anotehr study

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We tried this and it didnt work for us; but here's evidence that it did work

for someone -

Treatment of eosinophilic gastroenteritis with montelukast

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To the Editor:

We are reporting what we believe is the first case of a patient successfully

treated with a leukotriene modifier for symptoms related to eosinophilic

gastroenteritis. One of us (C. F.) initially saw a 13-year-old girl for a

3-year history of progressive nonbilious vomiting. Medical history was

remarkable for allergic rhinitis treated with medications and allergen

immunotherapy but no history of food allergies. Review of previous allergy

skin testing showed absence of reactivity to foods. Her previous allergist

had tried an elimination diet with no symptomatic improvement. A complete

blood cell count showed 574 eosinophils/mL (8% of total neutrophils). The

diagnosis was made by demonstration of marked eosinophilia in biopsy

specimens of the esophagus, gastric antrum, and duodenum and elimination of

other potential etiologies. Stool cultures and a barium esophagram with

small bowel follow through were unremarkable. Symptoms continued despite

treatment with oral cromolyn, ranitidine, and hydroxyzine. Montelukast 10 mg

given orally daily was started, with complete symptom resolution. Follow-up

showed one vomiting episode in 4 months of treatment with montelukast. There

was a decrease in peripheral eosinophilia (574 vs 342 eosinophils/mL)

compared with baseline 2 months after medications were started. Cromolyn,

ranitidine, and hydroxyzine were discontinued with no recurrence of

symptoms.

Tissue injury in eosinophilic gastroenteritis has been shown to correlate

with the number of activated degranulated eosinophils present.1 Cytokines

including GM-CSF, IL-3, and IL-5 promote eosinophil proliferation and

differentiation in the bone marrow as well as being eosinophil chemotaxins

to sites of inflammation.2 It has been suggested that the release of these

cytokines with autocrine or paracrine activities by eosinophils in the

lamina propria of gastrointestinal tissue may lead to the persistent

eosinophilic infiltration in eosinophilic gastroenteritis.3 Eosinophil

recruitment may also be enhanced by chemotactic factors such as

platelet-activating factor, C-C chemokines, and cysteinyl leukotrienes.2

Cysteinyl leukotrienes are generated from arachidonic acid through LTC4

synthase by mast cells, eosinophils, alveolar macrophages, and basophils,

leading to end-organ inflammation.2 LTD4 has been shown to be a potent and

specific chemotactic factor for human eosinophils in vitro, which has been

completely inhibited by a selective leukotriene antagonist.4 Many factors

may play a role in directing eosinophils to a site of inflammation. Because

LTD4 is both produced by and is a chemotactic factor for eosinophils, this

may provide the rationale for treating a patient with eosinophilic

gastroenteritis with a leukotriene receptor antagonist. Further research,

including double-blind placebo-controlled clinical studies, is needed to

clarify the potential role leukotrienes play in the inflammation seen in

eosinophilic gastroenteritis and to assess the potential role for

leukotriene modifiers in the treatment of this disease.