Thrombin lag time is increased in children with mild asthma

Background: Inflammation and coagulation are closely linked events. Thrombin is the key enzyme in coagulation system and also has roles in inflammation. Objective: The aim of our study was to evaluate thrombin generation in children with mild asthma. Methods: Forty-two children with mild asthma and 49 healthy children were included in the study. All patients performed spirometry. Thrombin generation tests (TGT) were performed with a calibrated automated thrombogram (CAT) in children without asthma exacerbation during the last six months. During CAT assay thrombogram curves were obtained. The area under the curve showed endogenous thrombin potentials and indicated the total amount of endogenous thrombin generated; the peak height showed the highest thrombin value, thrombin lag time and time to thrombin peak were measured. Results: Thrombin lag time was significantly longer in children with asthma (3.98 ± 1.2 min) compared to those in the control group (3.29 ± 0.6min) (p < 0.01). Children with asthma also had longer thrombin tail time compared to the control group (19.5 ± 8.9 min vs. 16.7 ± 2.9 min, p = 0.02). Thrombin peak was inversely correlated with FEF 25-75 (r = -0.41, p < 0.01). Thrombin lag time was inversely correlated with FEF 25-75 (r = -0.39, p < 0.01). Conclusion: Inflammation in mild asthma seems to disturb coagulation but this disturbance may not be so strong as to increase thrombin levels and may only affect the initiation phase of thrombin generation

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Thrombin lag time is increased in children with mild asthma.

BACKGROUND: Inflammation and coagulation are closely linked events. Thrombin is the key enzyme in coagulation system and also has roles in inflammation. OBJECTIVE: The aim of our study was to evaluate thrombin generation in children with mild asthma. METHODS: Forty-two children with mild asthma and 49 healthy children were included in the study. All patients performed spirometry. Thrombin generation tests (TGT) were performed with a calibrated automated thrombogram (CAT) in children without asthma exacerbation during the last six months. During CAT assay thrombogram curves were obtained. The area under the curve showed endogenous thrombin potentials and indicated the total amount of endogenous thrombin generated; the peak height showed the highest thrombin value, thrombin lag time and time to thrombin peak were measured. RESULTS: Thrombin lag time was significantly longer in children with asthma (3.98±1.2min) compared to those in the control group (3.29±0.6min) (p<0.01). Children with asthma also had longer thrombin tail time compared to the control group (19.5±8.9min vs. 16.7±2.9min, p=0.02). Thrombin peak was inversely correlated with FEF 25-75 (r=-0.41, p<0.01). Thrombin lag time was inversely correlated with FEF 25-75 (r=-0.39, p<0.01). CONCLUSION: Inflammation in mild asthma seems to disturb coagulation but this disturbance may not be so strong as to increase thrombin levels and may only affect the initiation phase of thrombin generation.

The efficacy of platelet-rich plasma gel in MRSA-related surgical wound infection treatment: an experimental study in an animal model.

INTRODUCTION: The wound healing properties of platelet-rich plasma (PRP) gel have been documented in many studies. PRP gel has also become a promising agent for treating surgical site infections. In this study, we investigated the antibacterial activity and wound healing effectiveness of PRP in an animal model of Methicillin-resistant Staphylococcus aureus subsp. aureus (MRSA N315)-contaminated superficial soft tissue wounds. MATERIALS AND METHODS: Subcutaneous wounds in Wistar Albino male rats were created by making two cm midline incisions followed by inoculation of microorganisms. Study groups comprised of Sham (no treatment), PRP alone, MRSA alone, MRSA + PRP, MRSA + Vancomycin, and MRSA + Vancomycin + PRP groups. We inoculated 0.1 mL (3 × 108 CFU/mL) of MRSA in contaminated groups. After 8 days, all rats were killed, wounds were excised and subjected to histopathologic examination, and MRSA counts were determined. RESULTS: MRSA counts in MRSA, MRSA + PRP, MRSA + Vancomycin and MRSA + Vancomycin + PRP groups were 5.1 × 106 (SD ± 0.4) CFU/mL, 4.3 × 106 (SD ± 0.7) CFU/mL, 2.3 × 106 (SD ± 0.3) CFU/mL, 1.1 × 106 (SD ± 0.4) CFU/mL, respectively. The inflammation scores of MRSA + PRP, MRSA + Vancomycin, and MRSA + Vancomycin + PRP groups were significantly lower than the MRSA group. MRSA + Vancomycin + PRP group inflammation score was significantly lower than the MRSA + PRP group. DISCUSSION: All treatment groups were effective in wound healing and decreasing the MRSA counts. MRSA + PRP combined created identical inflammation scores to the PRP group. More in vivo studies are required to corroborate these findings.