In view of the excellent results we had obtained using
KETOTIFEN in the treatment of respiratory
allergies, we decided to carry out a study of its protective action in cases of
allergies of purely alimentary etiology; that is, in patients symptoms only appeared after the ingestion of certain foodstuffs. The subjects of this study were 16 patients, 8 men and 8 women, aged from 13 to 49. The diagnosis of
food allergy was reached by means of a clear and detailed history, skin tests, hemagglutination tests and positive oral provocation tests with the tested
antigens in all patients. The basal oral provocation tests were carried out when the patients were fasting, using progressively larger doses of the
antigens until a positive response was obtained, consisting of an exact reproduction of the symptomatology described in the history. After an interval of at least 10 days, a second oral provocation test was performed under identical conditions, using the same dose of
antigens, after a treatment consisting of 1
capsule (1 mg.) of
KETOTIFEN every 12 hours during the 5 days prior to the test. Clinical symptoms appearing singly or together in the OPT were dermal in 8 patients (50%), respiratory in 7 patients (42.85%) and gastrointestinal in 3 patients (18.75%). In 7 patients whose
shock organ was the expiratory system, (group A) shows the decrease in FEV1 in each patient. It clearly shows that the patients had a smaller decrease in FEV1
after treatment, as compared with baseline values after OPT. On the other hand, 9 patients whose
shock organ was the skin and the gut (group B), the protection ws complete in 6 patients (66%). The
drug was well tolerated, the only side effects observed being
somnolence in one patient and dryness of the mouth in another (12.5%). No changes were observed in the hemogram, ESR, blood tests, pulse,
blood sugar and urinalysis. The most recent studies of the mechanism of action of
KETOTIFEN are suggestive, but have not yet provided a complete explanation. This
drug inhibits the release of
histamine and
SRS-A from mast cells, basophils and neutrophils. The fact that, as distinct from DSCG, it acts on neutrophils, inhibiting the release of
SRS-A, suggests that its mode of action does not only concern those reactions mediated by
IgE.