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Original Article


Detection of Local Mast-Cell Activity in Patients With Food Hypersensitivity


CGB Peterson,1,2 T Hansson,2,3 A Skott,4 U Bengtsson,5 S Ahlstedt,4,6 J Magnusson5,7

1 Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden
2 Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden
3 Department of Medicine, Rheumatology Unit, Karolinska Institute, Stockholm, Sweden
4 Phadia AB, Uppsala, Sweden
5 Asthma and Allergy Research Group, Department of Respiratory Medicine and Allergy, Sahlgrenska University Hospital, Gothenburg, Sweden
6 Institute of Environmental Medicine, Center for Allergy Research, Karolinska Institute, Stockholm, Sweden
7 Department of Rheumatology and Infl ammation Research, Sahlgrenska University Hospital, Gothenburg, Sweden

J Investig Allergol Clin Immunol 2007; Vol. 17 (5): 314-320



Background: Mast cells play a central role in many inflammatory diseases and assessment of their activation may be of use to provide objective confi rmation of the outcome of food challenge in the diagnosis of food hypersensitivity. However, to date, assessment of mastcell activation using serum markers has been unsuccessful.

Objective: The aim of this study was to explore whether locally released tryptase could be detected in stool samples from patients with food hypersensitivity.

Methods: Nine patients (median age, 55 years; range, 26 - 68 years) with food hypersensitivity confi rmed by double-blind placebo-controlled food challenge were included in the study. Tryptase concentration was assessed in stool samples collected before and after an open food challenge at home and symptoms were recorded throughout the study. Tryptase concentration was also assessed in stool samples from
16 apparently healthy individuals (median age, 44 years; range, 27 - 72 years).

Results: Measurement of fecal tryptase levels in 16 healthy control subjects revealed an upper limit of the normal range (mean + 2 SD of log transformed data) of 10 ng/g. Fecal tryptase levels exceeded 10 ng/g in 7 out of 9 patients in one or more samples obtained during the study. The tryptase levels varied between patients in response to the food challenge and the individual mean levels of tryptase correlated with the corresponding levels of the infl ammatory marker eosinophil protein X (ρ = 0.7500, P = .02).

Conclusion: Measurement of tryptase levels in stool samples is feasible using the method described here. Our results revealed elevated concentrations of fecal tryptase in patients with food hypersensitivity. However, several factors, including food exposure, may account for the increase in fecal tryptase and further studies are necessary to elucidate the role of mast cells in food hypersensitivity.

Key words: Asthma. Mast cell. Tryptase. Eosinophil. EPX. Food hypersensitivity. Gastrointestinal.