病毒性肝炎患者1055例中巨细胞病毒活动性感染的研究

对1992年4～11月入院的急性病毒性肝炎散发病例,用ELISA捕捉法测定急性期抗CMV-IgM与IgG。结果:患者1055例中抗CMV-1gM(+)37例,占3.51％,次于甲肝48.62％,乙肝44.26％,高于戊肝3.13％、丁肝3.02％、丙肝1.14％。排列病毒性肝炎病原谱第三位。在肝炎各类型分布中,重肝18.18％,慢活肝13.33％,慢迁肝3.86％,急肝1.34％,肝硬化未检出。37例患者中,原发感染1例,再发感染36例。随机抽查125例不同年龄肝炎患者,其抗CMV-IgG(+)109例,阳性率87.2％,抗体GMT372。由于感染普遍,对于成人患者CMV感染多为再发而极少原发。本文37例CMV感染者均为合并感染。合并感染有5种模式,即乙、巨二重12例,乙、丁、巨三重15例,甲、乙、巨三重3例,甲、乙、丁、巨四重4例,乙、丙、丁、巨四重3例。5种模式均有HBV存在,机体免疫功能下降是乙肝病人临床多发主要原因,反过来CMV感染进一步加重机体免疫功能抑制,这就构成恶性循环。在有丁肝合并感染22例患者中(占59.46％),慢活肝(63.64％)与重肝(9.09％)比例较大,合并感染无疑会加重病情变化。     

PCR技术诊断巨细胞病毒宫内感染的临床价值

采用聚合酶链反应（ＰＣＲ）技术及酶联免疫吸附试验（ＥＬＩＳＡ）法对６６例血清抗居细胞病毒抗体ＩｇＭ（ＣＭＶ－ＩｇＭ）阳性孕妇的新生儿脐血进行了巨细胞病毒脱氧核糖核酸（ＣＭＶ－ＤＮＡ）与ＣＭＶ－ＩｇＭ检测。结果显示，其ＣＭＶ－ＤＮＡ阳性率明显高于ＣＭＶ－ＩｇＭ阳性率，差异非常显著。表明用ＰＣＲ技术检测胎儿脐血ＣＭＶ－ＤＮＡ有助于巨细胞病毒（ＣＭＶ）宫内感染的早期诊断，且ＣＭＶ宫内感染影响胎儿发生发育     

巨细胞病毒与乙肝病毒持续感染的关系

对感染乙型肝炎病毒(HBV)的个体中巨细胞病毒(CMV)感染的情况进行研究。选取HBV慢性感染或携带者99例,康复组121例,健康对照组60例。分别测定血清CMV-IgG抗体、尿中CMV-DNA及各组相关的生化指标。结果:持续感染组ALT、AST、TBA、Glob高于康复组和正常对照组(P<0．01)。其它指标各组间差异均不显著;三组CMV-IgG阳性率均在95％以上,无显著差异。取对照组中CMV-IgG阳性者的OD均值0．3做为强阳性的cut-off值,三组的CMV-IgG强阳性率分别是65％、51％和40％,持续感染组高于康复组和对照组;三组CMV-DNA扩增结果分别为3例、2例和1例,差别不显著。在受检对象中,按CMV-IgG强阳性与否分组,对HBV的持续感染率进行统计,HBV的持续感染率CMV-IgG强阳性组43％,显著高于非强阳性组27％(P< 0．01)。提示CMV-IgG强阳性是HBV持续感染的危险因素。     

免疫功能低下宿主巨细胞病毒肺炎

巨细胞病毒是引起免疫功能低下宿主肺部感染最常见的病原之一,在临床上起病急、进展快,如不能及时诊断和干预,往往会在短期內发展为急性肺损伤甚或急性呼吸窘迫综合征及多器官功能衰竭,病死率高,预后差.实验室病毒学检测对早期诊断具有重要作用.在治疗上除了对症支持、保证氧合外,早期应用更昔洛韦抗病毒联合静脉丙种球蛋白,在一定程度上可改善预后,降低病死率.除非有明确细菌感染的指征或有创呼吸治疗,一般不主张给予联合抗生素治疗,以避免治疗进一步复杂化.     

非肝病及慢性乙型肝炎患者肝组织中巨细胞病毒的检测

目的：探讨巨细胞病毒（CMV）在非肝病患者及慢性乙型肝炎患者肝组织中的表达、分布特点及相关关系。方法：采用免疫组化方法以抗－CMV单克隆抗体对31例非肝病及76例慢性乙型肝炎肝组织进行检测，用抗－HBcAg多克隆抗体和抗－CMV单克隆抗体双标记技术在部分慢性乙型肝炎患者同一张肝组织切片上显示两种病毒分布特点。结果：31例非肝病肝组织中检出CMV Ag7例（22．6％），明显低于慢性乙型肝炎患者（43／76，56．6％），P＜0．01。在两组标本中CMV Ag均在肝细胞胞浆内表达。非肝病患者肝组织中阳性细胞数量较慢性乙型肝炎患者少，后者阳性细胞多近汇管区分布，数量多时，也可在肝小叶内弥漫分布。轻度和重度慢性乙型肝炎患者中CMV的检出率比较，差异无显著性，但慢性乙肝炎患者中CMV表达阳性细胞明显多于轻度慢性乙型肝炎（P＜0．05）。双标记染色显蒜CMV Ag和HBcAg多数可表达于肝小叶内同一区域肝细胞甚至同一肝细胞内，也可见于肝小叶中不同部位。结论：非肝病患者中CMV感染并不少见，慢性乙肝炎患者更易重叠CMV感染，并且其感染程度与肝组织的活动性病变密切相关。     

巨细胞病毒感染的免疫应答

巨细胞病毒 (Ｃｙｔｏｍｅｇａｌｏｖｉｒｕｓ ,ＣＭＶ)是疱疹病毒科 β属的ＤＮＡ病毒 ,在自然界中广泛存在 ,正常人群中自然感染普遍 ,发达国家人群血清ＣＭＶ抗体检出率约 4 0 %～ 6 0 % ,发展中国家超过 90 % [1] 。人是人类ＣＭＶ的唯一宿主 ,可累及肺、肾、肝、肠道、视网膜等脏器 ,无临床症状者称无症状性ＣＭＶ感染 (或隐性ＣＭＶ感染 ) ,出现临床症状者称症状性ＣＭＶ感染或ＣＭＶ病。健康人群ＣＭＶ感染多为隐性感染或症状轻微 ,在新生儿、器官移植受者、爱滋病等免疫功能低下的人群 ,ＣＭＶ感染可引起严重临床症状 ,如致命的间质…     

催化信号扩增法检测人巨细胞病毒被膜磷蛋白65的实验分析

目的建立一种新型的快速诊断肾移植受者人巨细胞病毒（HCMV）活动性感染的方法。方法采用免疫组织化学催化信号扩增法，通过抗HCMV被膜磷蛋白65（pp65）单克隆抗体AAC10对外周血WBC中的HCMVpp65抗原进行标记识别，并与荧光定量PCR（FQ-PCR）方法进行比较。结果检测的102例肾移植受者中，血浆HCMVDNA阳性66例，HCMVpp65抗原阳性56例，血浆HCMVDNA阴性患者中无pp65阳性，两种方法检测的符合率为90．2％，相关性好（r=0．831）；HCMV病患者31例，两者均阳性；同时检测40名健康者，结果pp65抗原全为阴性。结论催化信号扩增法敏感、简便，能更准确地反映HCMV感染的活动状况，有助于肾移植术后HCMV病的早期诊断，并可指导抗病毒治疗。     

人巨细胞病毒先天感染小鼠大脑皮质的病理学特征

目的　研究人巨细胞病毒（ Ｈ Ｃ Ｍ Ｖ） 经小鼠胎盘垂直传播致胎鼠大脑皮质感染的病理学特征。方法　在８ ～１２周龄 Ｂ Ａ Ｌ Ｂｃ 雌雄小鼠腹腔内接种 Ｈ Ｃ Ｍ Ｖ 后, 交配, 待孕鼠妊娠第７ 天及临产时处死动物; 无菌将雌胎鼠双侧大脑皮质取出, 应用常规组织切片 Ｈ Ｅ 染色、脑压印片地高辛标记 Ｈ Ｃ Ｍ Ｖ 寡核苷酸探针原位杂交及病毒分离的方法进行检测分析。结果　组织学检查发现, 雌、胎鼠脑微血管扩张充血, 脑实质有中性粒细胞和单核细胞浸润, 部分神经细胞已变性坏死。在胎鼠脑组织切片上, 还可见到软化灶及受染神经细胞核内 Ｈ Ｃ Ｍ Ｖ 特征性嗜碱性包涵体。原位杂交显示, 病毒核酸存在于待产胎鼠脑神经细胞及胶质细胞核内及胞浆内。在胎鼠脑组织悬液中分离出该病毒。结论　 Ｈ Ｃ Ｍ Ｖ 能通过 Ｂ Ａ Ｌ Ｂｃ 小鼠胎盘致发育中子鼠大脑皮质感染, 发生侵袭性脑膜脑炎性病理改变。     

Insulin degludec in the first trimester of pregnancy: Report of two cases

Insulin degludec is an extra‐long‐acting insulin analog that allows for enhanced efficacy and flexibility in the injection time. However, it is not approved for use during pregnancy. We report the pregnancy outcome and newborn conditions in two women with type 1 diabetes who continued preconception degludec treatment during embryogenesis. No pregnancy complication or congenital neonatal malformation was observed. Both babies presented with hypoglycemia and required neonatal intensive care unit admission. Degludec treatment did not cause adverse effects in the mothers or malformations in the newborns. The observed neonatal complications were probably independent of early pregnancy degludec treatment.     

肾移植术后巨细胞病毒肺炎的临床研究

目的:探讨肾移植术后巨细胞病毒(CMV)肺炎的临床特点及诊疗对策。方法:回顾34例肾移植术后CMV肺炎患者临床资料,总结临床特点和治疗措施。结果:34例患者,治愈30例,占88.24%,死亡4例(其中放弃治疗后死亡2例)。治愈患者除1例出现移植肾排斥反应外,其余功能均正常。高剂量更昔洛韦联用糖皮质激素组,在需使用呼吸机几率和死亡率方面均低于未使用糖皮质激素的常规剂量更昔洛韦组(P=0.045和0.010)。结论:早期及时诊断,适时适量应用激素,足剂量长疗程抗病毒治疗,及早进行高流量给氧或辅助呼吸等综合治疗是提高治愈率、降低病死率的关键。     

孕妇妊娠早期甲状腺功能及碘营养状况

目的 探讨全民食盐加碘后孕妇妊娠早期甲状腺功能及碘营养状况。方法 选择单纯食用合格碘盐补碘的60名孕妇作为研究组，于妊娠12～15周采集血、尿标本，化学发光免疫分析法测定血清FT3、FT4和TSH水平，放射免疫分析法测定血清TMAb和TGAb水平，酸消化砷铈接触分光光度法测定尿碘水平，与60名该地区非妊娠健康女性进行比较。结果 (1)研究组孕妇血清FT3、FT4水平高于对照组，血TSH水平低于对照组，差异具有显著性；(2)研究组孕妇血清TMAb和TGAb水平低于对照组，差异具有显著性；(3)研究组孕妇尿碘中位数为117．60μg／L，低于WHO推荐值。结论 全民食盐加碘后，孕妇甲状腺功能得到明显改善，但单纯食用碘盐不能满足孕妇任娠期生理需求，需要特别给予补充。     

The effect of late-onset CMV infection on the outcome of renal allograft considering initial graft function

Background

Delayed graft function (DGF) increases the renal allograft failure risk. Late-onset Cytomegalovirus (CMV) infection's effect on the association between DGF and allograft failure has not been determined.

Methods

In this retrospective cohort, we included all renal allograft recipients at London Health Sciences Centre from January 1, 2014 to December 30, 2017, and continued clinical follow-up until February 28, 2020. We determined whether late-onset CMV infection affects the association between DGF and allograft failure in stratified and Cox proportional hazard analyses.

Results

Of 384 patients (median age [interquartile range]: 55 [43.3–63]; 38.7% female), 57 recipients (14.8%) were diagnosed with DGF. Patients with DGF were at a greater risk of CMV infection than patients without DGF (22.8% vs. 11.3%, p = .017). Late-onset CMV infection (odds ratio [OR]: 4.7, 95% CI: 2.07–10.68) and rejection (OR: 9.59, 95% CI: 4.15–22.16) significantly increased the risk of allograft failure in recipients with DGF. Patients with DGF had a significantly greater risk of graft failure than those without DGF (17.5% vs. 6.1%, p = .007). In the adjusted Cox hazard model, CMV infection significantly increased the risk of allograft failure (aHR: 3.19, 95% CI: 1.49–6.84).

Conclusion

Late-onset CMV infection considerably increased the risk of graft failure in patients with DGF. A hybrid preventive model including prophylaxis followed by CMV-specific cell-mediated immunity monitoring may decrease the risk of allograft failure in recipients with DGF.

     

造血干细胞移植后巨细胞病毒感染患者糖蛋白B基因分型的初步研究

目的初步探讨造血干细胞移植(HSCT)后巨细胞病毒(CMV)感染患者CMV糖蛋白(G)B基因分型及其与致病性的关系。方法研究了2001年3月至2003年12月在我院行HSCT的患者38例,均采用巢式PCR方法检测CMV GBDNA为阳性,对PCR产物用RsaⅠ和HinfⅠ内切酶进行了酶切分型。结果Ⅰ型19/38例(50.0%),Ⅱ型3/38例(7.9%),Ⅲ型14/38例(36.8%),Ⅰ与Ⅲ混合型2例。Ⅰ型感染预后良好,Ⅲ型与致死性间质性肺炎(IP)发生有明显的相关性。Ⅰ、Ⅲ型患者移植物抗宿主病(GVHD)的发生率差异无统计学意义。结论CMVGB蛋白的基因分型与CMV的IP发生有关,与GVHD的发生无明显相关性。     

Liver biopsy for visceral leishmaniasis diagnosis in pregnancy: report of 2 cases

Visceral leishmaniasis (VL) or kala-azar is a zoonosis caused by intracellular protozoa of the Leishmania genus and is transmitted to humans by the bite of phlebotomine sandflies. It particularly affects cells in the phagocytic mononuclear system, accompanied by disturbances of cellular and humoral immunity. VL is potentially fatal and is characterized by fever, hepatosplenomegaly, diarrhea, epistaxis, jaundice, anemia, leucopenia, thrombocytopenia, hypoalbuminemia and hyperglobulinemia. Diagnostic suspicion is based on epidemiological, clinical and laboratory data and is confirmed by detecting the parasite in infected tissue. Splenic aspiration is the most sensitive method, followed by bone marrow aspiration (BMA) by sternal puncture, liver biopsy and lymph node aspiration; but, due to safety concerns, BMA is the most recommended method. VL is included as a target disease by players in drug research and development. Severe liver dysfunction associated with VL is uncommon. We report two VL cases in pregnant women from Bauru, Sao Paulo state, Brazil, considered an endemic area. The first of them developed hepatic failure due to fulminant hepatitis. In both cases, BMA was unable to find the protozoan; thus, liver biopsy was the only means of making the diagnosis.     

流式细胞术检测PP65抗原血症诊断巨细胞病毒性肝炎

巨细胞病毒（CMV）性肝炎是新生儿及免疫抑制状态下人群较常见和严重的疾病之一,常并发肝外脏器感染,引起多脏器功能损伤.早期、特异地诊断活动性CMV感染,已成为监测其感染、早期抗病毒治疗的关键.本研究通过流式细胞术对CMV性肝炎患者进行低基质磷脂蛋白65（PP65）抗原血症测定,并同时定量测定尿CMV DNA及血CMV-IgM,以探讨流式细胞术检测PP65抗原血症对CMV性肝炎的诊断价值.     

Successful primary percutaneous coronary intervention in the first trimester of pregnancy

A 28‐year‐old patient, medical nurse, in 10th week of her second pregnancy suffered ventricular fibrillation just after entering the waiting room of the emergency department. After she was successfully defibrillated, electrocardiography revealed a large acute anteroseptolateral ST elevation myocardial infarction. Urgent coronarography was done (premedication with 300 mg of aspirin and 600 mg of clopidogrel) with 90 min door‐to‐balloon time. Proximal left anterior descending occlusion was found, primary percutaneous coronary intervention was done using Amazonia CroCo 3.0/12 bare‐metal stent, and Thrombolysis in Myocardial Infarction III flow was achieved. During the procedure, the patient was wrapped in lead apron. Because of postresuscitational agitation, procedure was done in intravenous anesthesia. The revealed risk factors were smoking and hypercholesterolemia. PAI‐1 gene 4G/4G genotype and Apo E gene E2/E4 genotype were also found. Estimated X‐ray dosage that fetus received during the procedure was 0.45 mSv, which is less than the upper safe limit in pregnancy. All drugs given to our patient (clopidogrel, aspirin, ivabradine, bisoprolol, anesthetics, low‐molecular‐weight heparin, and unfractionated heparin) have B or C Food and Drug Administration Pregnancy Category. Fetal ultrasonography showed normal fetal growth, and, after consultation with our team, the patient decided to maintain the pregnancy. Before discharge echocardiography showed left ventricle of normal size with anteroseptolateral hypokinesia, small apical aneurysm, left ventricular ejection fraction of 40–45%, and diastolic dysfunction grade II, without pulmonary hypertension. At the 36th week of pregnancy, the patient was hospitalized and closely monitored; clopidogrel and aspirin were discontinued, and low‐molecular‐weight heparin was administered. She gave birth to a normal boy by vaginal delivery with epidural anesthesia and without any complication. © 2010 Wiley‐Liss, Inc.     

Fetal RHD genotyping in maternal serum during the first trimester of pregnancy

Fetal RHD genotype determination is useful in the management of sensitized RhD-negative pregnant women. It can be ascertained early during pregnancy by chorionic villus sampling (CVS) or amniocentesis. However, these procedures are invasive, resulting both in an increased risk of fetal loss and in an increased severity of immunization due to fetomaternal haemorrhage. A reliable determination of RHD genotype by fetal DNA analysis in maternal serum during the first trimester of pregnancy is reported in this study. One hundred and six sera from RhD-negative pregnant women were obtained during the first trimester of pregnancy. These sera were tested for the presence of RHD gene using a new real-time polymerase chain reaction assay and the results compared with those obtained later in pregnancy on amniotic fluid cells and by RHD serology of the new-born. All sera from women carrying a RhD-positive fetus (n = 62) gave positive results for RHD gene detection and sera from women carrying a RhD-negative fetus (n = 40) were negative. The high level of accuracy of fetal RHD genotyping obtained in this study could enable this technique to be offered on a routine basis for the management of RhD-negative patients during the first trimester of pregnancy.