新加坡急性重症呼吸道综合征(SARS):指征病例和密切接触者病例的临床特征

急性重症呼吸道综合征(SARS)是一种新出现的病毒性传染病。2003年3月在新加坡暴发流行。本文描述了该暴发指征病例及其密切接触者病例的临床特征、实验室结果和胸部X光片特点。新加坡的暴发从2003年3月中旬开始直至现在。由1名从香港返回的旅游者引入。     

台湾急性重症呼吸道综合征(SARS)的控制策略

SARS以惊人的速度在全球范围内播散，几个星期内波及许多医院和公共卫生机构。至2003年4月14日，全球已有超过20个国家有疫情发生，共有临床诊断病例3169例。在许多地区，疾病由感染的旅游者引入，迅速在医务人员和家庭密切接触者中播散开来。在疫情严重的香港和河内，病例中分别有46％和63％是医务人员。在新加坡和多伦多，医院内传播也是最主要的暴发类型。     

严重急性呼吸综合征患者心血管系统表现初步临床观察

目的:本文回顾分析了35例确诊严重急性呼吸综合征(SARS)患者在心血管系统方面的临床表现.方法:35例确诊为SARS的患者,其中男性19例,女性16例,平均年龄37.7岁(15～82岁),临床观察项目包括体温、血氧饱和度、心率、血清酶,以及X线影像和超声心动图检查.结果:35例患者中,有10例(28.6%)患者X线胸片显示心脏增大,以右心增大或全心增大为主,其中3例呈现肺动脉段突出,10例中6例为重症患者.X线胸片显示急性期(发病1～2周)心脏影像开始增大,恢复期(发病3～4周),大多数患者(9例)心脏影像恢复正常.10例患者心脏在急性期时平均心胸比率为0.59±0.03,恢复期平均心胸比率为0.51±0.02,二者有显著差异(P＜0.05).所有患者心率加快并长时间呈偏高水平,在体温正常后,平均心率仍在95次/分以上.有5例患者在发热期间发生过心肌酶(肌酸激酶,CK)增高,3～5天后,心肌酶恢复正常.所有患者在恢复期期间行超声心动图检查,仍有1例显示左、右心室增大,其余患者心脏大小均已恢复正常.结论:本组临床观察显示,SARS是以肺部为突出表现的呼吸道传染病,亦可累及心脏使一部分患者心脏增大.随着SARS病情好转大多数增大的心脏可恢复正常,其机制需进一步研究证实.     

传染性非典型肺炎肺部影像学与临床表现关系

目的　探讨传染性非典型肺炎的肺部 X线特征及其与临床表现的关系。方法　分析 39例传染性非典型肺炎的肺部 X线及临床表现。结果　肺部 X线改变出现在发热 4 .4± 2 .2日之后 ;35例病灶分布在下叶背段及后基底段为主。 2 0例 (5 1.3% )在治疗中肺部病灶进展 ,呈大片状阴影 ;19例在出现肺部病灶增加时 ,体温下降 ,全身中毒症状明显好转。在 2 2例重症中 ,治疗前外周血淋巴细胞 <1.2× 10 9/ L有 18例。结论　传染性非典型肺炎是一组起病急、肺部病灶出现快和以双肺下叶背段及后基底段病变为主的肺炎。对于血淋巴细胞计数减少的患者 ,要注意发展成重症肺炎的可能     

SARS病人的心脏损害及其预后

目的探讨SARS对病人心脏的影响.方法收集急性期和恢复期SARS病人的临床、实验室和物理检查资料进行统计分析.结果急性期89例住院病人均有胸闷、气促、心悸、乏力等症状,心率(92.5±18.6)/min.38例病人有至少一项心肌酶指标增高.其中多脏器功能衰竭4例,死亡4例.51例未升高者中多脏器功能衰竭2例,死亡1例.恢复期76例病人中,胸痛38例,胸闷54例,气短57例,心悸51例.静息心率(65～85)/min,有35例轻微活动后心率大于100/min.结论SARS可引起心脏的多样损害,可能与病毒直接侵犯心肌、毒素对心肌的损害、免疫机制及严重的低氧血症所致的心肌损伤有关.SARS对心脏损害多预后良好.     

The Role of Severe Acute Respiratory Syndrome (SARS)-Coronavirus Accessory Proteins in Virus Pathogenesis

A respiratory disease caused by a novel coronavirus, termed the severe acute respiratory syndrome coronavirus (SARS-CoV), was first reported in China in late 2002. The subsequent efficient human-to-human transmission of this virus eventually affected more than 30 countries worldwide, resulting in a mortality rate of ~10% of infected individuals. The spread of the virus was ultimately controlled by isolation of infected individuals and there has been no infections reported since April 2004. However, the natural reservoir of the virus was never identified and it is not known if this virus will re-emerge and, therefore, research on this virus continues. The SARS-CoV genome is about 30 kb in length and is predicted to contain 14 functional open reading frames (ORFs). The genome encodes for proteins that are homologous to known coronavirus proteins, such as the replicase proteins (ORFs 1a and 1b) and the four major structural proteins: nucleocapsid (N), spike (S), membrane (M) and envelope (E). SARS-CoV also encodes for eight unique proteins, called accessory proteins, with no known homologues. This review will summarize the current knowledge on SARS-CoV accessory proteins and will include: (i) expression and processing; (ii) the effects on cellular processes; and (iii) functional studies.     

Severe Acute Respiratory Syndrome

Severe acute respiratory syndrome (SARS) is a newly emerged infection that is caused by a previously unrecognized virus - a novel coronavirus designated as SARS-associated coronavirus (SARS-CoV). From November 2002 to July 2003 the cumulative number of worldwide cases was >8000, with a mortality rate of close to 10%. The mortality has been higher in older patients and those with co-morbidities. SARS has been defined using clinical and epidemiological criteria and cases are considered laboratory-confirmed if SARS coronavirus is isolated, if antibody to SARS coronavirus is detected, or a polymerase chain reaction test by appropriate criteria is positive. At the time of writing (24 May 2004), no specific therapy has been recommended. A variety of treatments have been attempted, but there are no controlled data. Most patients have been treated throughout the illness with broad-spectrum antimicrobials, supplemental oxygen, intravenous fluids, and other supportive measures. Transmission of SARS is facilitated by close contact with patients with symptomatic infection. The majority of cases have been reported among healthcare providers and family members of SARS patients. Since SARS-CoV is contagious, measures for prevention center on avoidance of exposure, and infection control strategies for suspected cases and contacts. This includes standard precautions (hand hygiene), contact precautions (gowns, goggles, gloves) and airborne precautions (negative pressure rooms and high efficiency masks). In light of reports of new cases identified during the winter of 2003-4 in China, it seems possible that SARS will be an important cause of pneumonia in the future, and the screening of outpatients at risk for SARS may become part of the pneumonia evaluation.     

A deficient public health system as a contributing cause of Severe Acute Respiratory Syndrome (SARS) epidemic in mainland China

SARS (Severe Acute Respiratory Syndrome) is a newly emerging infectious disease which spread over 32 countries and areas, infected more than 8,000 people and causing more than 900 deaths from November 2002 to August 2003. More than 90% of the SARS cases and death were reported from China. Nevertheless, we still know little about this disease, particularly in etiology. SARS, as an emergency of Public Health System (PHS), alarmed health workers throughout the world proving there is still the potential for an epidemic of an emerging infection both in developed and developing areas. Many reports indicated that the insufficiency of the PHS of China was one of the critical factors contributing to the outbreak of SARS. In this study, we attempt to demonstrate some of the categories of PHS that contributed to the SARS epidemic. Two of the categories studied were the living environment and health resources. In the living environment area, the population and population density were examined. Health resources include the medical facilities, health workers, and per capita public health expenditures. An understanding of these areas is important to prevent future epidemic.     

急性呼吸窘迫综合征在重症急性胰腺炎治疗过程中的临床意义

目的 探讨急性呼吸窘迫综合征（ARDS）在重症急性胰腺炎（SAP）治疗过程中的临床意义.方法 回顾性分析2003年7月至2006年7月收治的76例SAP患者的临床特点、病程演变趋势和治疗效果,其中29例合并ARDS,经有效呼吸支持,病人情况不稳定,脏器功能无好转.及时行外科手术干预治疗.结果 76例SAP存活64例,死亡12例,存活率84.21%;SAP病程中合并ARDS 29例,存活21例,死亡8例,存活率72.41%,其中手术干预15例,存活10例,死亡5例,存活率66.67%.结论 正确认识和处理SAP病程中并发ARDS,合理选择外科干预方式,对于决定SAP预后至关重要.     

严重急性呼吸综合征的病原学

严重急性呼吸综合征（severe acute respiratory syndrome,SARS）是由SARS冠状病毒（SARS-Cov）引起的急性呼吸系统传染病,在我国又称为传染性非典型肺炎。主要通过短距离飞沫、接触患者呼吸道分泌物及密切接触传播。临床上以起病急、发热、头痛、肌肉酸痛、乏力、干咳少痰、腹泻、白细胞减少等为特征,严重者出现气促或呼吸窘迫。     

SARS的影像学诊断

目的 探讨严重的急性呼吸综合征(SARS)的影像学特征。方法 回顾临床诊断的50例SARS的影像学检查方法与诊断价值。结果 50例均行胸片(后前位和右侧位或左侧位)检查，其中12例患多次摄床边胸片，11例患行HRCT检查，未行MRI检查。50例胸片均发现阴影，双侧肺内片状密度增高影27例(54％)和／或磨玻璃样影22例(44％)，一侧肺内片状密度增高影19例(38％)，双侧肺内间质改变呈网状阴影4例f病变短期内呈游走性和进展。吸收慢并且恢复后部分病例肺内纤维化；1例经胸部透视对肺内和胸膜病变进行了鉴别；11例经HRCT检查进一步了解肺内和纵隔病变。结论 凡临床诊断或疑似SARS病例短期内应进行影像学检查，并进行短期拍胸片动态观察。     

Effectiveness of Ribavirin and Corticosteroids for Severe Acute Respiratory Syndrome

ObjectiveRibavirin and corticosteroids were used widely as front-line treatments for severe acute respiratory syndrome; however, previous evaluations were inconclusive. We assessed the effectiveness of ribavirin and corticosteroids as the initial treatment for severe acute respiratory syndrome using propensity score analysis.MethodsWe analyzed data on 1755 patients in Hong Kong and 191 patients in Toronto with severe acute respiratory syndrome using a generalized propensity score approach.ResultsThe adjusted excess case fatality ratios of patients with severe acute respiratory syndrome receiving the combined therapy of ribavirin and corticosteroids within 2 days of admission, compared with those receiving neither treatment within 2 days of admission, were 3.8% (95% confidence interval, ?1.5 to 9.2) in Hong Kong and 2.1% (95% confidence interval, ?44.3 to 48.5) in Toronto.ConclusionsOur results add strength to the hypothesis that the combination of ribavirin and corticosteroids has no therapeutic benefit when given early during severe acute respiratory syndrome infection. Further studies may investigate the effects of these treatments later in disease course.     

Relationship Between Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and the Etiology of Acute Kidney Injury (AKI)

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since it was first recognized in December 2019, it has resulted in the ongoing worldwide pandemic. Although acute hypoxic respiratory failure (AHRF) and acute respiratory distress syndrome (ARDS) are the main features of the disease, the involvement of other organs needs to be explored. There has been a growing concern regarding the association between acute kidney injury (AKI) and poor outcomes in SARS-CoV-2 patients. Based on current observational data, AKI is the 2^nd most common cause of morbidity and mortality behind ARDS in SARS-CoV-2 patients. Angiotensin-converting enzyme 2 (ACE2) receptor has been shown to be the cornerstone of SARS-CoV-2 infection and possibly plays a significant role in the occurrence of renal injury. The pathogenesis of AKI is likely multifactorial that involves not only direct viral invasion but also dysregulated immune response in the form of cytokine storm, ischemia to kidneys, hypercoagulable state, and rhabdomyolysis, among others. We performed a literature search of the Pubmed and Google Scholar database from 1996 to 2020 using the following keywords: severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019, angiotensin-converting enzyme 2 receptor, and acute kidney injury to find the most pertinent and highest-quality of evidence. Any cited references were reviewed to identify relevant literature. The purpose of this review is to discuss, explore, and summarize the relationship between AKI in SARS-CoV-2 patients, with a focus on its epidemiology, association with ACE2 receptors, and pathophysiology of AKI.