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 Womens and Childrens 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 |
Abstract |
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. |
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