Premium
Biochip Array Analysis of Various Mediators of Inflammation in Disseminated Intravascular Coagulation
Author(s) -
Rahman Saud,
Hoppensteadt Debra,
Cunanan Josephine,
Davis Rachael,
Sadeghi Nasir,
Fareed Jawed
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.951.4
Subject(s) - disseminated intravascular coagulation , thrombomodulin , fibrinolysis , medicine , inflammation , lipocalin , coagulation , endothelial dysfunction , systemic inflammation , tumor necrosis factor alpha , pathophysiology , pathology , immunology , thrombin , platelet
Disseminated intravascular coagulation is a polypathologic syndrome which involves blood, endothelial and target organ dysfunction resulting in the generation of various mediators of vascular dysfunction, hemostatic aberrations and hemodynamic disturbances. In addition, various disorders of target organs such as kidney, liver, heart and brain are observed. Uncontrolled protease generation results in the formation of various mediators of inflammation such as neuron specific enolase (NSE), neutrophil gelatinase associated lipocalin (NGal) and soluble tumor necrosis factor receptor 1 (TNF R1). Endothelial damage results in the generation of thrombomodulin (TM) and endogenous coagulation/fibrinolysis results in D‐ Dimer formation. In order to study the circulating levels of these mediators, a Biochip array method (Randox, Oceanside, CA) was utilized with samples obtained from clinically diagnosed DIC (n=100) and normal individuals (n=10). Circulating levels of these mediators were markedly increased in DIC patients in comparison to normals. The most striking increase was noted in NGal (4–6 fold) and TNF R1 (10 fold). Other mediators were also increased in the DIC group, however the data was broadly scattered. These results indicate that NGal and TNF R1 along with other mediators play a major role in the pathophysiology of DIC.