AIDS并发巨细胞病毒性视网膜炎

目的探讨艾滋病(AIDS)并发巨细胞病毒(CMV)性视网膜炎的临床特点和治疗转归.方法观察分析北京协和医院确诊为AIDS并发CMV视网膜炎的5例患者的临床和实验室资料、治疗转归.结果 5例CMV视网膜炎患者的9只眼均经眼底散瞳检查确诊.全部患者均为AIDS晚期患者,CD+4T淋巴细胞计数3～36/mm3,在确诊CMV视网膜炎时均已合并其它机会性感染.平均年龄29.2±5.1岁.临床症状有视物模糊、视力下降等.眼底检查有典型的视网膜血管炎,表现为沿血管分布的黄白色病损、黄白色颗粒及视网膜出血,但玻璃体透明或轻微混浊.4例接受更昔洛韦(GCV)治疗的患者病情均得到控制,眼底病变消退,但其中1例视力丧失(失明)无法恢复;1例患者未特殊治疗死于多种机会感染.结论中国CMV视网膜炎的表现和国外文献报道的类似,多发生于晚期AIDS患者,不及时治疗将导致视力丧失,早期诊治非常重要.建议对于CD+4 T细胞计数<50/mm3以及存在眼外CMV感染的AIDS患者,应常规作眼底检查;反之,对于拟诊CMV视网膜炎的所有患者,均应常规筛查血清HIV抗体.     

45例AIDS合并巨细胞病毒性视网膜炎临床特点分析

目的探究AIDS合并巨细胞病毒(cytomegalovirus,CMV)性视网膜炎临床诊断及治疗措施。方法收集2012年2月—2014年2月收治的45例AIDS合并CMV性视网膜炎患者临床资料并进行回顾性分析,分析患者一般资料、临床特征、实验室检查结果、治疗及转归。结果患者眼部常见的症状为视力下降和视物模糊,分别为41例(91.11%)和23例(51.11%),另有3例(6.67%)发生失明。眼底检查发现视网膜血管炎和视神经炎,分别为31例(68.89%)和5例(11.11%),另有5例(11.11%)发生视网膜脱离。患者CD4+T细胞计数平均为(56.3±12.6)个/μl,CMV-Ig M阳性15例(33.33%),CMV抗原阳性18例(40.00%)。应用替诺福韦+拉米夫定+依非韦伦进行抗病毒治疗后,19例治愈(42.22%),19例好转(42.22%),7例无效(15.56%)。结论 AIDS患者免疫功能缺损,易合并眼部CMV感染造成视网膜炎症,临床以视力下降和视力模糊为主,眼底检查常见为视网膜血管炎和视神经炎,积极治疗可获得显著效果。     

AIDS合并巨细胞病毒脑炎临床分析

目的探讨艾滋病（AIDS）合并巨细胞病毒脑炎（CMVE）的临床特点及治疗转归。方法回顾性地收集北京地坛医院2011年3月-2013年2月收治的8名合并CMVE的AIDS病人的临床资料,分析其症状和体征、辅助检查、病毒学检查及治疗转归情况。结果 8例病人脑脊液CMV脱氧核糖核酸（DNA）或CMV-IgM抗体阳性,但血清中CMV DNA可阴性。7例CD4＋淋巴细胞计数均〈30/μL,轻症、早期病人可不伴随神经精神症状,头颅核磁共振（MRI）检查可无异常,7例患者经抗CMV及高效抗反转录病毒治疗（HAART）后均获得临床好转。结论合并CMVE易出现在CD4＋淋巴细胞计数低的AIDS病人中,及时对可疑病人进行脑脊液CMV DNA或CMV-IgM抗体检查,有利于早期诊断和治疗。     

艾滋病合并巨细胞病毒性肺炎的临床特点和治疗

目的 探讨艾滋病合并巨细胞病毒性(CMV)肺炎的临床特点和治疗方法.方法 分析2008年1月～2010年12月艾滋病合并巨细胞病毒性肺炎10例患者的临床资料,对艾滋病合并巨细胞病毒性肺炎的临床特点和治疗方法进行总结.结果 在10例患者中,CMV肺炎的症状明显早于体征,患者均出现发热,同时伴有咳嗽、气促、呼吸困难等临床表现;血氧饱和度降低,血气分析提示低氧血症;血CMV-IGM及CMV-DNA检测均为阳性.采用更昔洛韦联合膦甲酸钠抗病毒治疗,同时采取HAART、加用较大剂量的甲强龙或丙种球蛋白和适量的胸腺肽等的个体化免疫调节方案等综合治疗方法,5例治愈,治愈率为50％.2例患者死于呼吸衰竭.结论 艾滋病合并CMV肺炎临床特点以发热、咳嗽为主,病情迅速发展出现高热、呼吸困难、低氧血症以及呼吸窘迫综合征,治疗不及时死亡率高.     

肾移植患者巨细胞病毒感染的诊断、预防及治疗

巨细胞病毒（ｃｙｔｏｍｅｇａｌｏｖｉｒｕｓ,ＣＭＶ）是肾移植患者感染性合并症中最为重要的一种病原微生物。临床上,部分重症病例可因ＣＭＶ肺炎,急性呼吸窘迫综合征而危及生命,部分病例可因救治过程中不得不撤减抗排斥药物而移植肾失功,被迫摘肾。提高对ＣＭＶ感染的认识,早期诊断ＣＭＶ感染,及时采取积极有效地预防治疗措施,可减少ＣＭＶ感染的发生,挽救部分患者的生命［１,２］。本文介绍肾移植患者ＣＭＶ感染的诊断、预防及治疗现状。１　ＣＭＶ感染的病理生理特点ＣＭＶ是一种疱疹病毒,它本身具有的二大特性,即潜伏隐袭…     

巨细胞病毒与炎症性肠病的关系

巨细胞病毒（cytomegalovirus,CMV）为机会致病性病毒,多数人呈隐性或潜伏感染,显性CMV感染常发生在免疫功能抑制者。炎症性肠病（1BD）是一种慢性、复发性的肠道炎症疾病,患者常使用激素或免疫抑制剂治疗,因而有很高的CMV易感性。近年研究表明CMV感染可能在炎症性肠病病情发展变化中起关键作用,CMV通过直接或间接作用致组织损伤,目前新发展的检测技术或联合多种检测手段可增加CMV检出的敏感性和特异性,而不少研究表明难治性IBD时应用抗CMV病毒治疗可明显改善病情。本文就CMV在IBD疾病进展中的作用和关系,以及对CMV的最新检测技术和治疗策略的研究进展作一综述。     

肾移植术后巨细胞病毒感染的诊断及治疗

目的：介绍本单位对巨细胞病毒（ＣＭＶ）感染的诊断和治疗体会。方法：１９９６年５月至１９９７年５月我院共做肾移植８５例，其中７例发生ＣＭＶ感染，诊断主要依据发热、肺炎、神经根炎及视网膜炎等。实验室检查主要用ＰＣＲ方法测血、尿及眼分泌物中的ＣＭＶ－ＤＮＡ。胸片显示肺纹理增加。治疗主要用更莫昔洛韦，疗程１０－２４天。结果：７例中３例治愈，１例因ＣＭＶ感染诱发慢性排异反应，行移植肾切除，另３例均死于严重的     

巨细胞病毒在炎症性肠病中的研究进展

炎症性肠病（IBD）是一种病因尚不十分清楚的慢性非特异性炎症性疾病,在国内的发病率逐年增高。巨细胞病毒（CMV）属疱疹病毒科B属双链DNA病毒,近年随着IBD与CMV研究的深入,发现CMV在IBD的发生和疾病进展中起一定作用,且对IBD的临床诊治亦有一定指导价值。本文就CMV的检测方法学、其在IBD患者中的流行病学情况和相关研究进展作一综述。     

巨细胞病毒感染与炎症性肠病的关系

人巨细胞病毒(human cytomegalovirus,HCMV)是常见的机会性致病病毒,在免疫功能正常个体中常表现为隐性或潜伏感染,在免疫功能受损个体中常呈现显性感染.炎症性肠病(inflammatory bowel disease,IBD)是一种慢性、复发性的肠道炎症性疾病;IBD患者由于营养不良及使用免疫抑制剂等原因,感染HCMV的风险明显增加.IBD合并HCMV感染的患者逐渐增多,HCMV感染加重IBD病情的现象引起了临床医师的共同关注.研究表明HCMV感染可能在IBD病情发展变化中起重要作用,及时诊断IBD患者中HCMV的感染并正确治疗对患者的预后有很大改善作用.本文就巨细胞病毒感染与IBD中的关系及其治疗进展作一综述.     

以腹痛为主要表现的获得性免疫缺陷综合征临床分析

[目的]探讨以腹痛为主要表现的获得性免疫缺陷综合征(AIDS)的临床特征,以提高对该病的认识。[方法]对22例AIDS患者的临床资料进行回顾分析,并结合文献进行复习。[结果]全部患者均有腹痛(100%),其他主要症状为腹胀(77.3%)、腹泻(59.1%)、吞咽困难或吞咽疼痛(22.7%)、口腔炎或口腔真菌感染(18.2%)、纳差(72.7%)、乏力(68.2%)、不明原因发热(31.8%)、体质量减轻(40.9%)等,2例(9.0%)面部出现米糠样皮疹。胃镜下主要表现为胃黏膜充血水肿、糜烂,结肠黏膜主要表现为弥漫性或局限性充血水肿、糜烂或浅表溃疡等。[结论]AIDS以腹痛等消化系统症状为主要表现者比较多见,但临床表现无特异性,临床医务人员尤其是消化内科医师要不断提高对该病的认识,早诊早治,减少误诊。     

Pulmonary diseases in children with severe combined immune deficiency and DiGeorge syndrome

Pulmonary disease is a common presenting feature and complication of T-cell immunodeficiency. We retrospectively reviewed 15 children with severe combined immune deficiency (SCID) and 19 children with DiGeorge syndrome at the time of their first presentation to the Royal Children's Hospital in the 15-year period from 1981 to 1995. In children with SCID, pulmonary disease was a common (67%) presenting feature and the organisms identified were Pneumocystis carinii (PCP) (n = 7), bacteria (n = 4), viruses (n = 3), and a fungus (n = 1). Late pulmonary complications included lower respiratory tract infections, bronchiolitis obliterans, and lymphointerstitial pneumonitis. Pulmonary infections were common (17 occasions) and the organisms identified were bacteria (n = 7), viruses (n = 6), fungi (n = 3), and Mycobacterium tuberculosis (n = 1). Pulmonary complications were responsible for 5 of 9 deaths. PCP was not identified as a late complication in any child, presumably as a result of effective prophylactic therapy. Although pulmonary disease was not a major presenting feature in children with DiGeorge syndrome, pulmonary complications were common. These included recurrent bacterial and viral infections and bronchomalacia, which complicated management and predisposed to morbidity and mortality, even in those without a T-cell defect. We conclude that pulmonary disease is a common manifestation in children with SCID and DiGeorge syndrome. Pediatr. Pulmonol. 1997; 24:324–330. © 1997 Wiley-Liss, Inc.     

获得性免疫缺陷综合征相关消化系统疾病表现72例

目的 探索获得性免疫缺陷综合征（AIDS）患者相关消化系统疾病的发生率、临床表现、发病机制及诊断.方法对1000例共用针具静脉注射海洛因者进行问诊、体检及理化检查,按美国疾病预防控制中心CDC诊断标准筛选出CD4＋T淋巴细胞＜400/μl、人类免疫缺陷病毒（HIV）载量＞400拷贝/ml并有消化系统损害的72例作为观察对象.结果 AIDS相关消化系统疾病发生率为1.4%-98.6%不等,其中口咽部和胃肠道病变71例（98.6%）,肝胆胰病变59例（81.9%）.主要表现为发热、腹泻、进行性消瘦、持续性全身淋巴结病、机会性感染、恶性病变、多器官多系统损害.结论 AIDS相关消化系统疾病主要由HIV直接损害、机会性感染、肿瘤及免疫病理损害所致.     

Cytomegalovirus polyradiculopathy in HIV-infected patients

Cytomegalovirus polyradiculopathy, a late complication of HIV infection, is characterized by lower extremity weakness, urinary retention, and sacral dysesthesias. We describe four patients (mean CD4 T-cell count=25 cells/mm³) who developed this “infectious cauda equina syndrome.” The characteristic cerebrospinal fluid (CSF) findings, notably atypical for a viral infection, included polymorphonuclear leukocytosis (mean white blood cell count=1512 cells/mm³, 72% polymorphonuclear leukocytes), elevated protein level (mean=370 mg/dl), and hypoglycorrhacia (mean=28 mg/dl). Physicians who treat patients with HIV should be familiar with this syndrome because early intervention, prior to microbiologic confirmation, provides the best hope for improving neurologic function. Presented at a meeting of the American Society of Microbiology, Atlanta, GA, May 1993. The views expressed in this article are those of the authors and do not reflect the official policy of the U.S. Department of Defense or other departments of the United States Government.     

获得性免疫缺陷综合征合并肠结核1例

文献报道获得性免疫缺陷综合征(acquired immune deficiency syndrome,AIDS)合并肠结核很少,临床表现和内镜特点不典型,易误诊.本文对1例手术证实为合并肠结核的AIDS病例进行分析,旨在提高对AIDS继发肠病的诊断认识,减少误诊误治.     

Dyshematopoiesis in combined immune deficiency with congenital neutropenia

This report describes a patient with combined immune deficiency associated with congenital neutropenla (CID/CN) and reports a partial characterization of his hematopoletic abnormalities. The CID/CN syndrome described is characterized by neutropenla and by deficiencies in B-lymphoid and T-lymphoid cell number and function. Red cell and platelet counts were normal. In vitro assays indicate that the myeioid lineage was developmentally arrested at the level of the committed monocyte/granulocyte progenitor (CFU-GM), while precursors to the CFU-GM progenitor were normal. In vitro studies showed that the defect in myeiold development was not corrected with G-CSF or GM-CSF. However, combinations of cytokines present in conditioned media from the T-cell lines MO or C5MJ, or defined multiple cytokine combinations containing IL-1, IL-3, GM-CSF, kit ligand, IL-6, and IL-9, restored myelopoiesis in-vitro. In contrast, CBMJ-conditioned media did not correct deficiencies in immune function in the patient's lymphocytes and accessory cells. No abnormalities in the production of G-CSF, GM-CSF, M-CSF, or IL-1 from the patient could be identified to account for the defects in myelopoiesis orimmune function. © 1994 Wiley-Liss, Inc.     

Thrombotic thrombocytopenic purpura associated with the acquired immune deficiency syndrome

A bisexual male presented with acute thrombotic thrombocytopenic purpura (TTP) in association with established acquired immune deficiency syndrome. The patient had classic clinical and laboratory findings of TTP and responded well to plasmapheresis therapy. Previously reported cases of TTP in association with human immunodeficiency virus (HIV) infection are briefly reviewed. Basic concepts in the pathogenesis of TTP are examined in reference to HIV infection.     

Acquired,non‐amyloid related factor X deficiency: review of the literature

Summary. Factor X (FX) deficiency is a rare coagulopathy due to congenital deficiency (Stuart–Prower disease) or in association with primary amyloidosis. Acquired and isolated FX deficiency occurring in the absence of a plasma cell dyscrasia has only been infrequently described. After recently diagnosing and treating a case of acquired, isolated FX deficiency, we embarked upon a review of the literature to help guide clinicians who may face this clinical situation. The literature was reviewed to identify cases of isolated, acquired FX deficiency unrelated to congenital deficiency, use of vitamin K antagonists, or amyloidosis. There were 34 cases of acquired FX deficiency identified, occurring in association with malignancy, drug exposure and infection. The majority of described cases (38%) were preceded by a non‐specific respiratory viral illness. The initial presentation was variable, ranging from no bleeding to life‐threatening haemorrhage. Twenty per cent of patients had musculoskeletal bleeding resembling patients with haemophilia. Both the prothrombin time and the activated partial thromboplastin time were markedly prolonged in nearly all patients. In 26% of patients, a specific FX inhibitor was identified. Numerous therapies have been utilized in patients with acquired FX deficiency including high‐dose glucocorticoids, plasma exchange with fresh frozen plasma and intravenous immunoglobulin. In 18% of patients, the coagulopathy resolved spontaneously. All patients achieved a complete recovery. Acquired factor X deficiency is a rare disorder, commonly associated with a preceding viral illness and a circulating FX inhibitor. Although multiple treatment modalities have been described with variable success, in many cases, it is a self‐limited condition.     

Acquired von Willebrand factor deficiency during high-dose infusion of recombinant factor VIII

Constant infusion of factor VIII (FVIII) into patients with haemophilia A after major surgery has been recommended as optimal treatment to avoid peaks and valleys in the circulating levels of FVIII and to allow the use of much lower doses of FVIII than are historically required.
One of our young patients with severe (<0.01 U/ml FVIII) haemophilia suffered a subdural haematoma for which he received treatment with 815 190 recombinant FVIII (rFVIII) units over a period of 52 d. 2 weeks after admission, because of low FVIII levels and the presence of FVIII inhibitors, the infusion rate was increased to >100 U/kg/h for 14 d. During this time the FVIII level fluctuated between 0.6 and 4.2 U/ml. For some period it was not possible to detect ristocetin co-factor activity in this patient's plasma and the von Willebrand factor (VWF) level and VWF multimer pattern resembled those of a patient with von Willebrand's disease. Subsequently, when the rFVIII dose was increased 2-fold, this was not reflected by the plasma level of FVIII although antibodies were not detected.
The data suggest that the prolonged infusion of very high levels of rFVIII which is deficient in von Willebrand factor can result in depletion of VWF from existing stores, producing a laboratory picture which is consistent with the diagnosis of von Willebrand's disease. Further, in the absence of complexing with VWF, FVIII appears to be cleared from the circulation at an increased rate. This is expensive and potentially compromising. Therefore, when administering very high doses of FVIII concentrates devoid of VWF for prolonged periods of time, ristocetin cofactor and VWF levels should be monitored.     

浅表淋巴结肿大的151例艾滋病患者淋巴结病理学分析

目的 探讨浅表淋巴结肿大的HIV/AIDS患者的淋巴结病理类型及其特点.方法 取浅表淋巴结肿大的151例HIV/AIDS患者的淋巴结组织进行病理学检查,通过HE、抗酸、过碘酸雪夫和淀粉酶消化后过碘酸雪夫染色,光学显微镜下观察,描述和分析其病理结果及其与CD4+T淋巴细胞计数的关系.数据行卡方检验.结果 在151例HIV/AIDS患者的淋巴结病理结果中,表现为良性病变的有145例,占96.0%,表现为恶性肿瘤的有6例,占4.0%,其中结核病72例,淋巴结反应性增生34例,淋巴真菌感染23例(其中青霉病19例),AIDS相关淋巴结病14例,非霍奇金淋巴瘤5例,良性纤维组织细胞病1例,结核伴发真菌感染1例,间叶性恶性肿瘤1例.在所有患者中,CD4+T淋巴细胞计数<100×106/L的有83例,占55.0%.青霉病随着CD4+T淋巴细胞计数的减少,发病率明显升高(x2=7.757,P=0.021).结论 HIV/AIDS患者浅表淋巴结肿大的原因大多数为感染性疾病,主要为结核病及真菌感染,且多数发生在CD4+T淋巴细胞计数低下的患者,最常见的恶性肿瘤为非霍奇金淋巴瘤.

Abstract：

Objective To investigate the pathological types and features of lymph nodes in human immunodeficiency virus(HIV)/acquired immune deficiency syndrome(AIDS)patients with superficial lymphadenectasis.Methods The tissues of lymph nodes were obtained from 151 HIV/AIDS patients with superficial lymphadenectasis for pathological examination.The pathological results were observed by light microscope after Hematoxylin-Eosin(HE),acid-fast,periodic acid-Schiff (PAS),and digested-PAS(D-PAS)staining.The pathological results of lymph nodes were described and the correlation between pathological changes and CD4+T lymphocyte count was analyzed.Chisquare test was used for the statistic analysis.Results The benign lesions were found in 145 patients (96.0%),while the malignant tumors were found in 6 patients(4.0%).The pathological findings in the 151 HIV/AIDS patients included tuberculosis(72 patients),lymph node reactive hyperplasia(34patients),lymphatic fungal infections(23 patients,including penicillium diseases in 19 cases),AIDSrelated lymphadenectasis(14 cases),non-Hodgkin lymphoma(5 cases),benign fibrous histiocytoma (1 case).In addition,there were 83 patients(55.0%)with CD4+T lymphocyte count lower than 100×106/L.The frequency of penicillium diseases was higher in patients with lower CD4+T lymphocyte count(x2=7.757,P=0.021).Conclusions The major reasons for superficial lymphadenectasis in HIV/AIDS patients are infectious diseases,such as tuberculosis and fungal infections,which are common in patients with lower CD4+T lymphocyte counts.Non-Hodgkin lymphoma is the most common malignant tumor in this patient population.