This study shows that there is no difference in age and gender distribution between the atopic and non atopic groups of children. The age of onset of MPP is still mainly in school-age children, but there is also a trend of onset in infants and young children. There was no statistically significant difference in hospital stay and fever duration between the two groups of children, but the atopic group had a higher incidence of wheezing, longer duration of lung rales, and higher levels of eosinophils and IgE compared to the non atopic group. Research by Qian Shenghua et al. has shown that MP is one of the main pathogens causing wheezing diseases in children, and recurrent wheezing in children is closely related to allergens, allergy history, and atopic constitution [7]. Fan et al. [8]also confirmed that atopic constitution plays an important role in children's wheezing and coughing. Some studies suggest[9] that the antigen of Mycoplasma pneumoniae stimulates the body to produce autoantibodies, while the body activates the complement system to release inflammatory factors, causing an imbalance in the THL/TH2 ratio and stimulating B cells to produce IgE and an increase in the synthesis and secretion of eosinophils, resulting in wheezing[10]. After MP infection in children with atopic constitution, excessive inflammatory response leads to sustained tissue inflammation damage in the body, causing severe immune pathological processes and pathological damage, resulting in recurrent wheezing, long cough and wheezing time, and prolonged rales, ultimately leading to prolonged hospitalization.
The results of this study showed that there was no difference in CRP, PCT, D-dimer and other indicators between the two groups of children, but the lactate dehydrogenase levels in the atopic group were higher than those in the non atopic group. Wang Zhihua et al.'s research [11]also confirmed this. LDH is widely present in various tissues of the body, such as the brain, kidneys, liver, myocardium, and lungs. When cells are invaded by pathogens, the cell membrane is damaged, and a large amount of LDH is released into the extracellular space, causing a significant increase in LDH in serum [12]. Therefore, LDH, as a marker of tissue destruction, is a warning indicator for severe Mycoplasma pneumoniae pneumonia [13–16]. Studies have shown that atopic constitution is a risk factor for severe and refractory Mycoplasma pneumoniae pneumonia [17]. Compared to children with non atopic constitution, children with atopic constitution have a more severe condition and greater inflammatory response, resulting in a more significant increase in serum LDH. This can also serve as a basis for systemic administration of glucocorticoids. There was no difference in the use of glucocorticoids between the two groups of children in the study, but the atopic group had a longer duration of glucocorticoid use. Corticosteroids have anti-inflammatory, anti allergic, and immune suppressive effects, making them the most effective anti-inflammatory drugs currently available. Children with atopic constitution have high airway reactivity and long wheezing time, which should be taken seriously and given targeted treatment plans.
This study found that the pulmonary imaging of children in the atopic group was mainly characterized by bronchiolitis, while children in the non atopic group were mainly characterized by consolidation. Li Xufeng et al.[18] found that the imaging of Mycoplasma pneumoniae pneumonia showed a close correlation between bronchiolitis type changes and atopic constitution. Huang Kunling et al. also stated [19]that MP bronchiolitis often occurs in infants and preschool children with a family or personal history of allergies. This may be related to the strong immune response in children with atopic constitution. MP adheres to respiratory epithelial cells through P1 adhesin, activating the body's immune response, inducing the production of pro-inflammatory factors by its own epithelial cells, and secreting CARDS toxins [16, 20]. Krishnan M et al. [21] found that CARDS toxin can cause non programmed cell death in targeted cells, while the host initiates an innate immune response, damaging the structure of the bronchioles, and then abnormal repair processes lead to fibrous tissue proliferation, causing lumen narrowing, and in severe cases, even leading to the occurrence of occlusive bronchiolitis. In recent years, with the increase of MP infection rate, there has been an increasing trend of MP induced bronchiolitis, and the probability of left occlusive bronchiolitis has gradually increased. It should be fully valued by clinical physicians.