This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Erin, E. M. Articles by Hansel, T. T. Search for Related Content PubMed Articles by Erin, E. M. Articles by Hansel, T. T.

Study of Infliximab Treatment in Asthma

We are in agreement with the comments of Dr. Edwards and Prof. Polosa on our study employing a monoclonal antibody directed against TNF- in patients with moderate asthma (1). Indeed, the major message from our article is that this type of therapy now merits assessment in larger scale, longer term clinical trials of patients with severe asthma. We concur that these studies should include asthma exacerbations as a major clinical endpoint. Further encouragement for examining therapy directed against TNF- is provided by a recently published study in 10 patients with severe refractory asthma who noted improvements in asthma-related quality-of-life, lung function, and bronchial hyperresponsiveness (2), and an open-label study in 17 patients with severe asthma that recorded improvements in asthma symptoms, lung function, and bronchial hyperresponsiveness (3).

Therapy of severe allergic asthma with anti-IgE therapy (omalizumab) has convincingly demonstrated that this agent can improve asthma control and decrease the rate of severe asthma exacerbations and emergency visits (4–9). Furthermore, it is notable that in patients with more severe disease, the effects on exacerbations can be more convincing than those on symptoms. In our study of infliximab in moderate asthma, we agree that there were trends toward improvement in morning PEF, and that these changes became more convincing with time, so that a longer term study with higher doses is rational. Finally, the measurement of cytokines, such as TNF-, in induced sputum might be a useful way to select those patients who may respond to therapy directed against TNF-, and could have utility in monitoring therapeutic responses.

Edward M. Erin, Onn Min Kon, Peter J. Barnes and Trevor T. Hansel

National Heart and Lung Institute, Royal Brompton Hospital, London, United Kingdom

FOOTNOTES

Conflict of Interest Statement:E.M.E. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. O.M.K. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. P.J.B. has received funding and has served on scientific advisory boards for GlaxoSmithKline, AstraZeneca, Boehringer-Ingelheim, Novartis, Altana, Pfizer, and Millennium. T.T.H. has received research grants in 2004 to May 2006 from GlaxoSmithKline ($250,000), Novartis ($500,000), and Oxogen ($360,000).

REFERENCES

1. Erin EM, Leaker BR, Nicholson GC, Tan AJ, Green LM, Neighbour H, Zacharasiewicz AS, Turner J, Barnathan ES, Kon OM, et al. The effects of a monoclonal antibody directed against tumor necrosis factor- in asthma. Am J Respir Crit Care Med 2006;174:753–762.[Abstract/Free Full Text]
2. Berry MA, Hargadon B, Shelley M, Parker D, Shaw DE, Green RH, Bradding P, Brightling CE, Wardlaw AJ, Pavord ID. Evidence of a role of tumor necrosis factor alpha in refractory asthma. N Engl J Med 2006;354:697–708.[Abstract/Free Full Text]
3. Howarth PH, Babu KS, Arshad HS, Lau L, Buckley M, McConnell W, Beckett P, Al Ali M, Chauhan A, Wilson SJ, et al. Tumour necrosis factor (TNFalpha) as a novel therapeutic target in symptomatic corticosteroid dependent asthma. Thorax 2005;60:1012–1018.[Abstract/Free Full Text]
4. Soler M, Matz J, Townley R, Buhl R, O'Brien J, Fox H, Thirlwell J, Gupta N, Della CG. The anti-IgE antibody omalizumab reduces exacerbations and steroid requirement in allergic asthmatics. Eur Respir J 2001;18:254–261.[Abstract/Free Full Text]
5. Busse W, Corren J, Lanier BQ, McAlary M, Fowler-Taylor A, Cioppa GD, van As A, Gupta N. Omalizumab, anti-IgE recombinant humanized monoclonal antibody, for the treatment of severe allergic asthma. J Allergy Clin Immunol 2001;108:184–190.[CrossRef][Medline]
6. Humbert M, Beasley R, Ayres J, Slavin R, Hebert J, Bousquet J, Beeh KM, Ramos S, Canonica GW, Hedgecock S, et al. Benefits of omalizumab as add-on therapy in patients with severe persistent asthma who are inadequately controlled despite best available therapy (GINA 2002 step 4 treatment): INNOVATE. Allergy 2005;60:309–316.[CrossRef][Medline]
7. Holgate ST, Chuchalin AG, Hebert J, Lotvall J, Persson GB, Chung KF, Bousquet J, Kerstjens HA, Fox H, Thirlwell J, et al. Efficacy and safety of a recombinant anti-immunoglobulin E antibody (omalizumab) in severe allergic asthma. Clin Exp Allergy 2004;34:632–638.[CrossRef][Medline]
8. Ayres JG, Higgins B, Chilvers ER, Ayre G, Blogg M, Fox H. Efficacy and tolerability of anti-immunoglobulin E therapy with omalizumab in patients with poorly controlled (moderate-to-severe) allergic asthma. Allergy 2004;59:701–708.[CrossRef][Medline]
9. Bousquet J, Cabrera P, Berkman N, Buhl R, Holgate S, Wenzel S, Fox H, Hedgecock S, Blogg M. Cioppa GD. The effect of treatment with omalizumab, an anti-IgE antibody, on asthma exacerbations and emergency medical visits in patients with severe persistent asthma. Allergy 2005;60:302–308.[CrossRef][Medline]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Erin, E. M. Articles by Hansel, T. T. Search for Related Content PubMed Articles by Erin, E. M. Articles by Hansel, T. T.