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.