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Proteomic analysis reveals platelet factor 4 and beta‐thromboglobulin as prognostic markers in severe acute respiratory syndrome
Author(s) -
Poon Terence C.W.,
Pang Ronald T.K.,
Chan K.C. Allen,
Lee Nelson L.S.,
Chiu Rossa W.K.,
Tong YuKwan,
Chim Stephen S.C.,
Ngai Sai M.,
Sung Joseph J.Y.,
Lo Y.M. Dennis
Publication year - 2012
Publication title -
electrophoresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.666
H-Index - 158
eISSN - 1522-2683
pISSN - 0173-0835
DOI - 10.1002/elps.201200002
Subject(s) - ards , beta thromboglobulin , medicine , logistic regression , pathogenesis , platelet factor 4 , western blot , immunology , platelet activation , platelet , gastroenterology , biology , lung , gene , biochemistry
Previously, we reported that proteomic fingerprints were present in sera of patients with severe acute respiratory syndrome ( SARS ), and could separate patients into subgroups with different prognoses. In the present study, we examined the prognostic values of the SARS ‐associated proteomic features by biostatistical analysis, and deciphered the identities of those with prognostic values. Data of 20 SARS ‐associated serum proteomic features and ten serological variables from 38 SARS adult patients before treatment were subjected to multivariate logistic regression. Proteomic features of m/z 6634, m/z 7769, m/z 8635, and m/z 8865 were identified as independent prognostic markers. After purification by cation‐exchange chromatography and gel electrophoresis, proteomic features of m/z 7769 and m/z 8865 were found to be platelet factor 4 (PF4) and beta‐thromboglobulin (beta‐TG) by tandem mass spectrometry, respectively. The associations of decreased serum PF 4 and increased serum beta‐ TG levels with poor prognosis were confirmed by W estern blot. Previous studies suggest that PF 4 and beta‐ TG are involved in the pathogenesis of acute respiratory distress syndrome ( ARDS ) in a negative and positive way, respectively. Our results suggest that PF 4 and beta‐ TG may also play similar roles in the development of ARDS in SARS patients.