4. Discussion
We hope to investigate the appropriate drug therapy based on a novel classification system for adenoids based on their appearance. Thus, we divided the appearance of adenoids into three types: edematous type, common type, and fibrous type, and the pathological description was consistent with the appearance of adenoids.
In our study, we found that 70.67% (106/150) AH patients with AR, and of them 68% (72/106) of adenoids were the edematous type. The results showed that AR was the risk factor for the development of AH. Among the patients with AR, adenoids are mostly edematous type. Since the adenoid tissue is closer to the nasal anatomy, these areas have the same lymphatic drainage. Studies have indicated that local allergic inflammation may play an important role in childhood AH[8]. AR, asthma, and allergic dermatitis were risk factors for the development of AH [9].
Intranasal corticosteroids are known to significantly affect the production and/or activity of various pro-inflammatory mediators locally in the nasal mucosa, along with a decrease in vascular permeability and edema. This anti-inflammatory effect might reduce the immunological activation shown in hypertrophied adenoid tissue[10]. We found the expression of CGR-α and CGR-β were higher in the edematous type but not in common and fibrous types. It is indicated that glucocorticoid was only useful in the edematous type adenoid.
Leukotrienes are the key inflammatory mediators in the respiratory system and are usually involved in the pathogenesis of childhood diseases, such as asthma. They are also systemically and locally involved in the process of inflammation in AH[11]. Studies have confirmed the overexpression of CysLTR1 [12] and CysLTR2[13] in the adenoid tissue. Also, treatment with leukotriene receptor antagonist has been shown to reduce the adenoid volume [14]. In this study, we found that CysLTR1, CysLTR2 were stably expressed in all types of adenoid tissues. It is indicated that leukotriene receptor antagonist was the most important drug for the treatment of AH.
Additionally, we found that eosinophil count was higher in edematous type compared with the common type, and there was a positive correlation between eosinophil count in blood and in the adenoid tissue. But there was no correlation between the history of allergic diseases and the number of eosinophils in adenoid tissue. When only lateral radiographs is available without fiberoptic nasal endoscopic results, we consult on blood routines. If a patient’s blood routine shows an increased eosinophil count, eosinophils in adenoid tissue are also likely more abundant. According to our research results, we can preliminarily judge that the adenoid tissue of this patient is edematous, and the treatment of nasal glucocorticoid combined with leukotriene receptor antagonist is appropriate. On the contrary, if a patient’s blood routine shows a low eosinophil count, leukotriene receptor antagonists alone can be selected to treat AH.