Predicting the severity of systemic inflammatory response syndrome (SIRS)-associated coagulopathy with hemostatic molecular markers and vascular endothelial injury markers.
BACKGROUND
The changes in biomarkers of coagulation or fibrinolysis, anticoagulation, inflammation, and endothelial damage occur in patients with systemic inflammatory response syndrome (SIRS). The purpose of this study is to assess the prognostic value of these markers in patients with SIRS-associated hypercoagulopathy.


METHODS
Sixty-six SIRS patients with a platelet count less than 15.0 x 10(4)/mm3 in three university hospital intensive care units were enrolled in this prospective, comparative study. Blood samples were obtained on day 0 and day 2. Twelve hemostatic, inflammatory, and vascular endothelial indices were measured and the data were compared between the severe group (patients with a total maximum Sequential Organ Failure Assessment score of 10 or more and nonsurvivors; n = 25) and the less-severe group (Sequential Organ Failure Assessment score <10; n = 41).


RESULTS
Significant changes between the groups were observed in platelet count, fibrin or fibrinogen degradation products, interleukin-6, soluble thrombomodulin, antithrombin (AT) activity, and protein C activity, both on day 0 and on day 2. In contrast, the d-dimer, soluble fibrin, plasmin-[alpha]2-antiplasmin complex, and E-selectin levels were higher in the severe group only on day 2. No significant difference was seen regarding the thrombin-AT complex and total plasminogen activator inhibitor on both days. A comparison of the areas under the receiver operating characteristic curve revealed the AT activity to be the best predictor of a progression of organ dysfunction.


CONCLUSIONS
The changes in some hemostatic molecular markers and vascular endothelial markers were conspicuous in patients with organ dysfunction. The AT activity is considered to be the most useful predictor of organ dysfunction.
Iba
Toshiaki
T
Division Acute and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine. iba-jun@umin.ac.jp
Gando
Satoshi
S
Murata
Atsuo
A
Kushimoto
Shigeki
S
Saitoh
Daizoh
D
Eguchi
Yutaka
Y
Ohtomo
Yasuhiro
Y
Okamoto
Kohji
K
Koseki
Kazuhide
K
Mayumi
Toshihiko
T
Ikeda
Toshiaki
T
Ishhikura
Hiroyasu
H
Ueyama
Masashi
M
Ogura
Yuji
Y
Endo
Shigeatsu
S
Shimazaki
Shuji
S
D000990:Antithrombin III; D019540:Area Under Curve; D015415:Biomarkers / Q000097:blood; D001778:Blood Coagulation Disorders / Q000097:blood* / Q000209:etiology*; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000293:injuries* / Q000378:metabolism; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D005341:Fibrinolysin / Q000378:metabolism; D006487:Hemostasis; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood; D010976:Platelet Count; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D018746:Systemic Inflammatory Response Syndrome / Q000145:classification / Q000150:complications*; D018180:Thrombomodulin / Q000097:blood; D000979:alpha-2-Antiplasmin / Q000378:metabolism
D015415:Biomarkers; D019040:E-Selectin; D005338:Fibrin Fibrinogen Degradation Products; D015850:Interleukin-6; D018180:Thrombomodulin; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D005337:Fibrin; D005340:Fibrinogen; D010447:Peptide Hydrolases; D005341:Fibrinolysin