OBJECTIVE: To investigate the changes in plasma levels of thrombomodulin (TM) and D-dimer (DD) in children with different types of Mycoplasma pneumoniae pneumonia (MPP), and their role in the pathogenesis of MPP in children. METHODS: Fifty-two children with MMP were divided into lobar pneumonia (n=30) and interstitial pneumonia groups (n=22) and another 30 healthy children were selected as the control group. Plasma levels of TM and D-D were measured using enzyme-linked immunosorbent assay and latex-enhanced immunoturbidimetric assay, respectively. RESULTS: The lobar pneumonia, interstitial pneumonia and control groups had median plasma TM levels of 23.83, 15.56 and 8.78 μg/L respectively, with significant differences between the three groups (P<0.01). The lobar pneumonia and interstitial pneumonia groups had significantly higher plasma TM levels than the control group (P<0.01), and the lobar pneumonia group had a significantly higher plasma TM level than the interstitial pneumonia group (P<0.05). Median plasma D-D levels in the lobar pneumonia and interstitial pneumonia groups were significantly higher than the reference value (P<0.01). The lobar pneumonia group had a significantly higher plasma D-D level than the interstitial pneumonia group (0.35 μg/mL vs 0.13 μg/mL; P<0.01), and the percentage of patients with elevated plasma D-D levels was significantly higher in the lobar pneumonia group than in the interstitial pneumonia group (87% vs 59%; P<0.05). CONCLUSIONS: Children with MPP, especially those with lobar pneumonia, have increased plasma levels of TM and D-D. This suggests that damage to vascular endothelial cells and blood hypercoagulability may be involved in the pathogenesis of MPP.
OBJECTIVE: To investigate the changes in plasma levels of thrombomodulin (TM) and D-dimer (DD) in children with different types of Mycoplasma pneumoniae pneumonia (MPP), and their role in the pathogenesis of MPP in children. METHODS: Fifty-two children with MMP were divided into lobar pneumonia (n=30) and interstitial pneumonia groups (n=22) and another 30 healthy children were selected as the control group. Plasma levels of TM and D-D were measured using enzyme-linked immunosorbent assay and latex-enhanced immunoturbidimetric assay, respectively. RESULTS: The lobar pneumonia, interstitial pneumonia and control groups had median plasma TM levels of 23.83, 15.56 and 8.78 μg/L respectively, with significant differences between the three groups (P<0.01). The lobar pneumonia and interstitial pneumonia groups had significantly higher plasma TM levels than the control group (P<0.01), and the lobar pneumonia group had a significantly higher plasma TM level than the interstitial pneumonia group (P<0.05). Median plasma D-D levels in the lobar pneumonia and interstitial pneumonia groups were significantly higher than the reference value (P<0.01). The lobar pneumonia group had a significantly higher plasma D-D level than the interstitial pneumonia group (0.35 μg/mL vs 0.13 μg/mL; P<0.01), and the percentage of patients with elevated plasma D-D levels was significantly higher in the lobar pneumonia group than in the interstitial pneumonia group (87% vs 59%; P<0.05). CONCLUSIONS:Children with MPP, especially those with lobar pneumonia, have increased plasma levels of TM and D-D. This suggests that damage to vascular endothelial cells and blood hypercoagulability may be involved in the pathogenesis of MPP.