Eosinophilic esophagitis

To the Editor: In the February 2015 issue of Cleveland Clinic Journal of Medicine, Dr. David A. Katzka reviewed the major clinical features of eosinophilic esophagitis and, having presented its allergic component, rightly assessed the inherent difficulties of detecting and eliminating food allergens involved in the development and course of this disease.¹ The inadequacies of serologic testing were mentioned, as well as the difficulties of endoscopy and biopsy “painstakingly performed with the removal and reintroduction of every suspected food allergen, requiring multiple biopsies weekly, which is impractical for safety and economic reasons.”¹

In a meta-analysis, Arias et al² showed that such an individualized approach for each food is not really necessary. Elemental diets with graded reintroduction of grouped foods were effective in detecting and treating the responsible food allergies in 90.8% of cases (95% confidence interval [CI] 84.7–95.5). In fact, the more pragmatic, simple, and inexpensive six-food-elimination diet was also reasonably effective (72.1% of cases, 95% CI 65.8–78.1). Both outcomes are far superior to elimination strategies directed at immunoglobulin E (IgE), which were effective in only 45.5% of cases (95% CI 35.4–55.7%).²

Franciosi and Liacouras³ described a practical and comprehensive elimination-reintroduction protocol consisting of four steps that, in combination with symptom diaries, can easily identify responsible foods.

In our practice, graded elimination-reintroduction diets—which, depending on history, may range from the basic six-food-elimination diet to the fully developed Franciosi-Liacouras protocol—along with food IgE testing and judicial use of IgG testing against selected foods, have yielded detection and successful treatment rates comparable to the 90.8% rate reported by Arias et al.² Upon identification of food allergens, a dual approach of diet restrictions and food immunotherapy is initiated. As a result of this approach, patients only need to undergo a single endoscopy and biopsy to demonstrate decreased eosinophil counts, usually 1 year after initiation of allergy treatment.

Of course, pharmacologic management is necessary in the treatment of eosinophilic esophagitis. However, the inclusion of montelukast in the standard first-line regimen for eosinophilic esophagitis is not yet a firmly established practice. Not all eosinophilia can be equated to allergy, and not all allergic inflammation is leukotriene-dependent. Furthermore, too little is known about the secondary effects of leukotrienes on immune regulation and whether their blockade is really desirable in eosinophilic esophagitis. But it is known that leukotriene receptor antagonists, especially montelukast, can trigger Churg-Strauss vasculitis, a syndrome whose eosinophil activation, homing pattern, and subsequent proliferation—as well as its exclusive prevalence in allergic patients with asthma and chronic sinusitis—bear some similarity to those of eosinophilic esophagitis.

To the Editor: In the February 2015 issue of Cleveland Clinic Journal of Medicine, Dr. David A. Katzka reviewed the major clinical features of eosinophilic esophagitis and, having presented its allergic component, rightly assessed the inherent difficulties of detecting and eliminating food allergens involved in the development and course of this disease.¹ The inadequacies of serologic testing were mentioned, as well as the difficulties of endoscopy and biopsy “painstakingly performed with the removal and reintroduction of every suspected food allergen, requiring multiple biopsies weekly, which is impractical for safety and economic reasons.”¹

In a meta-analysis, Arias et al² showed that such an individualized approach for each food is not really necessary. Elemental diets with graded reintroduction of grouped foods were effective in detecting and treating the responsible food allergies in 90.8% of cases (95% confidence interval [CI] 84.7–95.5). In fact, the more pragmatic, simple, and inexpensive six-food-elimination diet was also reasonably effective (72.1% of cases, 95% CI 65.8–78.1). Both outcomes are far superior to elimination strategies directed at immunoglobulin E (IgE), which were effective in only 45.5% of cases (95% CI 35.4–55.7%).²

Franciosi and Liacouras³ described a practical and comprehensive elimination-reintroduction protocol consisting of four steps that, in combination with symptom diaries, can easily identify responsible foods.

In our practice, graded elimination-reintroduction diets—which, depending on history, may range from the basic six-food-elimination diet to the fully developed Franciosi-Liacouras protocol—along with food IgE testing and judicial use of IgG testing against selected foods, have yielded detection and successful treatment rates comparable to the 90.8% rate reported by Arias et al.² Upon identification of food allergens, a dual approach of diet restrictions and food immunotherapy is initiated. As a result of this approach, patients only need to undergo a single endoscopy and biopsy to demonstrate decreased eosinophil counts, usually 1 year after initiation of allergy treatment.

Of course, pharmacologic management is necessary in the treatment of eosinophilic esophagitis. However, the inclusion of montelukast in the standard first-line regimen for eosinophilic esophagitis is not yet a firmly established practice. Not all eosinophilia can be equated to allergy, and not all allergic inflammation is leukotriene-dependent. Furthermore, too little is known about the secondary effects of leukotrienes on immune regulation and whether their blockade is really desirable in eosinophilic esophagitis. But it is known that leukotriene receptor antagonists, especially montelukast, can trigger Churg-Strauss vasculitis, a syndrome whose eosinophil activation, homing pattern, and subsequent proliferation—as well as its exclusive prevalence in allergic patients with asthma and chronic sinusitis—bear some similarity to those of eosinophilic esophagitis.

To the Editor: In the February 2015 issue of Cleveland Clinic Journal of Medicine, Dr. David A. Katzka reviewed the major clinical features of eosinophilic esophagitis and, having presented its allergic component, rightly assessed the inherent difficulties of detecting and eliminating food allergens involved in the development and course of this disease.¹ The inadequacies of serologic testing were mentioned, as well as the difficulties of endoscopy and biopsy “painstakingly performed with the removal and reintroduction of every suspected food allergen, requiring multiple biopsies weekly, which is impractical for safety and economic reasons.”¹

In a meta-analysis, Arias et al² showed that such an individualized approach for each food is not really necessary. Elemental diets with graded reintroduction of grouped foods were effective in detecting and treating the responsible food allergies in 90.8% of cases (95% confidence interval [CI] 84.7–95.5). In fact, the more pragmatic, simple, and inexpensive six-food-elimination diet was also reasonably effective (72.1% of cases, 95% CI 65.8–78.1). Both outcomes are far superior to elimination strategies directed at immunoglobulin E (IgE), which were effective in only 45.5% of cases (95% CI 35.4–55.7%).²

Franciosi and Liacouras³ described a practical and comprehensive elimination-reintroduction protocol consisting of four steps that, in combination with symptom diaries, can easily identify responsible foods.

In our practice, graded elimination-reintroduction diets—which, depending on history, may range from the basic six-food-elimination diet to the fully developed Franciosi-Liacouras protocol—along with food IgE testing and judicial use of IgG testing against selected foods, have yielded detection and successful treatment rates comparable to the 90.8% rate reported by Arias et al.² Upon identification of food allergens, a dual approach of diet restrictions and food immunotherapy is initiated. As a result of this approach, patients only need to undergo a single endoscopy and biopsy to demonstrate decreased eosinophil counts, usually 1 year after initiation of allergy treatment.

Of course, pharmacologic management is necessary in the treatment of eosinophilic esophagitis. However, the inclusion of montelukast in the standard first-line regimen for eosinophilic esophagitis is not yet a firmly established practice. Not all eosinophilia can be equated to allergy, and not all allergic inflammation is leukotriene-dependent. Furthermore, too little is known about the secondary effects of leukotrienes on immune regulation and whether their blockade is really desirable in eosinophilic esophagitis. But it is known that leukotriene receptor antagonists, especially montelukast, can trigger Churg-Strauss vasculitis, a syndrome whose eosinophil activation, homing pattern, and subsequent proliferation—as well as its exclusive prevalence in allergic patients with asthma and chronic sinusitis—bear some similarity to those of eosinophilic esophagitis.