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。     

SARS病原导致人体脏器发生的病理及超微结构改变

对SARS死亡患者的尸检标本进行了光镜和电镜观察。结果:SARS病原体引起人体多个脏器的超微结构发生病理变化,表现为肺泡壁增厚,肺泡腔有絮状渗出物、间质可见纤维素及少量炎细胞浸润;心肌纤维断裂,线粒体肿胀;脾和淋巴结细胞膜崩解破坏;肾小管上皮细胞坏死脱落。在病变组织中可见少量病原颗粒。提示:SARS病原引起人体的细胞免疫病理反应,引起机体多个脏器,特别是肺、心及免疫器官的损害。     

SARS患者尸检肺组织的免疫组织化学观察

目的 通过对严重急性呼吸综合征(severe acute respiratory syndrome,SARS)肺组织病变的免疫组织化学研究,结合组织学观察,探讨SARS肺部病变的特点及发病机制。方法 以常规HE染色组织学观察结合CD8、CD20、CD34、LCA、CD56、CD68及AEl／AE3等单克隆抗体免疫组织化学染色,分别观察淋巴细胞、巨噬细胞、肺泡上皮细胞及肺毛细血管等在肺病变中的数目及分布特点,观察肺组织内血管变化、肺泡上皮增生以及机化和纤维化改变,从而分析SARS肺病变的特点。结果 从病变早期至早期纤维化,SARS肺组织中毛细血管数目增多,血管分布符合肺泡壁结构轮廓;炎细胞反应表现为淋巴细胞数目下降而巨噬细胞数目显著增多;Ⅱ型肺泡上皮显著增生;在晚期纤维化及实变的肺组织中,血管数目减少,管腔增大,分布分散,失去肺泡壁的结构轮廓。结论 SARS肺部病变具有血管反应、渗出、增生及纤维化等特点,其中巨噬细胞渗出可能在发病过程中起关键作用。     

SARS多器官病理改变临床表现及其防治

严重急性呼吸综合征(Severe acute respiratory syndrome，SARS)是21世纪出现的一种全新的、以高感染率和高死亡率为特征，主要表现为急性肺部损伤的严重急性传染性疾病。研究表明其病原体是一种有别于普通型的新型高度变异的单链RNA病毒。WHO将其命名为严重急性呼吸综合征冠状病毒(SARS-associated corona virus，     

SARS Research in China

The first case of severe acute respiratory syndrome(SARS)in Guangdong province was reported on2Jan2003,whileretrospective survey has datedthe first index case on16Nov2002.In months that followed,pandemic of SARS widelyspread over the world until July2003,infecting8454people and claiming908deathsin39countries andregions global-ly.On16Dec2003,a32years old photographerlivinginsuburban Guangzhou presented withsymptoms of SARSinfec-tion.There were3other ensuing cases betweenthe end of2003and…     

SARS患者死因的病理机制探讨--急性肺损伤与继发感染

目的分析严重急性呼吸综合征(SARS)患者的临床病理特点,探讨SARS死亡原因的病理生理机制。方法以4例SARS患者的尸检肺组织、经皮或经支纤镜肺活检标本为观察对象,组织病理切片经常规HE染色,免疫组化,并与临床表现进行联系。结果2例发病早期患者肺组织病理切片可见Ⅱ型肺泡上皮细胞增生,肺泡壁明显增宽,血管充血水肿,纤维母细胞增生,肺泡腔见纤维素及红细胞渗出,单个核细胞浸润,透明膜形成。另2例病程较长的死亡病例可见肺组织内大量曲霉菌菌丝,血管内见真菌栓,血管壁破坏。免疫组织化学染色：B细胞的CD20 在肺组织中的表达为阴性;T细胞的CD45RO^ 表达阳性增加;吞噬细胞的CD68^ 阳性表达显著增加。结论SARS发病早期肺部主要表现为急性肺损伤,其发生机制可能与超敏反应有关,也是SARS患者早期死亡的主要原因,与免疫抑制有关的继发严重霉菌感染是晚期病人的重要死因。     

2003香港SARS病理改变图谱

SARS的病理形态表现: 1.淋巴细胞降低,血钠轻微降低,以上两项改变也见于军团菌肺炎,但在SARS病人军团菌肺炎检验为阴性。 2.大体上肺呈斑片状实变,死亡病例病变广泛。 3.尸检时肺实变为机化性肺炎的硬度(不是肺硬化pneumonic consolida-tion)。     

SARS患者首诊的胸部X线表现

目的分析严重急性呼吸综合征(SARS)首诊患者的胸部X线表现及其在诊断和鉴别诊断中的作用.方法回顾性分析79例SARS患者首诊胸部X线平片,其中男性40例,女性39例;平均年龄(34.1±12.3)岁(15～69岁);平均体温(38.8±0.58)℃.79例患者起病时间至首次胸部X线检查平均时间为(5.8±3.7)d.观察项目包括:病变部位、肺部的基本病变、胸腔积液、心包积液、肺门和纵隔淋巴结增大等.结果79例患者首诊X线胸像阴性者占总例数的45.5%,43例X线胸像阳性者肺内所见均以渗出性病变为主,占阳性总数的81.3%.首诊胸片阳性和阴性者的平均年龄和平均起病时间的比较差异无显著性(P＞0.05).79例患者首次胸片未见有心包积液、肺门和纵隔淋巴结增大.结论SRAS患者的胸部X线表现多以磨玻璃样病变为主,但特异性不强;SARS患者首诊胸部X线阴性者并不少见,且胸部X线阳性者出现时间也可能较晚,应引起临床上的重视.     

SARS流行病学研究

传染性非典型肺炎是通过近距离空气飞沫或密切接触等途径迅速传播的一种急性呼吸道传染病 ,世界卫生组织将这种急性呼吸道传染病称为严重急性呼吸综合征 (SARS)。作者主要是对 2 0 0 3年初在中国流行的SARS的传染源、传播途径、流行模式以及流行特征等方面的初步情况进行综述。     

SARS患者T淋巴细胞亚群的动态改变

目的研究严重急性呼吸综合征(severeacuterespiratorysyndrome,SARS)患者T淋巴细胞亚群动态变化的特点。方法收集本院确诊的46例SARS患者在发病后不同时间的抗凝血,用特异性荧光抗体标记,通过三色流式细胞仪检测其T淋巴细胞亚群、CD4+纯真细胞亚群(CD4+CD45RA+CD62L+)和CD8+激活亚群(CD8+CD38+),以56例健康献血员的结果作为正常人对照。结果与正常对照相比,SARS患者的CD4+细胞和CD8+细胞在感染1周内百分比正常,但计数均显著减少,分别为(306±140)/mm3和(270±143)/mm3,CD4+纯真细胞亚群的计数也明显降低至(96±49)/mm3,CD8+CD38+激活亚群的比例则明显升至(59.3±12.6)%犤正常人为(44.9±12.5)%犦。感染3～5周时,CD8+细胞计数和激活亚群的百分比均恢复正常,分别为(581±356)/mm3和(40.1±17.6)%。感染8～12周时,CD4+细胞和CD4+纯真细胞亚群的计数分别为(578±193)/mm3和(176±64)/mm3,仍低于正常水平,但与感染1周时相比均有异常显著的升高。结论SARS患者的T淋巴细胞免疫在细胞数量上严重受损,但在短期内有很明显的恢复,CD4+细胞和纯真CD4+细胞亚群的恢复需要比8～12周更长的时间。     

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.     

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.     

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.     

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.     

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。     

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.     

重症急性呼吸综合征临床特点分析

目的了解本地区重症急性呼吸综合症(severe acute respiratory syndrome,SARS)的临床特点及治疗和预后.方法回顾性分析广东省佛山市第一人民医院2002年11月～2003年2月收治的16例SARS病人的临床资料,分为普通型、重症两组.结果本组病例年龄在20～57岁,男9例,女7例,青壮年为主,44%为医护人员.潜伏期平均为6.7±3.4天.重症7例,占44%.重症SARS较普通型肺部病灶发现晚,发热持续时间长,多累及双肺,易并发急性呼吸窘迫综合症(ARDS),多器官功能损害.重症患者采用早期氧疗,充分镇静及抗病毒,抗细菌感染,激素,增强免疫功能等综合治疗.结论重症SARS患者临床表现严重,但经过积极综合治疗,及早氧疗、采取"肺保护性策略"人工通气,预防和处理好并发症,是可以治愈的.     

Fibromyalgia after severe acute respiratory syndrome: a case report

S ince November 2002, an infectious disease with unknown cause occurred in China and many countries had been involved. Cases were reported in 28 countries and more than 5050 individuals had been infected. Lung is the most frequently involved organ and can be fatal in severe cases. At the end of February 2003, it was defined as Severe Acute Respiratory Syndrome （SARS） by World Health Or clanization.     

利巴韦林在严重急性呼吸综合征中的应用

抗病毒药利巴韦林(ribavirin)被临床用于抗严重急性呼吸综合征(SARS)病毒，利巴韦林与激素联用对SARS的疗效肯定，但亦有一定不良反应。本文对其临床使用方法、疗效、不良反应及注意事项等作一综述。