PMID- 18458712
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20100617
LR  - 20211020
IS  - 0159-8090 (Print)
IS  - 0159-8090 (Linking)
VI  - 25
IP  - 2
DP  - 2004 May
TI  - Severe acute respiratory syndrome: clinical and laboratory manifestations.
PG  - 121-32
AB  - Severe acute respiratory syndrome (SARS) is a recently emerged infectious disease 
      with significant morbidity and mortality. An epidemic in 2003 affected 8,098 
      patients in 29 countries with 774 deaths. The aetiological agent is a new 
      coronavirus spread by droplet transmission. Clinical and general laboratory 
      manifestations included fever, chills, rigor, myalgia, malaise, diarrhoea, cough, 
      dyspnoea, pneumonia, lymphopenia, neutrophilia, thrombocytopenia, and elevated 
      serum lactate dehydrogenase (LD), alanine aminotransferase (ALT) and creatine 
      kinase (CK) activities. Treatment has been empirical; initial potent antibiotic 
      cover, followed by simultaneous ribavirin and corticosteroids, with or without 
      pulse high-dose methylprednisolone, have been used. The postulated disease 
      progression comprises (1) active viral infection, (2) hyperactive immune 
      response, and (3) recovery or pulmonary destruction and death. We investigated 
      serum LD isoenzymes and blood lymphocyte subsets of SARS patients, and found LD1 
      activity as the best biochemical prognostic indicator for death, while CD3+, 
      CD4+, CD8+ and natural killer cell counts were promising predictors for intensive 
      care unit (ICU) admission. Plasma cytokine and chemokine profiles showed markedly 
      elevated Th1 cytokine interferon (IFN)-gamma, inflammatory cytokines interleukin 
      (IL)-1beta, IL-6 and IL-12, neutrophil chemokine IL-8, monocyte chemoattractant 
      protein-1 (MCP-1), and Th1 chemokine IFN-gamma-inducible protein-10 (IP-10) for 
      at least two weeks after disease onset, but there was no significant elevation of 
      inflammatory cytokine tumor necrosis factor (TNF)-alpha and anti-inflammatory 
      cytokine IL-10. Corticosteroid reduced IL-8, MCP-1 and IP-10 concentrations from 
      5-8 days after treatment. Measurement of biochemical markers of bone metabolism 
      demonstrated significant but transient increase in bone resorption from Day 28-44 
      after onset of fever, when pulse steroid was most frequently given. With tapering 
      down of steroid therapy, there was a decrease in bone resorption marker together 
      with an increase in bone formation markers round Day 50, suggesting that some of 
      the bone loss might be reversed. Our research studies on the chemical pathology 
      and clinical immunology of SARS should have implications for the pathophysiology 
      and therapy of this potentially lethal infection.
FAU - Lam, Christopher W K
AU  - Lam CW
AD  - Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of 
      Wales Hospital, Shatin, Hong Kong. waikeilam@cuhk.edu.hk
FAU - Chan, Michael H M
AU  - Chan MH
FAU - Wong, Chun K
AU  - Wong CK
LA  - eng
PT  - Journal Article
PL  - Australia
TA  - Clin Biochem Rev
JT  - The Clinical biochemist. Reviews
JID - 8215797
PMC - PMC1904416
EDAT- 2008/05/07 09:00
MHDA- 2008/05/07 09:01
PMCR- 2004/05/01
CRDT- 2008/05/07 09:00
PHST- 2008/05/07 09:00 [pubmed]
PHST- 2008/05/07 09:01 [medline]
PHST- 2008/05/07 09:00 [entrez]
PHST- 2004/05/01 00:00 [pmc-release]
AID - cbr25_2p121 [pii]
PST - ppublish
SO  - Clin Biochem Rev. 2004 May;25(2):121-32.