血清学检测联合胃镜检查在青海胃癌高发地区早期胃癌筛查中的价值研究

目的评价血清胃蛋白酶原(PG)Ⅰ、PGR(PGⅠ/PGⅡ)及血清胃泌素(G17)水平检测联合胃镜检查在青海胃癌高发地区早期胃癌筛查中的应用价值。方法2014年10月至2019年10月,青海省4个胃癌高发区县8个自然村近25000人作为普查对象,通过问卷调查确定适龄目标人群(40~69岁)2700人,采用ELISA法检测血清PGⅠ、PGⅡ及G17水平并计算PGR(PGⅠ/PGⅡ),筛查出数值异常者949例作为胃癌高危人群并行胃镜检查及活检,根据胃镜及活检病理结果分成非萎缩性胃炎组、萎缩性胃炎组、消化性溃疡组、早期胃癌组、进展期胃癌组。观察不同胃黏膜病变中血清PGⅠ、PGR及G17表达水平,绘制受试者工作特征曲线(receiver-operator characteristic curve,ROC),计算PGⅠ、PGR及G17诊断早期胃癌、进展期胃癌的最佳临界值及其敏感度、特异度。结果胃镜检查949例,病理活检649例。检出非萎缩胃炎239例,萎缩性胃炎500例,消化性溃疡197例,胃癌13例(其中早期胃癌5例、进展期胃癌8例)。血清PGⅠ表达水平,早期胃癌组[(70.00±12.35)μg/L]、进展期胃癌组[(38.39±2.77)μg/L]明显低于非萎缩性胃炎组[(103.89±37.45)μg/L,P均<0.05],且早期胃癌组明显高于进展期胃癌组(P<0.05);PGR值早期胃癌组(3.74±1.40)、进展期胃癌组(2.05±0.59)明显低于非萎缩性胃炎组(9.18±4.10,P均<0.05),且早期胃癌组明显高于进展期胃癌组(P<0.05);血清G17表达水平,早期胃癌组[(18.03±4.52)pmol/L]、进展期胃癌组[(25.15±3.76)pmol/L]明显高于非萎缩性胃炎组[(14.99±7.12)pmol/L,P均<0.05],且早期胃癌组明显低于进展期胃癌组(P<0.05)。诊断早期胃癌的ROC分析显示,PGⅠ的最佳临界值为71.85μg/L,灵敏度和特异度分别为80.0%和59.0%;PGR的最佳临界值为5.04,灵敏度和特异度分别为100.0%和70.4%;G17的最佳临界值为15.65 pmol/L,灵敏度和特异度分别为80.0%和69.3%。诊断进展期胃癌的ROC分析显示,PGⅠ的最佳临界值为42.55μg/L,灵敏度和特异度分别为100.0%和95.3%;PGR的最佳临界值为2.79,灵敏度和特异度分别为100.0%和92.1%;G17的最佳临界值为20.55 pmol/L,灵敏度和特异度分别为100.0%和89.7%。结论通过血清学检测筛查出胃癌高危人群,然后对高危人群行胃镜及活检确诊,不仅可以提高早期胃癌的诊断率,而且可以节约医疗资源,是一种经济、高效的可行性方案,适合在青海省胃癌高发区推广使用。     

检测血清胃蛋白酶原和胃泌素-17诊断胃癌的临床价值

目的通过测定血清胃蛋白酶原(PG)Ⅰ、PGⅡ、胃泌素-17(G-17)和H.pylori-IgG抗体来预测胃癌高危,提高胃癌早诊率。方法本研究采用观察性病例-对照研究,共310例受检者纳入研究。在作血清试验前,所有患者均在胃镜下作多处活检,并根据病理结果将受检者分为胃癌组(141例,其中早期胃癌40例、进展期胃癌101例)、正常组(77例)和萎缩性胃炎组(92例)。每一例均用酶联免疫吸附试验(ELISA)定量测定空腹血清PGⅠ、PGⅡ和G-17,定性测定H.pylori-IgG抗体。结果PGⅠ和PGR(PGⅠ/PGⅡ)水平在胃癌组(28.74±11.55μg/L,1.66±1.01)明显低于正常组(123.99±32.25μg/L,10.09±1.89)和萎缩性胃炎组(58.63±25.35μg/L,4.36±2.57)(均P<0.01),根据接受者操作特征曲线(ROC)计算PGⅠ和PGR诊断胃癌的最佳界值分别为57.15μg/L(灵敏度99.3%,特异度84.5%)和2.99(灵敏度92.5%,特异度89.0%);而G-17水平胃癌组(20.86±8.24pmol/L)明显高于正常组(10.39±9.25pmol/L)和萎缩性胃炎组(8.59±6.08pmol/L)(均P<0.01)。根据ROC曲线计算G-17的最佳界值为14.61pmol/L(灵敏度75.2%,特异度71.3%)。进展期胃癌的PGⅠ和PGR水平较早期胃癌明显降低(P<0.01),而G-17差别不明显。萎缩性胃炎组和胃癌组的H.pylori-IgG抗体阳性率均明显高于正常组(P<0.01)。结论结合G-17水平明显升高而PGⅠ、PGR水平显著低下可作胃镜进行胃癌筛查,有助于提高胃癌早诊率。     

新型胃癌筛查评分系统对本地区早期胃癌患者的筛查价值

背景:早期胃癌的预后明显优于晚期胃癌,但由于缺乏完善的普查手段,导致早期胃癌检出率较低。血清胃蛋白酶原Ⅰ(PGⅠ)、PGⅡ、胃泌素-17(G-17)可用于早期胃癌的筛查。目的:探讨新型胃癌筛查评分系统对本地区早期胃癌患者的筛查价值。方法:纳入2017年4月—2018年12月收治的393例患者,依据病理结果分为对照组、胃溃疡组、异型增生组和早期胃癌组,检测PGⅠ、PGⅡ、G-17浓度、Hp抗体,并计算PGR。采用ROC曲线分析各指标筛查早期胃癌的价值。比较新型胃癌筛查评分系统、血清ABC法、新ABC法对早期胃癌的检出率。结果:与对照组相比,胃溃疡组PGⅠ、PGⅡ升高,PGR降低(P 0. 05);异型增生组和早期胃癌组PGⅡ、G-17升高,PGⅠ、PGR降低(P 0. 05)。与胃溃疡组相比,异型增生组PGⅠ、PGⅡ和PGR均降低(P 0. 05),早期胃癌组PGⅠ、PGR降低,G-17升高(P 0. 05)。PGⅠ、PGⅡ、G-17、PGR筛查早期胃癌的AUC分别为0. 858、0. 744、0. 791、0. 937。PGⅠ、G-17、PGR的临界值分别为≤68. 46μg/L、 12. 80 pmol/L和≤6. 90,三者联合的敏感性为90. 6%,特异性为91. 1%,AUC为0. 965。新型胃癌筛查评分系统对早期胃癌高风险人群的检出率显著高于血清ABC法(P 0. 05),而与新ABC法无明显差异(P 0. 05)。结论:血清PGⅠ、PGR明显降低且G-17升高提示可能发生早期胃癌。新型胃癌筛查评分系统对早期胃癌的筛查效率较高。     

血清G-17、PG Ⅰ、PG Ⅱ、Hcy在胃黏膜癌变进展中的表达及临床意义

背景早期胃癌阶段机体多项血清因子异常,其中血清胃泌素-17(gastrin-17, G-17)、胃蛋白酶原Ⅰ(pepsinogenⅠ, PG Ⅰ)、胃蛋白酶原Ⅱ(pepsinogenⅡ, PGⅡ)、同型半胱氨酸(homocysteine, Hcy)广受临床关注,推测四者联合检测可作为早期胃癌的诊断参考依据.目的检测血清G-17、PG Ⅰ、PG Ⅱ、Hcy在早期胃癌中的表达水平,并分析其对早期胃癌诊断的临床价值.方法回顾性分析本院230例高度怀疑为胃癌的患者的临床资料,根据胃镜及病理诊断结果将患者分为胃良性病变组(136例),早期胃癌组(53例),进展期胃癌组(41例).另回顾性分析同期118例健康受试者的临床资料,将其设置为健康组.比较4组血清G-17、PG Ⅰ、PGⅡ、Hcy水平;对比胃癌组、非胃癌组可能影响因素的差异,并采用Logistic回归分析法分析导致胃癌的危险因素;通过绘制受试者工作曲线(receiver operating curve, ROC),分析血清G-17、PG Ⅰ、PG Ⅱ、Hcy单独及联合检测对早期胃癌、进展期胃癌的诊断价值.结果进展期胃癌组、早期胃癌组、胃良性病变组、健康组血清G-17、PG Ⅱ、Hcy呈降低趋势(P0.05),血清PGI呈升高趋势(P 0.05),组间比较差异均有统计学意义(P0.05);胃癌组喜食烫食占比、高盐饮食占比,血清G-17、PG Ⅱ、Hcy水平均显著高于非胃癌组,血清PG Ⅰ显著低于非胃癌组(P0.05),经Logistic回归分析证实均为导致胃癌的危险因素; ROC结果显示,血清G-17、PG Ⅰ、PG Ⅱ、Hcy单独检测诊断早期胃癌的最佳截断点分别为13.46 pmol/L、60.98 ng/m L、27.56 ng/m L、23.01μmol/L,曲线下面积(area under the curve, AUC)分别为0.71、0.70、0.71、0.78、0.83;血清G-17、PG Ⅰ、PG Ⅱ、Hcy单独检测诊断进展期胃癌的最佳截断点分别为18.53 pmol/L、47.56 ng/m L、28.41ng/m L、27.63μmol/L, AUC分别为0.71、0.68、0.73、0.75、0.80.结论血清G-17、PG Ⅱ、Hcy在早期胃癌中呈异常高表达,血清PG Ⅰ呈异常低表达,四者联合检测对早期胃癌的诊断具有一定临床价值.     

胃蛋白酶原联合智能染色内镜对早期胃癌的诊断

[目的]探讨以时间分辨荧光免疫法测定血清胃蛋白酶原PG Ⅰ、PGⅡ以及PG Ⅰ/PGⅡ比值作为第一步筛查手段,联合智能染色内镜(i-Scan)筛查早期胃癌的诊断价值.[方法]入选患者在知情同意前提下随机行胃蛋白酶原检测,发现异常者,即行i-Scan检查,可疑病灶应用i-Scan引导的“靶向活检”,依据病理结果明确病变性质.根据胃镜检查及病理学结果,将受检者分为7组:胃溃疡组29例,慢性萎缩胃炎组50例,慢性浅表性胃炎组88例,早期胃癌组8例,进展期胃癌组22例,胃手术组19例,健康体检者46例为对照组.根据文献报道的胃良性病变的PG Ⅰ、PG Ⅰ/PGⅡ比值参考值范围,比较各组PG Ⅰ、PG Ⅰ/PGⅡ的变化.[结果]胃溃疡组患者血清PG Ⅰ及PGⅡ比对照组升高,PG Ⅰ/PGⅡ比值降低(P＜0.05).慢性浅表性胃炎组较对照组PG Ⅰ下降,PG Ⅰ/PGⅡ比值降低.早期胃癌组、进展期胃癌组血清PG Ⅰ及PG Ⅰ/PGⅡ比值较对照组及慢性浅表性胃炎组均显著降低(P＜0.05),早期胃癌组与进展期胃癌组相比PG Ⅰ及PG Ⅰ/PGⅡ比值均差异无统计学意义(P＞0.05).胃手术组PGⅠ值较对照组降低,PG Ⅰ/PGⅡ值降低(P＜0.05).与慢性浅表性胃炎组、对照组比较,萎缩性胃炎组、早期胃癌组、进展期胃癌组PG Ⅰ ＜60μg/L和PG Ⅰ/PGⅡ比值≤6患者出现概率增高(P＜0.05).[结论]血清PG Ⅰ、PGⅡ值及比值下降与胃癌早期发生密切相关.时间分辨荧光免疫分析法测定血清PG可作为人群胃癌的普查手段,无创,简便;胃蛋白酶原联合i Scan可提高胃癌早期诊断率.     

老年患者胃黏膜病变与血清胃蛋白酶原变化

目的探讨老年胃疾病患者胃黏膜病理改变过程中，血清胃蛋白酶原（PG）Ⅰ、Ⅱ的变化规律。方法选择我院消化内镜中心行胃镜检查老年患者306例，按病理诊断标准分为4组：非萎缩性胃炎组（对照组）40例。慢性萎缩性胃炎组95例，消化性溃疡组105例，胃癌组66例。用免疫放射法（IEMA）测定患者血清PGⅠ及PGⅡ，并计算PGⅠ／PGⅡ的比值（PGR）。结果（1）正常对照组PGⅠ为（150．17±63．51）μg／L，PGR为10、44±3．42。（2）与对照组比较，慢性萎缩性胃炎患者血清PGI降低为（118．81±40．99）μg／L，PGR降低为7．11±2．99（P〈0.05）；（3）胃癌患者血清PGI降低为（95．39±22、80）μg／L，PGR降低为5．86±3．87（P〈0．01）；（4）消化性溃疡患者血清PGⅠ（175．29±33、69）μg／L及PGⅡ（21．81±8．91）μg／L升高（P〈0．05）。结论血清PGⅠ、PGⅡ含量的变化及PGR值对癌前状态和早期胃癌的诊断具有重要的临床意义，当血清PGⅠ及PGⅡ严重降低时，应及时进行胃镜检查，以明确诊断。     

血清胃蛋白酶原诊断胃癌的临床价值

目的 探讨血清胃蛋白酶原（PG）诊断胃癌的临床价值.方法 选择非萎缩性胃炎患者36例（非萎缩性胃炎组）、胃溃疡患者39例（胃溃疡组）、萎缩性胃炎患者31例（萎缩性胃炎组）及胃癌患者42例（胃癌组）,采用胶乳增强免疫比浊法检测其血清PG Ⅰ、PGⅡ水平,计算PG Ⅰ/PGⅡ（PGR）.结果 非萎缩性胃炎组、胃溃疡组、萎缩性胃炎组及胃癌组的血清PG Ⅰ水平及PGR值逐渐降低,以胃癌组降低最明显,显著低于其他三组（P均＜0.01）;胃溃疡组血清PGⅡ水平显著高于其他三组（P均＜0.01）,其他三组血清PGⅡ水平比较差异无统计学意义（P均＞0.05）.以PG Ⅰ＜70 μg/L＋ PGR＜ 3.0为判断界值,其诊断胃癌的敏感性为78.6％、特异性为85.8％.结论 血清PG Ⅰ水平及PGR明显降低可作为胃癌及癌前病变的一项血清学诊断指标.     

老年胃黏膜病变患者血清胃蛋白酶原变化

目的 探讨老年胃疾病患者胃黏膜病理改变过程中,血清胃蛋白酶原(PG)Ⅰ、Ⅱ的变化规律.方法 选择我院消化内镜中心行胃镜检查老年患者276例,按病理诊断标准分为4组,非萎缩性胃炎组(对照组)34例,慢性萎缩性胃炎组(胃炎组)71例,消化性溃疡组(溃疡组)105例,胃癌组66例.用免疫放射法(IRMA)测定患者血清PGⅠ及PGⅡ,并计算PGⅠ/PGⅡ的比值(PGR).结果 对照组PG Ⅰ、PG Ⅱ和PGR分别为(149.26±62.45)/μg/L、(15.66±8.97)μg/L和10.62±3.30,慢性萎缩性胃炎组PG Ⅰ[(119.32±41.87)μg/L]、PGR(7.19±3.02)较对照组降低(P＜0.05),胃癌组PG Ⅰ[(95.39±22.80)μg/L]、PGR(5.86±3.87)较对照组明显降低(P＜0.01);溃疡组PG Ⅰ[(175.29±33.69)μg/L]、PGⅡ[(21.81±8.91)μg/L]较对照组升高(P＜0.05).结论 血清PGⅠ、PGⅡ含量的变化及PGR对癌前状态和早期胃癌的诊断具有重要的临床意义,当血清PGⅠ及PGR严重降低时,应尽早进行胃镜检查,以明确诊断.     

辽宁庄河地区居民血清胃蛋白酶原含量检测分析

目的 检测辽宁庄河居民血清胃蛋白酶原（PG）含量，以明确其基本人群分布特征，并探讨相关影响因素。方法 利用酶联免疫吸附试验（ELISA）方法对辽宁庄河地区6990名居民进行血清PGI、PGⅡ含量检测，并计算PGI／Ⅱ比值；利用胃镜及胃黏膜组织病理学检查进行胃疾病诊断；利用ELISA法检测血清幽门螺杆菌（Hp）IgG抗体滴度。结果 辽宁庄河地区居民血清PGⅠ、PGⅡ及PGI／Ⅱ中位值分别为86．9μ／L、10．6μg／L和8．1。男性血清PGⅠ、PGⅡ（95．2μg／L、12．1μ／L）显著高于女性（79．7μg／L、9．4μg／L；P=0．000），PGⅠ／Ⅱ（7．9）显著低于后者（8．3，P=0．000）。PGI／Ⅱ随年龄增高呈阶段性显著降低。PGⅠ／Ⅱ在胃黏膜由基本正常（10．4）向非萎缩性病变（8．8）、萎缩性病变（6．6）转变过程中呈显著性降低。Hp感染者血清PGⅠ、PGⅡ（88．7μg／L，11．4μg／L）显著高于非感染者（81．4μg／L，8．4μg／L；P=0．000），PGⅠ／Ⅱ（7．7）显著低于后者（9．6，P=0．000）。以PGⅠ／Ⅱ为指标筛选胃黏膜萎缩性病变，ROC曲线下面积为0．622，最适临界值为6．9，灵敏度53．2％，特异度67．5％。多因素Logistic回归分析，男性（OR：1．151，95％CI：1．042～1．272，P=0．006）、年龄≥61岁（OR：1．358，95％CJ：1．188～1．553，P=0．000）、萎缩性病变（OR：2．075，95％CI：1．870～2．302，P=0．000）及Hp感染（OR：1．546，95％CI：1．368～1．748，P=0．000）是明显影响PGⅠ／Ⅱ水平的因素。结论 辽宁庄河居民血清PG水平呈明显偏态分布，受性别、年龄因素影响，与胃疾病和Hp感染密切相关。PGⅠ／Ⅱ较之PGⅠ和PGⅡ，更适用于胃疾病筛查。     

血清胃蛋白酶原检测在慢性萎缩性胃炎筛查中的价值

目的探讨血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅰ/胃蛋白酶原Ⅱ(PGⅠ/PGⅡ)比值(PGR)与慢性萎缩性胃炎的关系,确定其在萎缩性胃炎中的变化规律。方法选择在我院消化科行胃镜检查符合入选研究标准的200例患者,根据组织病理学诊断结果分为慢性非萎缩性胃炎组(135例)和慢性萎缩性胃炎组(65例)。采用化学发光方法定量测定空腹血清PGⅠ、PGⅡ,并计算PGⅠ/PGⅡ比值(PGR)。结果慢性萎缩性胃炎组与非萎缩性胃炎组血清PGⅠ分别为(78.55±15.42)μg/L和(130.51±55.23)μg/L,有显著差异(P<0.05)。PGR分别为4.09±2.15和8.95±5.18,显著差异(P<0.05);以PGⅠ≤70μg/L且PGR≤3.0为界值来计算诊断慢性萎缩性胃炎的敏感性和特异性分别为72.3%和93.3%。结论检测血清PG及PGR可用于慢性萎缩性胃炎的筛查,如有异常,应进一步行胃镜检查以确诊并指导治疗。     

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。     

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。     

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。     

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.     

治疗高血压药物的经济学评价

重视高血压治疗中的经济学评价,对利用我国有限的卫生资源来遏制高血压对人民群众的危害有着重要的现实意义。药物经济学对于药物治疗的成本和治疗的结果给予同样的关注。因为治疗高血压的费用,不仅涉及药物价格,还包括患者的危险水平,降压疗效和对临床终点事件的影响,以及治疗的依从性和安全性。因此药物经济学更强调整体成本和价-效比。低危病人,若非药价低廉,治疗的价-效比不够理想。而在高危的患者,价-效比越小越经济而不是药费越便宜越好。