清细胞因子水平变化

目的研究聚乙二醇干扰素α-2b治疗慢性乙型肝炎患者外周血T淋巴细胞亚群和血清细胞因子水平的变化。方法 2014年1月~2016年1月我院收治的184例慢性乙型肝炎患者,92例接受聚乙二醇干扰素α-2b联合恩替卡韦治疗48 w,另92例只接受恩替卡韦治疗。使用流式细胞仪检测外周血T淋巴细胞亚群,采用放射免疫法检测血清IL-6、INF-ɑ、IL-4,采用酶联免疫吸附法检测血清IL-17、TGF-β1和HBV标记物,采用荧光定量PCR法检测血清HBV DNA、核转录因子RORγt、Foxp3、IL-17mRNA。结果在停药随访24 w,联合组与恩替卡韦组血清HBV DNA阴转率分别为86.96%和84.78%(P0.05);联合组血清HBeAg阴转率为28.89%(13/45),与恩替卡韦组的15.22%(7/46)比,无显著性差异(P0.05);联合组血清ALT水平为(34.6±11.6)U/L,显著低于恩替卡韦组【(64.6±20.5)U/L,P0.05】;联合组外周血CD3~+、CD4~+细胞和CD4~+/CD8~+比值分别为(75.6±14.5)%、(42.7±10.3)%和(1.4±0.6),显著高于恩替卡韦组【(66.8±14.4)%、(36.7±8.5)%和(1.0±0.5),P0.05】,CD8+细胞百分比为(29.3±7.3)%,显著低于恩替卡韦组【(34.8±8.5)%,P0.05】,两组NK细胞百分比比较无显著性差异(P0.05);治疗前两组血清IL-6、IL-17、IL-4、INF-ɑ、TGF-β1水平比较无显著性差异(P0.05),治疗后联合组血清IL-6水平为(6.8±1.2)pg/ml,显著高于恩替卡韦组【(3.5±0.8)pg/ml,P0.05】,IL-17水平为(0.7±0.3)pg/ml,显著低于恩替卡韦组【(2.8±0.9)pg/ml,P0.05】,IL-4水平为(1.4±0.5)pg/ml,显著低于恩替卡韦组【(3.8±1.5)pg/ml,P0.05】,INF-ɑ水平为(4.0±1.3)pg/ml,显著高于恩替卡韦组【(2.6±0.9)pg/ml,P0.05】,两组血清TGF-β1水平比较无显著性差异(P0.05);治疗前两组血清Foxp3、IL-17和RORγt mRNA水平比较无显著性差异(P0.05),治疗后联合组血清RORγt水平为(0.86±0.31),显著低于恩替卡韦组【(1.56±0.43),P0.05】,而两组血清Foxp3和IL-17mRNA水平比较无显著性差异(P0.05)。结论聚乙二醇干扰素α-2b能通过调控细胞因子和核转录因子水平,从多个环节调控慢性乙型肝炎患者免疫功能,发挥抗病毒作用。     

恩替卡韦治疗失代偿期乙型肝炎肝硬化3年疗效观察

目的 探讨恩替卡韦治疗失代偿期乙型肝炎肝硬化患者的疗效及其对血清肝纤维化指标的影响。方法 按照住院时间顺序编号,将190例失代偿期乙型肝炎肝硬化患者随机分为观察组95例和对照组95例,给予观察组口服恩替卡韦治疗,给予对照组水飞蓟等综合治疗。应用SPSS 17.0统计软件进行分析。结果 在治疗3年末,观察组血清HBV DNA载量为（2.01±1.1） lg copies/ml,显著低于对照组的（5.93±1.3） lg copies/ml（P<0.05）;观察组ALT为32.3±4.6 U/L、TBIL为13.2±3.3 μmol/L、ALB为35.1±4.6 g/L和INR为0.9±0.1,与对照组的（262.5±25.5 U/L、29.5±4.1 μmol/L、28.5±4.1 g/L和1.6±0.1）比,差异显著（P<0.05）;观察组血清HA、LN、IV-C和PCⅢ分别为180.7±20.6 ng/ml、190.8±23.4 ng/ml、153.7±19.3 ng/mL和31.21±5.62 ng/ml,显著低于对照组的（310.7±20.8 ng/ml、410.5±20.9 ng/ml、214.7±20.2 ng/ml和79.56±8.23 ng/ml,P<0.05）。结论 恩替卡韦治疗失代偿期乙型肝炎肝硬化可以显著降低血清HBV DNA水平,改善肝功能和阻断肝纤维化进展,且安全性高,延长了生存期。     

恩替卡韦联合水飞蓟宾葡甲胺治疗慢性乙型肝炎合并NAFLD患者疗效初步研究

目的观察恩替卡韦联合水飞蓟宾葡甲胺治疗慢性乙型肝炎合并非酒精性脂肪性肝病（NAFLD）患者的临床疗效及其对血清HBsAg、HBV DNA和血清肝纤维化指标的影响。方法2015年1月~2016年1月我院诊治的慢性乙型肝炎合并NAFLD患者80例,随机将患者分为对照组40例和观察组40例。对照组患者服用恩替卡韦,观察组患者服用恩替卡韦和水飞蓟宾葡甲胺,观察24 w。结果在治疗24 w末,观察组患者血清ALT和AST分别为（64.3±27.9）U/L和（42.0±24.5）U/L,均显著低于对照组【分别为（83.7±26.0）U/L和（57.6±26.6）U/L,P<0.05】;观察组血清Ⅲ型前胶原、Ⅳ型胶原蛋白、层粘连蛋白和透明质酸酶分别为（106.0±54.5）ng/L、（69.23±21.24）ng/L、（119.2±61.2）ng/L和（119.2±71.2）ng/L,均显著低于对照组【（147.6±76.6）ng/L、（86.74±21.30）ng/、（212.7±100.3）ng/L和（205.7±91.3）ng/L,P<0.05】;观察组与对照组患者血清HBV DNA水平分别为（2.3±0.9）Ig IU/ml和（2.7±1.0）Ig IU/ml,血清HBsAg水平分别为（4458.0±945.5）S/CO和（4744.0±1256.5）S/CO,差异均无统计学意义。结论应用恩替卡韦联合水飞蓟宾葡甲胺治疗慢性乙型肝炎合并NAFLD患者较恩替卡韦单药治疗可以更有效地改善肝酶谱及血清肝纤维化指标,但对血清HBsAg水平无明显影响。     

恩替卡韦联合甘草酸二铵治疗慢性乙型肝炎患者效果研究*

目的 探讨应用恩替卡韦联合甘草酸二铵治疗慢性乙型肝炎(CHB)患者的短期效果和血清细胞因子水平变化。方法 2019年1月～2020年2月我院收治的98例CHB患者,被随机分为对照组49例和观察组49例,两组均接受恩替卡韦治疗,在此基础上,给予观察组加用甘草酸二铵口服,两组均持续治疗观察12个月。采用放射免疫法检测血清透明质酸 (HA) 、层粘连蛋白(LN) 、IV型胶原( CIV) 、III型前胶原(PIIIP) 水平,采用ELISA法检测血清白介素 2(IL- 2)、白介素4(IL- 4)、白介素 10(IL- 10)和肿瘤坏死因子α(TNF-α)水平,使用流式细胞仪检测外周血 T 细胞亚群。结果 在治疗12个月末,观察组血清ALT复常率为87.8%,显著高于对照组的71.4%(P＜0.05);观察组血清ALT和AST水平分别为(32.3±6.9)U/L和(38.3±4.7)U/L,显著低于对照组【分别为(47.5±7.6)U/L和(52.9±5.1)U/L,P＜0.05】;观察组血清HA和PⅢP水平分别为(90.6±9.5)ng/mL和(141.6±32.6)ng/mL,显著低于对照组【分别为(126.8±14.6)ng/mL和(168.2±29.9)ng/mL,P＜0.05】;观察组血清IL-4和TNF-α水平分别为(48.8±7.9)ng/L和(11.3±1.9)ng/L,显著低于对照组【分别为(62.6±8.8)ng/L和(18.5±1.7)ng/L,P＜0.05】,而血清IL-10水平为(19.2±2.5)ng/L,显著高于对照组【(12.7±3.4)ng/L,P＜0.05】;观察组外周血CD4⁺细胞百分比和CD4⁺/CD8⁺细胞比值分别为(43.5±5.5)%和(1.6±0.2),显著高于对照组【分别为(38.4±4.7)%和(1.4±0.4),P＜0.05】。结论 应用恩替卡韦联合甘草酸二铵治疗CHB患者可有效改善患者肝功能,抑制肝纤维化进程,控制体内炎症反应,改善免疫功能紊乱。     

阿德福韦酯与恩替卡韦治疗HBeAg阳性慢性乙型肝炎患者临床疗效观察

目的：观察阿德福韦酯和恩替卡韦治疗初治的 HBeAg 阳性慢性乙型肝炎患者96 w 的临床疗效及不良反应。方法在初治的 HBeAg 阳性慢性乙型肝炎患者中,接受阿德福韦酯治疗的患者38例,接受恩替卡韦治疗的患者30例,比较两组患者治疗前基线 ALT、HBV DNA、HBsAg、HBeAg、肌酐及治疗96 w 时的疗效。结果阿德福韦酯治疗患者基线 ALT 水平为（186.6±124.5） U/L,HBV DNA 水平为（7.3±1.1） log10拷贝/毫升,恩替卡韦治疗患者基线 ALT 水平为（190.8±116.8） U/L,HBV DNA水平为（7.5±1.5） log10拷贝/毫升 ml,两组具有可比性（P＜0.05）;在治疗96 w 时,恩替卡韦治疗患者 HBV DNA 阴转率为98.2%,显著高于阿德福韦酯治疗患者的60.2%（P＜0.05）;恩替卡韦组 ALT 复常率为97.1%,与阿德福韦酯组的92.7%相比,无显著性相差（P＞0.05）;恩替卡韦组 HBeAg 阴转率28.8%,与阿德福韦酯组的26.2%相比,无显著性相差（P＞0.05）。结论恩替卡韦在降低患者血清 HBV DNA 载量方面优于阿德福韦酯,但在血清 HBeAg 转阴率、ALT 复常率方面两者相似。     

恩替卡韦联合复方甘草酸苷治疗乙型肝炎肝硬化患者疗效及对肠道菌群的影响*

目的 观察恩替卡韦联合复方甘草酸苷治疗乙型肝炎肝硬化患者的疗效及对肠道菌群的影响。方法 2013年1月～2020年12月我院诊治的乙型肝炎肝硬化患者73例,采用随机数字表法将其分为对照组40例和观察组33例,分别给予恩替卡韦或恩替卡韦联合复方甘草酸苷治疗48周。采用ELISA法检测血清肿瘤坏死因子α(TNF-α)、白介素-6(IL-6)和IL-10水平,使用法国生物梅里埃公司的ATB半自动微生物鉴定系统进行细菌鉴定,使用美国GE公司 LOGIQ E9或PHILIPS EPIQ7型彩色多普勒超声诊断仪检测门静脉内径(DPV)、脾静脉内径(DSV)和脾脏厚度(SPT)。结果 在治疗48周末,观察组血清丙氨酸氨基转移酶(ALT)水平为(43.7±7.6)U/L,显著低于对照组【55.9±6.5)U/L,P<0.05】,而血清白蛋白、总胆红素和凝血酶原时间分别为(35.3±4.5)g/L、(15.2±3.6)μmol/L和(13.3±0.8)s,与对照组【分别为(34.5±4.2)g/L、17.6±2.9)μmol/L和(13.9±0.7)s】比,差异无显著意义(P>0.05);观察组血清HBV DNA水平为(1.3±0.3)lg copies/ml,与对照组的(1.4±0.4)lg copies/ml比,无显著性差异(P>0.05);观察组粪便拟杆菌和双歧杆菌数分别为(7.9±0.8)lg GFU/g和(9.3±1.5)lg GFU/g,显著高于对照组【分别为(5.5±0.6)lg GFU/g和(7.6±1.0)lg GFU/g,P<0.05】,而大肠杆菌、肠球菌和乳酸杆菌数量分别为(7.3±0.9)lg GFU/g、(7.0±1.2)lg GFU/g和(9.8±0.6)lg GFU/g,与对照组【分别为(7.9±0.7)lg GFU/g、(7.3±1.3)lg GFU/g和(9.5±0.5)lg GFU/g】比,差异无显著意义(P>0.05);观察组血清TNF-α和IL-6水平分别为(39.6±6.5)ng/L和(33.5±5.9)ng/L,显著低于对照组【分别为(48.7±7.6)ng/L和(40.6±4.3)ng/L,P<0.05】,而两组血清IL-10水平无显著性差异【(20.3±4.1)ng/L对(23.7±4.2)ng/L,P>0.05】;观察组DPV、DSV和SPT分别为(12.9±0.9)mm、(9.2±1.3)mm和(42.5±5.1)mm,与对照组【分别为(13.1±1.0)mm、(9.7±1.4)mm和(43.8±4.9)mm】比,差异无显著性意义(P>0.05)。结论 应用恩替卡韦联合复方甘草酸苷治疗乙型肝炎肝硬化患者能帮助改善肝功能,或可促进肠道菌群的恢复,值得进一步观察。     

聚乙二醇干扰素α-2b治疗慢性乙型肝炎患者外周血T淋巴细胞亚群和血清细胞因子水平变化*

目的 研究聚乙二醇干扰素α-2b治疗慢性乙型肝炎患者外周血T淋巴细胞亚群和血清细胞因子水平的变化。 方法 2014年1月~2016年1月我院收治的184例慢性乙型肝炎患者,92例接受聚乙二醇干扰素α-2b联合恩替卡韦治疗48 w,另92例只接受恩替卡韦治疗。使用流式细胞仪检测外周血T淋巴细胞亚群,采用放射免疫法检测血清IL-6、INF-ɑ、IL-4,采用酶联免疫吸附法检测血清IL-17、TGF-β1和HBV标记物,采用荧光定量PCR法检测血清HBV DNA、核转录因子RORγt、Foxp3、IL-17mRNA。 结果 在停药随访24 w,联合组与恩替卡韦组血清HBV DNA阴转率分别为86.96%和84.78%（P>0.05）;联合组血清HBeAg阴转率为28.89%（13/45）,与恩替卡韦组的15.22%（7/46）比,无显著性差异（P>0.05）;联合组血清ALT水平为（34.6±11.6） U/L,显著低于恩替卡韦组【（64.6±20.5） U/L,P<0.05】;联合组外周血CD3+、CD4+细胞和CD4+/CD8+比值分别为（75.6±14.5）%、（42.7±10.3）%和（1.4±0.6）,显著高于恩替卡韦组【（66.8±14.4）%、（36.7±8.5）%和（1.0±0.5）,P<0.05】,CD8+细胞百分比为（29.3±7.3） %,显著低于恩替卡韦组【（34.8±8.5） %,P<0.05】,两组NK细胞百分比比较无显著性差异（P>0.05）;治疗前两组血清IL-6、IL-17、IL-4、INF-ɑ、TGF-β1水平比较无显著性差异（P>0.05）,治疗后联合组血清IL-6水平为（6.8±1.2）pg/ml,显著高于恩替卡韦组【（3.5±0.8） pg/ml,P<0.05】,IL-17水平为（0.7±0.3） pg/ml,显著低于恩替卡韦组【（2.8±0.9） pg/ml,P<0.05】,IL-4水平为（1.4±0.5）pg/ml,显著低于恩替卡韦组【（3.8±1.5）pg/ml,P<0.05】,INF-ɑ水平为（4.0±1.3） pg/ml,显著高于恩替卡韦组【（2.6±0.9）pg/ml,P<0.05】,两组血清TGF-β1水平比较无显著性差异（P>0.05）;治疗前两组血清Foxp3、IL-17和RORγt mRNA水平比较无显著性差异（P>0.05）,治疗后联合组血清RORγt水平为（0.86±0.31）,显著低于恩替卡韦组【（1.56±0.43）,P>0.05】,而两组血清Foxp3和IL-17mRNA水平比较无显著性差异（P>0.05）。 结论 聚乙二醇干扰素α-2b能通过调控细胞因子和核转录因子水平,从多个环节调控慢性乙型肝炎患者免疫功能,发挥抗病毒作用。     

聚乙二醇干扰素α-2a联合恩替卡韦治疗慢性乙型肝炎患者疗效及血清Pygo2和GP73水平变化

目的 分析聚乙二醇干扰素α-2a联合恩替卡韦治疗慢性乙型肝炎(CHB)患者的疗效及血清人尾肢同源蛋白2(Pygo2)和高尔基体糖蛋白73(GP73)水平的变化。方法 2018年2月~2019年2月我院收治的77例CHB患者,采用随机数字表法分为对照组36例和观察组41例,分别给予恩替卡韦或恩替卡韦联合聚乙二醇干扰素α-2a治疗24 w。采用聚合酶链式反应检测血清HBV DNA,采用化学发光法检测血清HBeAg和抗HBe,采用ELISA法检测血清Ⅲ型前胶原(PCⅢ)、层粘连蛋白(LN)、透明质酸(HA)和Ⅳ型胶原(Ⅳ-C)及Pygo2和GP73水平。结果 在治疗结束时,两组血清HBV DNA转阴率均为100.0%,但观察组血清HBeAg转阴率为36.6%,显著高于对照组(19.4%,P<0.05),HBeAg血清转换率为22.0%,显著高于对照组(8.3%,P<0.05);观察组血清ALT水平为(32.3±13.5)U/L,显著低于对照组【(46.1±19.7)U/L,P<0.05】;观察组患者血清LN水平为(84.7±31.5)μg/L,显著低于对照组【(117.6±40.3)μg/L,P<0.05】,Ⅳ-C水平为(79.8±16.1)μg/L,显著低于对照组【(97.4±19.5)μg/L,P<0.05】,PC-Ⅲ水平为(94.5±21.2)μg/L,显著低于对照组【(140.8±29.7)μg/L,P<0.05】,和HA水平为(107.1±25.2)μg/L,显著低于对照组【(160.5±35.0)μg/L,P<0.05】;观察组患者血清Pygo2水平为(50.8±5.9)μg/L,显著低于对照组【(55.4±7.3)μg/L,P<0.05】,GP73水平为(108.6±10.6)ng/mL,显著低于对照组【(121.5±13.2)ng/mL,P<0.05】。结论 联合应用恩替卡韦和聚乙二醇干扰素α-2a治疗CHB患者可取得比单用恩替卡韦更好的短期疗效,可能与联合治疗能有效降低血清Pygo2和GP73水平,缓解肝纤维化进程,从而显著改善肝功能和提高了血清学应答有关。     

国产恩替卡韦治疗慢性乙型肝炎患者早期抗病毒疗效观察*

目的 比较国产恩替卡韦与合资恩替卡韦治疗不同病毒载量的慢性乙型肝炎（CHB）患者24周的疗效。方法 57例CHB患者接受国产恩替卡韦治疗,40例接受合资产恩替卡韦治疗。国产药物治疗患者中血清HBeAg阳性39例,血清HBV DNA水平≥1×106 IU/m1者38例,合资产药物治疗患者HBeAg阳性26例,高病毒载量者27例。采用实时荧光定量PCR法检测血清HBV DNA水平,采用微粒子发光法检测血清HBsAg和HBeAg水平。结果 治疗前两组间各指标比较无显著性差异。在治疗24 w末,国产和合资产恩替卡韦治疗患者血清HBsAg水平分别为（3651.7±1403.2）IU/ml和（3713.9±1117.5） IU/ml（P＞0.05）;血清HBeAg阴转率分别为17.9%和19.2%（P＞0.05）;在高病毒载量患者,24 w末血清HBV DNA水平分别为[lg （3.0±0.5）和lg （2.9±0.4）,P＞0.05];在低病毒载量患者,则分别为【lg （2.6±0.3）和lg （2.5±0.5）,P＞0.05】。结论 两种恩替卡韦在降低血清HBsAg水平、促进血清HBeAg阴转和抗病毒疗效等方面疗效确切,无显著性差异。     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Study of constancy of hydrogen-consuming flora of human colon

The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H₂-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.