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Abstract
Background:
Plasma coagulation factor XIII (FXIII) catalyzes the formation of covalent bounds between fibrin monomers, thus stabilizing the fibrin clot and increasing its resistance to fibrinolysis. Alteration of FXIII may contribute to bleeding, wound dehiscence and recurrent abortion. However, standard clotting tests cannot detect the FXIII deficiency. In this study, we evaluated a newly developed FXIII test kit (CoalinkTM, PeopleBio Inc., Seoul, Korea) in patients with various clinical conditions.
Methods:
We evaluated the linearity and precision of the new FXIII test kit and compared the results of the new kit and the Pefakit FXIII assay. The FXIII was tested in idiopathic thrombocytopenic purpura (ITP) (n=40) patients, chronic renal failure (CRF) (n=20) patients, liver cirrhosis (LC) (n=40) patients, EDTA-induced pseudothrombocytopenia (EDTAIP) (n=10) patients, and in normal healthy persons (n=50). In the normal healthy persons, we determined a complete blood count (CBC), Ed-highlight-the second (n=50) is redundant. prothrombin time (PT) measurement and activated partial prothrombin time (aPTT) measurement and evaluated the results using the two assays.
Results:
Serial dilution experiments with five samples provided good linearity (r2=0.9717). The intra-and inter assay precisions (CV) were 2.3∼8.6% and 3.9∼14.9%, respectively (n=20). There was a significant correlation between the use of the new kit and the Pefakit FXIII assay (r=0.8798, n=50). The FXIII activities of the normal healthy persons, ITP, CRF, LC and EDTAIP patients were 103.3±23.3%, 79.7± 41.0%, 117.9±82.3%, 56.9±23.7% and 130.0±29.0%, respectively and they were significantly decreased in the ITP and LC patients (P＜0.05). The rates below 80% of the FXIII level were 67.5% in the ITP patients, 90.0% in the LC patients, 35.0% in the CRF patients and 0.0% in the EDTAIP patients. FXIII activities were closely related to platelet count (r=0.832, P＜0.05) and negatively correlated with PT (r= ?0.389, P＜0.05) and aPTT (r=?0.326, P＜0.05).
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Fig. 1
Quantitative measurement of FXIII and FXIIIa activities in clinical sample by using the transglutaminase activity. The mechanism is based on the cross-linking the HRP conjugated FXIII fibrinogen complex to casein coated plate by thrombin activated FXIIIa, which is in the clinical sample. The crosslinked HRP is detected with HRP chromogenic substrate.
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