Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe acute respiratory syndrome (SARS) is a viral disease, observed primarily in Southern China in November 2002, with variable flu-like symptoms and pneumonia, in approx. 5% leading to death from respiratory distress syndrome (RDS). The disease was spread over more than 30 states all over the globe by SARS-virus-infected travelers. WHO and CDC received first information about a new syndrome by the end of February 2003, after the first cases outside the Republic of China had been observed. A case in Hanoi, Vietnam, led to the first precise information about the new disease entity to WHO, by Dr. Carlo Urbani, a co-worker of WHO/Doctors without Borders, who had been called by local colleagues to assist in the management of a patient with an unknown severe disease by the end of February 2003. Dr. Urbani died from SARS, as did many other health care workers. In the meantime, more than 7,000 cases have been observed worldwide, predominantly in China and Hong Kong, but also in Taiwan, Canada, Singapore, and the USA, and many other countries, and more than 600 of these patients died from RDS. Since the beginning of March 2003, when WHO and CDC started their activities, in close collaboration with a group of international experts, including the Bernhard-Nocht-Institute in Hamburg and the Department of Virology in Frankfurt/Main, a previously impossible success in the disclosure of the disease was achieved. Within only 8 weeks of research it was possible to describe the infectious agent, a genetically modified coronavirus, including the genetic sequence, to establish specific diagnostic PCR methods and to find possible mechanisms for promising therapeutic approaches. In addition, intensifying classical quarantine and hospital hygiene measures, it was possible to limit SARS in many countries to sporadic cases, and to reduce the disease in countries such as Canada and Vietnam. This review article summarizes important information about many issues of SARS (May 15th, 2003).
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PMID:[Severe acute respiratory syndrome (SARS)]. 1287 9

The severe acute respiratory syndrome (SARS) is a highly infectious respiratory disease, to the best of our knowledge caused by a hitherto unknown corona virus. The virus has spread from South East Asia to many countries of the world. Three case reports of patients from the Prince of Wales Hospital of The Chinese University of Hong Kong demonstrate typical clinical courses. Fever, cough, in most cases non-productive, myalgia, chills, and rigor are the leading symptoms. Leucopenia and thrombocytopenia are the most prominent laboratory parameters, increased values for lactatedehydrogenase (LDH) reflect a more severe clinical course. Advanced age and coexisting conditions seem to influence the prognosis unfavourably. The chest roentgenogram may be normal initially but at a later stage progressive consolidations in the majority of peripheral parts of the lung are observed, which cannot be differentiated from pneumonias of other origin. Even young patients can enter a stage of respiratory compromise rather fast. A therapy against the cause of the disease is not known. Empirical therapy with ribavirin in combination with high dose corticosteroids have proved successful. The disease may progress into respiratory failure comparable with an acute respiratory distress syndrome (ARDS). Mortality is around five to ten per cent. Stringent hygiene and quarantine measures are mandatory to prevent the further spread of this threatening disease.
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PMID:[Severe acute respiratory syndrome (SARS)]. 1281 63

In order to investigate the clinical pathology of severe acute respiratory syndrome (SARS), the autopsies of three patients who died from SARS in Nan Fang Hospital Guangdong, China were studied retrospectively. Routine haematoxylin and eosin (H&E) staining was used to study all of the tissues from the three cases. The lung tissue specimens were studied further with Macchiavello staining, viral inclusion body staining, reticulin staining, PAS staining, immunohistochemistry, ultrathin sectioning and staining, light microscopy, and transmission electron microscopy. The first symptom was hyperpyrexia in all three cases, followed by progressive dyspnoea and lung field shadowing. The pulmonary lesions included bilateral extensive consolidation, localized haemorrhage and necrosis, desquamative pulmonary alveolitis and bronchitis, proliferation and desquamation of alveolar epithelial cells, exudation of protein and monocytes, lymphocytes and plasma cells in alveoli, hyaline membrane formation, and viral inclusion bodies in alveolar epithelial cells. There was also massive necrosis of splenic lymphoid tissue and localized necrosis in lymph nodes. Systemic vasculitis included oedema, localized fibrinoid necrosis, and infiltration of monocytes, lymphocytes, and plasma cells into vessel walls in the heart, lung, liver, kidney, adrenal gland, and the stroma of striated muscles. Thrombosis was present in small veins. Systemic toxic changes included degeneration and necrosis of the parenchyma cells in the lung, liver, kidney, heart, and adrenal gland. Electron microscopy demonstrated clusters of viral particles, consistent with coronavirus, in lung tissue. SARS is a systemic disease that injures many organs. The lungs, immune organs, and systemic small vessels are the main targets of virus attack, so that extensive consolidation of the lung, diffuse alveolar damage with hyaline membrane formation, respiratory distress, and decreased immune function are the main causes of death.
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PMID:The clinical pathology of severe acute respiratory syndrome (SARS): a report from China. 1284 23

Severe acute respiratory syndrome (SARS) is a newly described and highly contagious respiratory infection. Many adult patients will develop progressive hypoxia, and a large proportion will develop respiratory distress syndrome (RDS), possibly related to massive and uncontrolled activation of the immune system. The mortality has been reported to be quite high, especially in the elderly with comorbid conditions. The causative agent has been identified as a novel coronavirus, and children appear to acquire the infection by close-contact household exposure to an infected adult. However, the severity is much milder and the clinical progression much less aggressive in young children. The exact pathophysiology of SARS is still unclear, and the medical treatment of SARS remains controversial. The main treatment regime used in Hong Kong is a combination of ribavirin and steroid. To date, there have been no reported case fatalities in children with this disease. The success of reducing the burden of this infection in children will depend on proper isolation of infected adults early in the course of illness. Strict public health policy and quarantine measures are the key in controlling the infection in the community.
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PMID:Severe acute respiratory syndrome in children. 1295 37

Severe acute respiratory syndrome (SARS) is a newly emerged disease that rapidly spread around the world. The disease originated in southern China and a novel coronavirus (SARS CoV) has been implicated as the causative organism. The path this virus took to set up human infection remains a mystery, though preliminary data point to origins in an animal reservoir. Nosocomial transmission of SARS CoV has been a striking feature in this epidemic. The clinical illness is similar to many acute respiratory infections, although a large proportion of patients show a rapid deterioration with respiratory distress towards the end of the second week of illness. The management principles are broadly similar to treating any community acquired pneumonia but the infection control measures take a pivotal role. There is no proven antiviral agent against SARS CoV. The most remarkable feature about the SARS epidemic was the speed with which the global community acted in a coordinated way to control it.
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PMID:Severe acute respiratory syndrome (SARS): a review. 1513 36

Severe Acute Respiratory Syndrome (SARS) caused by new corona--virus SARS-Co-V was not identified at humans and animals up to this time. A characteristic feature of this disease is biphasic course. First high fever, parainfluenza syndrome followed by increasing respiratory distress. The main role in transmission is droplet way, things contaminated by excreta, blood transfusion is not excluded. Pathomorphological changes are: bronchial epithelial denudation, loss of cilia, squamous metaplasia, a giant cells infiltrate of macrophages in the alveoli, haemophagocytosis, atrophy white pulp of the spleen. Diagnosis is based on clinical picture and epidemiological data supported by positive serology, PCR or presence virus in cell culture. In treatment ribavirin, steroids and mechanical ventilation are used.
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PMID:[Severe acute respiratory syndrome (SARS)--new, unknown disease?]. 1517 7

Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease with a significant morbidity and mortality. The major clinical features include persistent fever, chills/rigor, myalgia, malaise, dry cough, headache and dyspnoea. Respiratory failure is the major complication of SARS and approximately 20% of patients may progress to acute respiratory distress syndrome requiring invasive mechanical ventilatory support. However, the severity is much milder in infected young children. Treatment of SARS was empirical in 2003 due to our limited understanding of this new disease. Protease inhibitors (lopinavir/ritonavir) in combination with ribavirin may play a role as antiviral therapy in the early phase, whereas the role of IFN and systemic steroid in preventing immune-mediated lung injury deserves further investigation. Knowledge of the genomic sequence of the SARS coronavirus has facilitated the development of rapid diagnostic tests. In addition, other antiviral treatment, RNA interference, monoclonal antibody, synthetic peptides, and vaccines are being developed. This paper provides a review of the epidemiology, clinical features and possible treatment strategies of SARS.
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PMID:Advancements in the battle against severe acute respiratory syndrome. 1526 83

In mid-April 2003, a major outbreak of severe acute respiratory syndrome (SARS) developed in Taiwan. During the outbreak, SARS-associated coronavirus (SARS-CoV) was documented in 346 patients and 73 of them died. Autopsy was performed in 9 of the suspected SARS patients who died during the outbreak, but SARS was the cause of death in only 1 of these patients. Here we report the histological features of this patient and their clinicopathological correlations. The patient, a 36-year-old Indonesian woman, was a caretaker working for a Taiwanese family. She stayed in Taipei Jen-Chi Hospital from April 10 to April 19 to take care of her elderly employer. She developed fever on April 21 and respiratory distress on April 25, and received ribavirin, intravenous immunoglobulin, and steroid. The respiratory distress persisted and worsened, and intubation was performed on April 27. The respiratory condition improved initially after mechanical ventilation, but subcutaneous emphysema and pneumomediastinum developed on May 1. Her condition deteriorated rapidly and she died on May 2, 11 days after the onset of fever. Autopsy was performed on the same day. Histologically, the lungs showed severe diffuse alveolar damage and bronchopneumonia, but no viral inclusion. The spleen and lymph nodes revealed lymphoid depletion and the liver showed microvesicular steatosis. No specific pathological change was seen in the gastrointestinal tract and kidneys. SARS-CoV genome was detected in the nasopharyngeal aspirate and the autopsy lung specimen.
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PMID:Clinicopathology of severe acute respiratory syndrome: an autopsy case report. 1549 31

Tracheoesophageal fistula is an uncommon complication usually associated with chronic usage of ventilator and pressure necrosis of the tracheoesophageal wall. A 56-year-old female patient with severe acute respiratory syndrome (SARS) with tracheoesophageal fistula is reported. She was intubated for ventilatory support 3 days after admission because of progressive respiratory distress. Methylprednisolone pulse therapy followed by a maintenance dosage was given due to persistence of bilateral pulmonary fibrosis. Thirty three days after admission, she underwent tracheostomy because of difficulty in weaning from the ventilator. Ten days after tracheostomy, she developed tracheoesophageal fistula, which was confirmed by bronchoscopy and panendoscopy. Tracheal resection and primary repair for the esophageal defect was performed via a cervical incision combined with partial sternotomy. She was weaned from the ventilator soon after the surgery and discharged 34 days after the operation. In SARS patients with persistent pulmonary fibrosis and under prolonged corticosteroid treatment, special care should be given to avoid intubation-related tracheal injury during the period of ventilatory support. The tracheoesophageal fistula, once developed, can be repaired in a single stage after improvement of the nutritional status.
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PMID:Surgical treatment of tracheoesophageal fistula in a patient with severe acute respiratory syndrome complicated with extensive pulmonary fibrosis. 1562 43

Findings coming from autopsies and serum of SARS patients suggest an important immune-inflammatory implication in the evolution to respiratory distress. Conditions such as HIV infection or treatment with immunosuppressors (in cancer or autoimmune diseases) are not among the bad prognosis factors for development of distress. To date, there have been no reported case fatalities in children, probably due to their more immature immune system. Our conclusions follow: (1) The milder form of SARS in children and the apparent protective factor that immunosupression represent rules out a significant viral cytopathic effect (they would be the most affected). (2) The evidence for immune implication in distress strongly supports immunomodulators for therapy: phosphodiesterase inhibitors (due to their down-modulating activity on proinflammatory cytokines); inhaled corticoids (aimed at producing a local immunomodulation); teophylline or nedocromil sodium (which prevents inflammatory cell recruitment into the airway wall). (3) An early immunomodulatory therapy, based on the levels of proinflammatory cytokines and clinical parameters to evaluate the respiratory function such as arterial oxygen saturation, could prevent the occurrence of distress. (4) Vaccine design should consider the immune origin of distress. (5) Physicians should be aware of mildly symptomatic patients (children, immuno-compromised hosts) to avoid transmission to immunocompetent adults.
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PMID:Severe acute respiratory syndrome, a pathological immune response to the new coronavirus--implications for understanding of pathogenesis, therapy, design of vaccines, and epidemiology. 1567 50


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