SARS尸检的肺部病理改变

目的 通过研究严重急性呼吸综合征(severe acute respiratory syndrome,SAPS)患者的尸检肺部标本。总结SAPS的肺部病变特点及发病机制。方法 详细检查SARS患者肺脏标本的大体特点,并用常规方法研究显微光镜下SAPS累及各肺叶的病变特点。结果 7例SAPS患者的双肺均明显膨胀,镜下表现以弥漫性肺泡损伤(DAD)不同时期的病变为主。7例均有肺水肿及透明膜形成,肺水肿尤以早期明显。病程超过3周者开始有肺泡内机化及肺间质纤维化,造成肺泡的纤维性闭塞。几乎每例都可见到小血管内的微血栓和肺出血、散在的小叶性肺炎、肺泡上皮脱落、增生等病变。2例可见曲霉菌感染,l例累及左全肺及右肺部分区域,l例出现在肺门淋巴结。肺门淋巴结多表现为充血、出血及淋巴组织减少,窦组织细胞增多。结论 SAPS肺可能为SAPS病毒造成的弥漫性肺泡损伤,表现为肺泡上皮及毛细血管的严重损伤导致肺水肿和肺泡及细支气管的纤维索性渗出性炎症,出现透明膜。继而出现肺泡内机化及肺泡间隔的成纤维细胞增生,共同使肺泡萎陷、机化,最终形成纤维化实变。肺门淋巴组织的减少可能是此病影响免疫系统的又一形态学表现。     

SARS冠状病毒N蛋白单克隆抗体在SARS尸检组织中的表达

目的 观察SARS死者的尸检组织中SARS冠状病毒(SARS-CoV)的存在与分布情况。方法 应用免疫组化技术检测4例尸检标本肺、脾脏、淋巴结、脑、垂体、心、肝、肾、胰腺、气管、食道、胃肠道和骨髓等组织的SARS-CoVN蛋白。结果 肺泡上皮、肺、脾、淋巴结内浸润的单核细胞／巨噬细胞、脑神经元、肝细胞、肾远曲小管上皮细胞、胰腺腺泡细胞、垂体嗜酸细胞、甲状旁腺嗜酸性细胞、肾上腺皮质细胞、气管及支气管浆液腺上皮细胞、食道粘膜鳞状上皮、胃肠道柱状上皮细胞及胃壁细胞、骨髓早幼粒细胞及小静脉内皮细胞等细胞质内SARS-CoVN蛋白单克隆抗体均为阳性。结论 SARS-CoV可侵犯全身多种器官和组织。SARS-CoVN蛋白单克隆抗体在胃肠道、肾远曲小管及汗腺细胞内的阳性表达，对研究SARS—CoV传播途径具有重要意义。     

肾综合征出血热肺组织中C3的免疫组织化学检测

本文应用免疫组织化学方法(ABC法)对10例肾综合征出血热尸检肺组织中C3进行检测，发现C3分散地存在干肺的多种细胞内和细胞间隙中。此研究结果，为肾综合征出血热的免疫发病机理提供了实验依据．     

3例SARS患者肺组织病理学观察及核转录因子-κB的表达

为观察严重急性呼吸综合征 (SARS)患者肺损伤的病理学特点及核转录因子 κB(NF κB)在肺组织中的表达 ,探讨急性肺损伤时NF κB的活化及其与肺损伤的关系 ,对 3例SARS死亡病例进行尸体解剖 ,HE染色观察肺组织的病理改变 ;采用免疫组织化学SP法检测肺组织NF κBp65活性。结果 :肺部病变主要表现为弥散性肺间质炎症及肺泡损伤 ,肺泡上皮细胞凋亡脱落及肺透明膜形成 ,肺间隔明显增宽 ,以淋巴细胞和单核细胞为主的炎细胞浸润。 3例肺组织NF κBp65检测均为阳性 ,阳性信号表达于肺泡上皮细胞、巨噬细胞及淋巴细胞的胞质及胞核内。结果提示 :SARS患者的肺组织表现为急性肺损伤 ,NF κB在SARS患者肺组织的损伤中起重要的作用     

从尸检肺组织病理特点反思ARDS患者机械通气策略

色性呼吸窘迫综合征(acute respiratory distress syndrome ,ARDS)是在严重感染、休克、创伤、烧伤及重症急性胰腺炎等非心源性疾病作用下,以色性呼吸窘迫和进行性低氧血症为主要表现的常见危重症,机械通气是纠正ARDS患者顽固性低氧血症最主要的呼吸支持手段~([1]).     

原位杂交检测尸检组织中SARS-CoVRNA

目的 从分子水平检测急性重症呼吸综合征(SARS)患者的病变组织中SARS病毒(SARS-associatcd coronavirus，SARS—CoV)的存在和分布情况。方法 应用原位杂交技术检测因SARS死亡患者的肺、脾脏、淋巴结、垂体、胰腺、甲状旁腺、肾上腺、胃肠道、皮肤、脑、肝、肾、血管、四肢横纹肌组织、骨髓、心脏、卵巢、子宫和睾丸等组织的SARS-CoVRNA的表达和定位。结果 尸检组织多部位(包括肺泡上皮细胞、气管及支气管浆液腺上皮细胞、肺内单核／巨噬细胞、脾脏和淋巴结的单核／巨噬细胞、胰腺腺泡细胞、垂体嗜酸性细胞、肾上腺皮质细胞、甲状旁腺嗜酸性细胞、食道鳞状上皮、胃肠道上皮细胞及胃粘膜壁细胞、皮肤汗腺细胞、大脑神经元细胞、肝细胞、肾远曲小管上皮细胞、骨髓早幼粒细胞及小静脉内皮细胞)SARS-CoVRNA阳性。结论 SARS-CoV可侵犯全身多种器官；SARS-CoV在机体的分布情况与冠状病毒受体CD13分布相似：皮肤汗腺、消化道上皮及肾远曲小管上皮细胞SARS-CoVRNA阳性对确定SARS传播途径具有重要意义。     

致死性SARS的肺病理学改变

自去年11月以来,一场爆发流行的重症急性呼吸道综合征(SARS)使全球五大洲的33个国家受到不同程度的影响。截至2003年5月中旬,全球报告的SARS病例数为7053例,死亡506例。至少在6个国家中发生了局部的SARS传播。 SARS病的临床表现特征为发热、呼吸困难、淋巴细胞减少、胸部X光片显示有快速的进行性病变;但上呼吸道症状并不明显,某些患者偶有腹泻症状。目前用于治疗传统非典型肺炎的抗生素类药物对其无效,与SARS相关的冠状病毒(SARS-CoV)被认为与此病有关。虽然该病毒似乎是发生SARS所必需的,但它并不局限于肺病理学部位。     

严重急性呼吸综合征冠状病毒在肺组织内各种类型细胞中的表达

目的:了解肺组织内被严重急性呼吸综合征冠状病毒(severe acute respiratory syndrome -associated coronavirus, SARS-CoV)感染的靶细胞类型, 并对SARS诱发的肺损伤发病机制进行探讨.方法: 运用SARS-CoV基因组序列合成的地高辛标记cDNA探针,对北京市7例及安徽省1例确诊的SARS死亡病例的肺组织进行原位杂交检测,在原位杂交基础上,进一步运用免疫组织化学方法显示SARS-CoV感染的靶细胞类型,如Cytokeratin(CK)标记上皮细胞,CD34标记血管内皮细胞,CD68标记巨噬细胞,Vimentin标记纤维母细胞, CD3标记全T细胞. 结果:原位杂交检测显示,8例患者肺组织中都表达SARS-CoV RNA,阳性信号位于靶细胞胞浆内,呈紫蓝色(NBT-BCIP).原位杂交和免疫组化结果显示:支气管上皮细胞、Ⅱ型肺泡上皮细胞、血管内皮细胞、巨噬细胞、纤维母细胞及T淋巴细胞在所有SARS病例中都受到了病毒感染.原位杂交阳性(紫蓝色,NBT-BCIP)和免疫组化阳性(红棕色,AEC)信号同时表达于靶细胞胞浆中而呈紫红色.结论:通过对SARS患者肺组织原位杂交和免疫组织化学双重标记研究表明,肺组织内支气管上皮细胞、Ⅱ型肺泡上皮细胞、血管内皮细胞、巨噬细胞及纤维母细胞等多种细胞成分广泛受到了SARS-CoV攻击,肺组织内多种细胞成分弥漫性受损以及所释放的炎性介质在肺损伤的发病过程中起着重要作用.     

免疫组织化学方法在肺癌病理诊断中的应用

应用免疫组织化学方法，观察低分子细胞角蛋白（ＣＫ－ＬＭＷ）、神经烯醇化酶（ＮＳＥ）、嗜铬粒蛋白（ＣｇＡ）、突触泡蛋白（Ｓｙｎ）和α１－抗胰蛋白酶（α１－ＡＴ）在细支气管肺泡癌、肺乳头状腺癌、肺大细胞癌癌组织中的表达。结果发现，三型肺癌均有神经内分泌分化，细支气管肺泡癌和乳头状腺癌具有多种细胞分化成分。结果支持肺癌细胞来源于共同干细胞的假说。同时说明，在肺癌病理诊断上，免疫组织化学方法具有较为实用的     

A retrospective study of 78 patients with severe acute respiratory syndrome

Objective To summarize the clinical features of severe acute respiratory syndrome (SARS) and to discuss diagnosis and management of the disease. Methods A retrospective study was conducted on 78 cases of SARS referred to the Guangzhou Institute of Respiratory Diseases (GIRD) between December 22, 2002 and near the end of March 2003. Items reviewed cover all data concerning clinical manifestations, laboratory investigation and radiology. Results The patients in the study consisted of 42 males and 36 females, aged 20-75 yrs (mean age 37.5±11.6 yrs), including 44 affected health-care professionals. Clinical symptoms seen in the group were fever (100.0%), cough (88.5%), and dyspnea (79.5%). There were 12 cases (15.3%) with WBCs <4.0×10(9)/L, 49 cases (62.8%) ranging between （4.0-10.0）×10(9)/L and 17 cases (21.8%) over 10.0×10(9)/L. The average was（7.58±4.96）×10(9)/L, with 0.75±0.14 (neutrophil) and 0.18±0.11 (lymphocyte). Chest films and CT scanning revealed changes related to pneumonia. The transmission of the disease was likely via close contact with contagious droplets. The prevalences of acute lung injury (ALI, in 37cases) and acute respiratory distress syndrome (ARDS, 21 out of 37 cases) were considerably high among the patients. Seven patients who developed ARDS complicated with multiple organs dysfunction syndrome (MODS) died. Conclusions A history of close contact, fever, sign of pneumonia by X-ray and normal-to-lowered WBC counts are favorable for the diagnosis of SARS. Recognition of ALI as the important index for critical SARS and comprehensive supportive management are of paramount in decreasing the mortality of the disease.     

Pathogenesis of severe acute respiratory syndrome

Severe acute respiratory syndrome （SARS） first emerged in Guangdong province, China in November 2002. During the following 3 months, it spread rapidly across the world, resulting in approximately 800 deaths. In 2004, subsequent sporadic cases emerged in Singapore and China. A novel coronavirus, SARS-CoV, was identified as the etiological agent of SARS.1＇2 This virus belongs to a family of large, positive, single-stranded RNA viruses. Nevertheless, genomic characterization shows that the SARS-CoV is only moderately related to other known coronaviruses.3 In contrast with previously described coronaviruses, SARS-CoV infection typically causes severe symptoms related to the lower respiratory tract. The SARS-CoV genome includes 14 putative open reading frames encoding 28 potential proteins, and the functions of many of these proteins are not known.4 A number of complete and partial autopsies of SARS patients have been reported since the first outbreak in 2003. The predominant pathological finding in these cases was diffuse alveolar damage （DAD）, This severe pulmonary injury of SARS patients is caused both by5 direct viral effects and immunopathogenetic factors, Many important aspects of the pathogenesis of SARS have not yet been fully clarified. In this article, we summarize the most important mechanisms involved in the complex pathogenesis of SARS, including clinical characters, host and receptors, immune system response and genetic factors.     

严重急性呼吸综合征682例临床分析

目的探讨严重急性呼吸综合征(severe acute respiratory syndrome,SARS)的临床特点.方法回顾性统计分析北京小汤山医院收治的682例SARS临床病例资料.结果682例SARS患者的年龄分布于13～76岁.356例(52.2%)有明确的接触史,有171例(25.1%)发病前曾到过医院.677例(99.3%)患者出现发热,5例患者体温正常.其它主要症状包括咳嗽(44.3%)、气促(12.2%)、腹泻(8.9%);外周血白细胞计数正常或降低占87.4%;ALT和CPK升高的比例分别为16.4%、2.5%;全部患者都有肺部病变,累及双肺占69.8%;死亡6例.结论该病有较强的传染性,医院是重要的传播场所;发热、咳嗽、胸片异常及外周血白细胞正常或降低是该综合征的主要临床特点.     

Pathological study on severe acute respiratory syndrome

Objective To study the pathological characteristics of severe acute respiratory syndrome (SARS)and its relationship to clinical manifestation.Methods Tissue specimens from 3 autopsies of probable SARS cases were studied by microscope,and the clinical data was reviewed.Results The typical pathological changes of lungs were diffuse hemorrhaging on the surface. A combination of serous, fibrinous and hemorrhagic inflammation was seen in most of the pulmonary alveoli with the engorgement of capillaries and detection of micro-thrombosis in some of these capillaries. Pulmonary alveoli thickened with interstitial mononuclear inflammatory infiltrates, suffered diffuse alveolar damage, experienced desquamation of pneumocytes and had hyaline-membrane formation, fibrinoid materials, and erythrocytes in alveolar spaces. There were thromboembolisms in some bronchial arteries. Furthermore, hemorrhagic necrosis was also evident in lymph nodes and spleen with the attenuation of lymphocytes. Other atypical pathological changes, such as hydropic degeneration, fatty degeneration, interstitial cell proliferation and lesions having existed before hospitalization were observed in the liver, heart, kidney and pancreas.Conclusion Severe damage to the pulmonary and immunological systems is responsible for the clinical features of SARS and may lead to the death of patients.     

传染性非典型肺炎并急性呼吸窘迫综合征的治疗

目的 探讨传染性非典型肺炎(世界卫生组织又称严重急性呼吸综合征,SARS)并急性呼吸窘迫综合征(ARDS)的治疗。方法 以2002年l2月至2003年3月,我院及广州医学院第一附院临床诊断SARS并ARDS的12例患为对象,回顾性分析呼吸机通气模式、糖皮质激素、深度镇静等方面的应用。结果 压力控制模式(PCV)优于同步间歇指令通气(SIMV)和持续气道正压通气(CPAP)及双相气道正压通气(BIPAP),早期规律使用糖皮质激素可减少死亡率,深度镇静可减少气胸出现。结论 PCV模式通气,早期规律使用糖皮质激素,深度镇静治疗SARS并ARDS疗效良好。     

SARS患者2例的诊断与治疗

目的探讨严重急性呼吸综合征(SARS)的诊断与治疗.方法观察南京地区2003年4月30日至5月30日收治的SARS确诊患者的流行病学、临床症状、实验室检查和X线胸片表现,比较SARS患者治疗前后临床症状、实验室检查和X线胸片的变化情况.结果共收治2例SARS患者,年龄分别为28和36岁.SARS患者在流行病学明显表现为密切接触传播.以发热为首发症状,其次为干咳和肌肉酸痛.发病期患者唾液和血液中SARS冠状病毒RNA为阳性.发病第11天患者血液中检测到SARS病毒抗体IgM,第12～16天时出现抗体IgG.入院后患者白细胞低于4×109L-1,淋巴细胞低于1.5×109L-1,血小板低于100×109L-1,治疗5 d后白细胞和血小板增加到正常范围,但淋巴细胞在第17天才恢复正常.患者丙氨酸氨基转移酶和乳酸脱氢酶明显升高,治疗10 d后降至正常范围.患者T细胞绝对计数明显降低,治疗21 d后恢复正常.X线胸片表现为双侧多叶病变,发病5～10 d渗出病变最严重.治疗上经验性应用抗生素、利巴韦利和调节免疫功能等.2例患者均用糖皮质激素治疗,疗程分别为18 d和24 d.1例行无创机械通气治疗,疗程5 d.2例患者全部存活.结论SARS通过密切接触传播,流行病学史和病原学检查是重要的诊断依据.SARS表现为多器官受损,综合支持治疗是行之有效的方法.     

严重急性呼吸综合征患者肺组织包被抗原的特异性研究

目的：探讨严重急性呼吸综合征(SARS)肺组织包被抗原在不同个体以及猪、羊、大鼠中的种属特异性。方法：匀浆SARS患者尸检肺组织、非SARS患者肺组织以及猪、羊、大鼠肺组织后分别包被，利用酶联免疫吸附试验(ELISA)，同时检测SARS患者及正常献血员血清中的IgG。结果：SARS患者及正常献血员血清用SARS尸检患者与非SARS患者肺组织包被抗原检测，两种组织包被抗原检测的阳性率间无统计学差异；而用非SARS患者肺组织包被抗原检测的阳性率和用羊、猪、大鼠肺组织包被抗原检测的阳性率均具有统计学差异。结论：SARS患者肺组织及非SARS患者肺组织中存在相同的抗原；其他动物中可能也存在该抗原，但可能因为其他抗原干扰而不适于用该方法检测。     

严重急性呼吸综合征患者糖皮质激素的应用

为探讨严重急性呼吸综合征(SARS)治疗过程中糖皮质激素的应用时机、疗程和效果，对7例SARS患者(其中男4例，女3例，平均年龄31．3岁)应用糖皮质激素治疗，甲泼尼龙平均剂量为126mg／d，平均疗程7．8d；口服泼尼松平均疗程12d。结果高热患者在治疗后2d体温恢复正常，肺部进行性病变者在3～5d内有所恢复，疗程结束时病灶明显吸收，无1例患者发生呼吸衰竭。提示糖皮质激素对改善SARS中毒症状，阻止病情进展有一定疗效。     

Digestive system manifestations in patients with severe acute respiratory syndrome

Objective To explore digestive system manifestations in patients with severe acute respiratory syndrome (SARS).Method The clinical data of 96 cases with SARS admitted into our hospital from February 6, 2003 to March 28, 2003 were retrospectively analyzed.Results Among the 96 cases, 26 cases (27%) had diarrhea, 17 (18%) had nausea, 6 (6%) had vomiting, 16 (17%) had bellyache, and 8 (8%) had ALT elevation.Conclusions Patients with SARS may have digestive system manifestations; diarrhea is the most common symptom.