A review of the literature on treatment for EGE showed that the first step is dietary restriction [5
]. It is recommended to perform skin prick testing to identify any food allergies [6
]. Although an association is evident between food allergy and EGE, the results of elimination diets are often poor [6
]. The next step is the use of steroids, which have been a mainstay of treatment in EGE. The dosage of PSL given at the onset of the condition is 20 to 40 mg/day for 6 to 8 weeks [6
]. About 90% of patients respond to this therapy [7
]. If patients require high doses of PSL for maintenance or are intolerant of steroid side effects, immunosuppressive drugs such as azathioprine may be helpful as steroid-sparing agents [7
]. Mast cell stabilizers, such as sodium cromoglycate, that prevent the release of histamine, platelet activating factors, and leukotrienes from mast cells, have also been reported to be effective [7
]. Montelukast, an antagonist of the leukotriene receptor Cys-LT1, was also found to be effective and useful as a steroid-sparing agent [8
]. Other case studies have investigated the effectiveness of new interleukin (IL)-4 and IL-5 inhibitors such as suplatast tosilate [9
] in EGE and anti-IL-5 monoclonal antibody mepolizumab in hypereosinophilic syndromes [10
The present case suggests that CAM was effective for the treatment of EGE. During the second relapse, when there was a gradual increase in the eosinophil count, CAM at 400 mg/day was effective in reducing the maintenance dose of PSL. During the third relapse, when eosinophil counts increased rapidly, CAM at an increased dose of 800 mg/day was effective. However, the third relapse occurred during monotherapy with CAM at 400 mg/day, suggesting that this form of treatment was not effective. The fact that CAM treatment could reduce the maintenance dose of PSL was advantageous in reducing the risk of steroid-induced hyperglycemia.
For bronchial asthma, which is caused by eosinophilic and neutrophilic inflammation, a trial of macrolide therapy yielded promising results. In the trial, patients received 200 mg/day of CAM for 8 weeks, after which symptoms, blood and sputum eosinophil counts, and sputum eosinophilic cationic protein levels were significantly decreased. The authors concluded that CAM had a bronchial anti-inflammatory effect associated with decreased eosinophilic infiltration [4
Although bronchial asthma could be controlled by only 200 mg/day of CAM in that trial, a dose of 800 mg/day was needed for control of EGE during the third relapse in the present patient. This suggests that eosinophil activity is higher in EGE than in bronchial asthma.
One study showed that CAM and erythromycin (EM) suppressed the IL-5-induced prolongation of eosinophil survival in a dose-dependent manner. When eosinophils were cultured in the presence of IL-5 with physiologic concentrations of EM or CAM (both 10 µg/mL), the effect of IL-5 was almost abolished, and the morphologic changes in eosinophils observed by electron microscopy were consistent with apoptosis [3
]. EM and its derivatives also inhibit proliferation and induce apoptosis of T-lymphocytes that secrete IL-5 [2
]. In addition to immunomodulatory effects, macrolides also have steroid-sparing effects because of their influence on corticosteroid metabolism.
Study evidence suggests that the macrolide mechanism of action in treating EGE involves anti-eosinophilic effects, anti-T lymphocytic effects, and steroid-sparing effects; however, because only one case is reported, more research is necessary before this treatment can be adopted.