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Oesophagus: S E A Attwood, C J Lewis, C S Bronder, C D Morris, G R Armstrong, and J Whittam Eosinophilic oesophagitis: a novel treatment using Montelukast Gut 2003; 52: 181-185 [Abstract] [Full text] [PDF]

Electronic letters published:

Eosinophilic oesophagitis: treatment using Montelukast

Ranjit Sinharay   (9 April 2003)

Eosinophilic oesophagitis: treatment using Montelukast 9 April 2003
Ranjit Sinharay, Consultant Physician Royal Gwent Hospital, Cardiff Road, Newport,Gwent NP20 2UB Send letter to journal: Re: Eosinophilic oesophagitis: treatment using Montelukast ranjitsinharay{at}hotmail.com Ranjit Sinharay	Dear Editor I read with interest the paper by Attwood et al.[1] 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 ).[1] 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, et al.[1] is a valuable contribution towards understanding the complex oesophageal condition of EO. Pathophysiology of EG or EO may be similar to that of asthma. Asthmatic patients demonstrate increased production of cysteinyl leukotrienes during acute asthma attacks.[2] 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.[3] No controlled trartment trial either 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) receptors. Because LTD4 is both produced by and is a chemotactic factor for eosinophils, this may provide the rationale for treating a patient eith EG or EO with a LTRAs. First reported case of successful Montelukast treatment for an young EG patient was published in 1999.[4] Montelukast was originally licensed in UK for use in asthma.[5] There has been some concern regarding association between the use of LTRA and Churg-Strauss syndrome (CSS) in asthma.[6,7] CSS is a rare form of eosinophilic vasculitis associated with asthma. This syndrome has previously been associated with the use of Zafirlukast.[7] The Committee on Safety of Medicines (CSM) has received 12 reports of CSS and pulmonary eosinophilia possibly associated with Montelukast.[8] There are other reports of Montelukast induced CSS in asthma patients [9] in the literature. Attwood, et al.[1] observed nausea in four patients and myalgia in one in the Montelukast group but there was no mentioning of CSS. In the previous report of Montelukast therapy in EG, it had been shown that Montelukast did not affect neither the tissue eosinophilia (TE) nor the symptoms in a patient with severe EG complicated by oesophageal stricture.[10] In another report Montelukast reduced pheripheral eosinophilia, but there was no mentioning of whether TE was reduced.[4] In the Attwood et al.'s paper,[1] treatment with Montelukast for a median period of 14 months in eight patients out of the cohort of twelve 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 1 of eight patients on Montelukast. LTRAs are an useful therapy for EO. While anti-leukotriene drugs are generally safe and effective for most patients, from the asthma-experience I conclude that the 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 furthere randomised control trials are going to be required to assess the full benefits of Montelukast therapy in EO. References (1) Attwood SEA, Lewis CJ, Bronder CS, Morris CD, Armstrong GR, Whittam J. Eosinophilic oesophagitis: a novel treatment using Montelukast. Gut 2003;52:181-85. (2) Bisgaard H. Pathophysiology of the cysteinyl leukotrienes and effects of leukotriene receptor antagonists in asthma. Allergy 2001; 56 (suppl 66): 7-11. (3) Daneshjoo R, J Talley N. Eosinophilic gastroenteritis. Curr Gastroenterol Rep 2002; 4: 366-72. (4) Neustrom MR, Friesen C. Treatment of eosinophilic gastroenteritis with montelukast. J Allergy Clin Immunol 1999; 104: 506. (5) Sampson A, Holgate S. Leukotriene modifiers in the traetment of asthma. BMJ 1998; 316: 1257-58. (6) Wechsler ME, Garpestad E, Flier SR, et al. Pulmonary infiltrates, eosinophilia and cardiomyopathy. JAMA 1998; 279: 455-57. (7) Churg J, Churg A. Zafirlukast and Churg-Strauss syndrome. JAMA 1998; 279: 1949-50. (8) Committee on the Safety of Medicines. Leukotriene antagonists: a new class of asthma treatment. Curr Probl Pharmacovigilance 1998; 24: 14. (9) Tuggey JM, Hosker HSR. Churg-Strauss syndrome associated with montelukast therapy. Thorax 2000; 55: 805-06. (10) Daikh BE, Ryan CK, Schwartz RH. Montelukast reduces peripheral blood eosinophilia but not tissue eosinophilia or symptoms in a patient with eosinophilic gastroenteritis and esophageal stricture. Ann Allergy Asthma Immunol 2003; 90: 23-27.