Background
Mycoplasma pneumoniae (MP) is a common pathogen of community‐acquired pneumonia in children. In the present study, serum amyloid A (SAA), C‐reactive protein (CRP), and procalcitonin (PCT) levels in children with MP infection were analyzed and the differential diagnoses of MP evaluated.
Methods
The study included 152 children with MP infection hospitalized in Tai’an Central Hospital in Shandong Province and 50 healthy children as controls. SAA, CRP, and PCT, as well as serum immunoglobulins and T lymphocyte subsets were analyzed during the acute and convalescent phases. Among the MP‐infected children, 30 cases were selected to monitor the SAA, immunoglobulins, and T lymphocyte subset levels for a week.
Results
The SAA, CRP, PCT, IgA, and IgM levels were significantly higher in the MP‐infected group than in the control group (F(SAA) = 83.91, p < 0.05; F(CRP) = 40.79, p < 0.05; F(PCT) = 60.58, p < 0.05; F(IgA) = 43.45, p < 0.05; F(IgM) = 233.88, p < 0.05). In addition, the levels of these factors were significantly higher in the acute phase than in the convalescent phase (p < 0.05). However, significant difference was not observed in the IgG level between these two groups (p > 0.05). The CD3+ and CD4+ levels in the MP‐infected group were lower than in the control group ( F(CD3+)= 60.58, P < 0.05; F(CD4+) = 89.05, p < 0.05), and the CD8+ level was higher than in the control group ( F(CD8+)= 96.96, p < 0.05). The CD3+, CD4+, and CD8+ levels were significantly different between the acute phase and the convalescent phase (CD3+: acute phase vs. convalescent phase, q = 2.79, p < 0.05; CD4+: acute phase vs. convalescent phase, q = 2.83, p < 0.05; CD8+: acute phase vs. convalescent phase, q = 3.15, p < 0.05). The changes in serum SAA levels in the MP‐infected group positively correlated with the changes in IgA, IgM, and CD8+ levels and negatively correlated with CD3+, CD4+, and CD4+/CD8+.
Conclusion
SAA, CRP, and PCT were specific markers for diagnosing early MP infection in children. These findings are important in the differential diagnosis of MP infection and clinical guidance for MP treatment.