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Eosinophilic oesophagitis: treatment using Montelukast
  1. R Sinharay
  1. Royal Gwent Hospital, Cardiff Rd, Newport, Gwent NP20 2UB, UK; ranjitsinharay{at}

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I read with interest the paper by Attwood and colleagues (Gut 2003;52:181–5) on eosinophilic oesophagitis (EO). According to the authors, the distinct clinical syndrome of EO is not usually seen either as a component of gastro-oesophageal reflux disease or as a variant of eosinophilic gastroenteritis (EG).

The diagnostic hallmark of EO is odynophagia and the diagnosis is always histology dependent (>20 eosinophils/high power field) (Gut 2003;52:181–5). In the paediatric setting, the condition is widely recognised but the adult EO may escape diagnosis due to general lack of awareness of the condition. In this respect, the paper by Attwood and colleagues (Gut 2003;52:181–5) is a valuable contribution towards understanding the complex oesophageal condition of EO.

The pathophysiology of EG or EO may be similar to that of asthma. Asthmatic patients demonstrate increased production of cysteinyl leukotrienes during acute asthma attacks.1 Cysteinyl leukotrienes have potent chemoattractant properties for eosinophils and play an important role in the pathophysiology of asthma.

In EG, accumulated eosinophils cause severe tissue damage characteristic of EG. Cysteinyl leukotrienes, along with cytokines interleukin 3 and 5 and granulocyte macrophage-colony stimulating factor play a role in the recruitment of eosinophils into the tissue causing the damage.2

No controlled treatment trial for EG or EO exist. Limited results have been achieved with oral cromolyn, ketotifen, and other antihistamines. Oral corticosteroids are effective but long term use is complicated by side effects.

Montelukast is a leukotriene receptor antagonist (LTRA) which actively and selectively blocks the leukotriene D4 (LTD4) receptor. Because LTD4 is both produced by and a chemotactic factor for eosinophils, this may provide the rationale for treating a patient with EG or EO with a LTRA. The first reported case of successful Montelukast treatment for an young EG patient was published in 1999.3

Montelukast was originally licensed in the UK for use in asthma.4 There has been some concern regarding association between the use of LTRA and Churg-Strauss syndrome (CSS) in asthma.5,6 CSS is a rare form of eosinophilic vasculitis associated with asthma. This syndrome has previously been associated with the use of Zafirlukast.6 The Committee on Safety of Medicines has received 12 reports of CSS and pulmonary eosinophilia possibly associated with Montelukast.7 There are other reports of Montelukast induced CSS in asthma patients8 in the literature.

Attwood and colleagues (Gut 2003;52:181–5) observed nausea in four patients and myalgia in one in the Montelukast group but there was no mention of CSS. In the previous report of Montelukast therapy in EG, it was shown that Montelukast did not affect tissue eosinophilia (TE) or symptoms in a patient with severe EG complicated by oesophageal stricture.9 In another report, Montelukast reduced peripheral eosinophilia but there was no mention of whether TE was reduced.3 In Attwood et al’s paper (Gut 2003;52:181–5), treatment with Montelukast for a median period of 14 months in eight patients out of a cohort of 12 patients with EO did not change the density of TE. However, subjective improvements were seen in seven patients with swallowing difficulties in Attwood’s series, one of eight patients on Montelukast.

LTRAs are a useful therapy for EO. While anti-leukotriene drugs are generally safe and effective for most patients, from the asthma experience I conclude that clinicians need to be vigilant of any development of CSS in all patients with eosinophilic oesophagitis undergoing treatment with Montelukast. I agree with the authors that further randomised control trials are required to assess the full benefits of Montelukast therapy in EO.


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