Clinical manifestations and inflammatory cytokine responses in patients with severe acute respiratory syndrome

Wang Huei Sheng, Bor Luen Chiang, Shan Chwen Chang, Hung Nern Ho, Jann Tay Wang, Yee Chun Chen, Cheng Hsiang Hsiao, Po Ren Hseuh, Wei Chu Chie, Pan Chyr Yang

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Background and Purpose: Severe acute respiratory syndrome (SARS) is a highly transmissible disease with significant morbidity and mortality. Death from SARS is most often due to rapidly progressive respiratory compromise (acute respiratory distress syndrome, ARDS) and subsequent multi-organ dysfunction. However, the mechanisms evoking respiratory distress and a fulminant systemic response remain unclear. In order to elucidate the pathogenic mechanisms of SARS, we analyzed clinical manifestations and levels of serum cytokines of SARS patients. Methods: Fourteen hospitalized patients with a diagnosis of SARS-associated coronavirus infection at National Taiwan University Hospital from March to May 2003 were included. Data on clinical manifestations, parameters of laboratory tests, complications and final outcomes of patients were collected retrospectively. Serial plasma inflammatory cytokines, including interleukin (IL)-1beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-alpha (TNF-α) of preserved serum were measured by enzyme immunoassay. Results: All 14 patients had fever, dry cough and dyspnea. Twelve were intubated during hospitalization. The median duration from onset of fever to the nadir level or most severe condition was 9 days for hypoxia, 7 days for lymphocytopenia, 6.5 days for thrombocytopenia, 9.5 days for maximal pulmonary infiltrates; to peak serum levels was 9 days for C-reactive protein (CRP), 10.5 days for IL-6, 13.5 days for IL-8 and 12 days for TNF-α; to defervescence was 13 days. There was no significant elevation of serum IL-1β levels in any of the 14 patients. There were no significant differences in peak levels of IL-6, IL-8 and TNF-α between patients with and without ARDS. The 8 patients who died tended to have higher peak levels of serum TNF-α compared to those who survived (14 vs 9.1 pg/mL; p = 0.06). Conclusion: Rapid elevation of inflammatory cytokines-IL-6, IL-8 and TNF-α might play a role in the development of SARS-related ARDS. The timing of elevations in inflammatory cytokines and CRP is correlated with progression of pulmonary infiltrates of SARS patients. The peak level of serum TNF-α tends to be higher in patients who die of SARS than in those who survive. Our results indicate that CRP and TNF-α might be used as prognostic markers of SARS.

Original languageEnglish
Pages (from-to)715-723
Number of pages9
JournalJournal of the Formosan Medical Association
Volume104
Issue number10
Publication statusPublished - Dec 1 2005
Externally publishedYes

Fingerprint

Hydroxycorticosteroids
SARS Virus
Severe Acute Respiratory Syndrome
Adult Respiratory Distress Syndrome
Taiwan
Retrospective Studies
Cytokines
Tumor Necrosis Factor-alpha
Interleukin-8
Interleukin-6
Serum
Interleukin-1beta
C-Reactive Protein
Fever
Coronavirus Infections
Lung
Lymphopenia
Interleukin-12
Immunoenzyme Techniques
Cough

Keywords

  • Hydroxycorticosteroids
  • Inflammatory cytokines
  • Respiratory distress syndrome, adult
  • Severe acute respiratory syndrome

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Sheng, W. H., Chiang, B. L., Chang, S. C., Ho, H. N., Wang, J. T., Chen, Y. C., ... Yang, P. C. (2005). Clinical manifestations and inflammatory cytokine responses in patients with severe acute respiratory syndrome. Journal of the Formosan Medical Association, 104(10), 715-723.

Clinical manifestations and inflammatory cytokine responses in patients with severe acute respiratory syndrome. / Sheng, Wang Huei; Chiang, Bor Luen; Chang, Shan Chwen; Ho, Hung Nern; Wang, Jann Tay; Chen, Yee Chun; Hsiao, Cheng Hsiang; Hseuh, Po Ren; Chie, Wei Chu; Yang, Pan Chyr.

In: Journal of the Formosan Medical Association, Vol. 104, No. 10, 01.12.2005, p. 715-723.

Research output: Contribution to journalArticle

Sheng, WH, Chiang, BL, Chang, SC, Ho, HN, Wang, JT, Chen, YC, Hsiao, CH, Hseuh, PR, Chie, WC & Yang, PC 2005, 'Clinical manifestations and inflammatory cytokine responses in patients with severe acute respiratory syndrome', Journal of the Formosan Medical Association, vol. 104, no. 10, pp. 715-723.
Sheng, Wang Huei ; Chiang, Bor Luen ; Chang, Shan Chwen ; Ho, Hung Nern ; Wang, Jann Tay ; Chen, Yee Chun ; Hsiao, Cheng Hsiang ; Hseuh, Po Ren ; Chie, Wei Chu ; Yang, Pan Chyr. / Clinical manifestations and inflammatory cytokine responses in patients with severe acute respiratory syndrome. In: Journal of the Formosan Medical Association. 2005 ; Vol. 104, No. 10. pp. 715-723.
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abstract = "Background and Purpose: Severe acute respiratory syndrome (SARS) is a highly transmissible disease with significant morbidity and mortality. Death from SARS is most often due to rapidly progressive respiratory compromise (acute respiratory distress syndrome, ARDS) and subsequent multi-organ dysfunction. However, the mechanisms evoking respiratory distress and a fulminant systemic response remain unclear. In order to elucidate the pathogenic mechanisms of SARS, we analyzed clinical manifestations and levels of serum cytokines of SARS patients. Methods: Fourteen hospitalized patients with a diagnosis of SARS-associated coronavirus infection at National Taiwan University Hospital from March to May 2003 were included. Data on clinical manifestations, parameters of laboratory tests, complications and final outcomes of patients were collected retrospectively. Serial plasma inflammatory cytokines, including interleukin (IL)-1beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-alpha (TNF-α) of preserved serum were measured by enzyme immunoassay. Results: All 14 patients had fever, dry cough and dyspnea. Twelve were intubated during hospitalization. The median duration from onset of fever to the nadir level or most severe condition was 9 days for hypoxia, 7 days for lymphocytopenia, 6.5 days for thrombocytopenia, 9.5 days for maximal pulmonary infiltrates; to peak serum levels was 9 days for C-reactive protein (CRP), 10.5 days for IL-6, 13.5 days for IL-8 and 12 days for TNF-α; to defervescence was 13 days. There was no significant elevation of serum IL-1β levels in any of the 14 patients. There were no significant differences in peak levels of IL-6, IL-8 and TNF-α between patients with and without ARDS. The 8 patients who died tended to have higher peak levels of serum TNF-α compared to those who survived (14 vs 9.1 pg/mL; p = 0.06). Conclusion: Rapid elevation of inflammatory cytokines-IL-6, IL-8 and TNF-α might play a role in the development of SARS-related ARDS. The timing of elevations in inflammatory cytokines and CRP is correlated with progression of pulmonary infiltrates of SARS patients. The peak level of serum TNF-α tends to be higher in patients who die of SARS than in those who survive. Our results indicate that CRP and TNF-α might be used as prognostic markers of SARS.",
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AU - Sheng, Wang Huei

AU - Chiang, Bor Luen

AU - Chang, Shan Chwen

AU - Ho, Hung Nern

AU - Wang, Jann Tay

AU - Chen, Yee Chun

AU - Hsiao, Cheng Hsiang

AU - Hseuh, Po Ren

AU - Chie, Wei Chu

AU - Yang, Pan Chyr

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N2 - Background and Purpose: Severe acute respiratory syndrome (SARS) is a highly transmissible disease with significant morbidity and mortality. Death from SARS is most often due to rapidly progressive respiratory compromise (acute respiratory distress syndrome, ARDS) and subsequent multi-organ dysfunction. However, the mechanisms evoking respiratory distress and a fulminant systemic response remain unclear. In order to elucidate the pathogenic mechanisms of SARS, we analyzed clinical manifestations and levels of serum cytokines of SARS patients. Methods: Fourteen hospitalized patients with a diagnosis of SARS-associated coronavirus infection at National Taiwan University Hospital from March to May 2003 were included. Data on clinical manifestations, parameters of laboratory tests, complications and final outcomes of patients were collected retrospectively. Serial plasma inflammatory cytokines, including interleukin (IL)-1beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-alpha (TNF-α) of preserved serum were measured by enzyme immunoassay. Results: All 14 patients had fever, dry cough and dyspnea. Twelve were intubated during hospitalization. The median duration from onset of fever to the nadir level or most severe condition was 9 days for hypoxia, 7 days for lymphocytopenia, 6.5 days for thrombocytopenia, 9.5 days for maximal pulmonary infiltrates; to peak serum levels was 9 days for C-reactive protein (CRP), 10.5 days for IL-6, 13.5 days for IL-8 and 12 days for TNF-α; to defervescence was 13 days. There was no significant elevation of serum IL-1β levels in any of the 14 patients. There were no significant differences in peak levels of IL-6, IL-8 and TNF-α between patients with and without ARDS. The 8 patients who died tended to have higher peak levels of serum TNF-α compared to those who survived (14 vs 9.1 pg/mL; p = 0.06). Conclusion: Rapid elevation of inflammatory cytokines-IL-6, IL-8 and TNF-α might play a role in the development of SARS-related ARDS. The timing of elevations in inflammatory cytokines and CRP is correlated with progression of pulmonary infiltrates of SARS patients. The peak level of serum TNF-α tends to be higher in patients who die of SARS than in those who survive. Our results indicate that CRP and TNF-α might be used as prognostic markers of SARS.

AB - Background and Purpose: Severe acute respiratory syndrome (SARS) is a highly transmissible disease with significant morbidity and mortality. Death from SARS is most often due to rapidly progressive respiratory compromise (acute respiratory distress syndrome, ARDS) and subsequent multi-organ dysfunction. However, the mechanisms evoking respiratory distress and a fulminant systemic response remain unclear. In order to elucidate the pathogenic mechanisms of SARS, we analyzed clinical manifestations and levels of serum cytokines of SARS patients. Methods: Fourteen hospitalized patients with a diagnosis of SARS-associated coronavirus infection at National Taiwan University Hospital from March to May 2003 were included. Data on clinical manifestations, parameters of laboratory tests, complications and final outcomes of patients were collected retrospectively. Serial plasma inflammatory cytokines, including interleukin (IL)-1beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-alpha (TNF-α) of preserved serum were measured by enzyme immunoassay. Results: All 14 patients had fever, dry cough and dyspnea. Twelve were intubated during hospitalization. The median duration from onset of fever to the nadir level or most severe condition was 9 days for hypoxia, 7 days for lymphocytopenia, 6.5 days for thrombocytopenia, 9.5 days for maximal pulmonary infiltrates; to peak serum levels was 9 days for C-reactive protein (CRP), 10.5 days for IL-6, 13.5 days for IL-8 and 12 days for TNF-α; to defervescence was 13 days. There was no significant elevation of serum IL-1β levels in any of the 14 patients. There were no significant differences in peak levels of IL-6, IL-8 and TNF-α between patients with and without ARDS. The 8 patients who died tended to have higher peak levels of serum TNF-α compared to those who survived (14 vs 9.1 pg/mL; p = 0.06). Conclusion: Rapid elevation of inflammatory cytokines-IL-6, IL-8 and TNF-α might play a role in the development of SARS-related ARDS. The timing of elevations in inflammatory cytokines and CRP is correlated with progression of pulmonary infiltrates of SARS patients. The peak level of serum TNF-α tends to be higher in patients who die of SARS than in those who survive. Our results indicate that CRP and TNF-α might be used as prognostic markers of SARS.

KW - Hydroxycorticosteroids

KW - Inflammatory cytokines

KW - Respiratory distress syndrome, adult

KW - Severe acute respiratory syndrome

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