Human mankind is aware of the existence of adverse reactions to foods since classical times. Hippocrates (460-370BC) reported urticaria and gastroin¬testinal upset following cow’s milk (CM) ingestion. Lucretius (98-55BC) wrote “Quod aliis cibus est aliis fuat acre venenum”. Galen (131- 219) described allergy to goat’s milk. At the turn of this century the first description of acute shock due to CM al¬lergy was published, and Schloss was the first to evaluate skin tests for the diagnosis .
Accordingly the aspiration to influence the natural incidence of atopic illness has piqued physicians’ imaginations for a long time. The phenotypic expression of IgE-mediated disorders, which appears regulated by multiple genetic factors and modulated by environmental experiences, has been a target for prevention medicine since the 1920s when dietary intervention was adopted in infancy. During the past 70 years, controversy has emerged from clinical studies designed to evaluate the effect of dietary and environmental exclusions on the subsequent manifestations of atopy. Since then, vast arrays of articles have been published, which were only matched by endless discussions on the terms to be used. The lack of a single, practical diagnostic test has contributed to the polarization of the scientific controversy between “believers” and “nonbelievers”. The problem posed by few diseases like atopic dermatitis (AD) is compounded by the difficulties experienced in its treatment. AD cannot benefit from pre-arranged therapeutic protocols, and is cause of invaluable and long-term physical and emotional suffering for children and parents. Therefore AD confronts doctors with one of the most demanding challenges [2,3].
In a 5-yr prospective study on 56 children (32M, 24F) affected with food hypersensitivity (FH) fulfill¬ing the criteria for the AD diagnosis3 a 4-wk diagnostic elimi¬na¬tion diet was prescribed for diagnostic purposes. CM and dairy prod¬ucts were avoided if AD appeared when milk was the only feeding. If AD occurred when egg and wheat were also given, these foods were avoided. Further foods were elimi¬nated following anamnestic data. Soy-milk (Isomil, Abbott), lamb-meat based-diet , and other
nutritionally ade¬quate food equivalents were employed. An open challenge test was done when skin lesions cleared-up. If no immediate reaction ensued, food was fed in a normal way, and the skin accurately checked by parents. At each visit the severity of skin lesions was evaluated. On the basis of the challenge test, a therapeutic elimination diet, ex¬cluding the offending foods, was given independently of IgE and/or skin test response. All patients were checked every year or more fre¬quently if necessary.
The following parameters were studied at the 5-yr follow-up: age; AD severity score; development of food tolerance; duration of symptoms; respira¬tory allergy (asthma and/or rhinitis). Total IgE determina¬tion was not per¬formed by 7 children, and skin tests and/or IgE to food/inhalant allergens by 13. Due to previous severe ana-phylactic reactions the challenge test to egg was not done in 7 patients and to CM in 3. The median age (MA) of the children at the first examination was 3 yr. MA at AD onset was 3mo, before the 4th mo of life in 27 babies (48%); between the 4th and 6th mo in 10 babies (18%), and after the 6th mo in 19 babies (34%). Mean sever¬ity score of AD was 17. Family history of atopy was positive in 23 pa¬tients (41%). Skin le¬sions were typical in 43 children (77%) and widespread or not typical (reverse pattern) in 13 (23%); 19 patients (34%) had respiratory al¬lergy.
CM formulas were given since birth in 23 (41%), before the 3rd mo in 18 (32%), after the 3rd mo in 15 cases (27%). Total IgE levels were higher than 2 SD for age in 39/49 chil¬dren (80%). Skin tests and/or IgE to food allergens were positive in 45/55 children (82%), and to inhalant allergens in 26/44 children (59%). Main offending foods were CM and egg in 40%, CM alone and egg in 14%, and wheat in 2% of children. Polysensitivity was present mainly towards CM, egg and wheat in 29% of patients. 10/56 children (18%) were sen¬sitive to wheat. At the follow- up the children’s MA was 6 yr+9mo. Skin lesions cleared up
in 32 (57%) children, persisted in 24 (43%). 60% of children
completely lost FH, 14% achieved a partial tolerance, in 26% FH
persisted. There was no differ¬ence in the MA of these 3 groups.
The MA for tolerance to CM was 3 yr+6mo, to egg 4 yr, and to
wheat 4 yr+ 6mo.
There was no age difference at the first examination and at
the follow-up in the groups with and without tolerance. There
was a significant difference (p=0.0001) in the age of AD onset in
the group with tol¬erance (MA 3 mo) and in the group without
tolerance. 28 children (50%) had respiratory allergy at the followup,
21 pa¬tients (37%) developed asthma, 2(4%) rhinitis, and
5(9%) asthma and rhinitis. The children were divided into two
groups: 24 with persisting AD, and 32 with cleared-up AD. There
was a signif¬icant relationship between AD outcome and the
age of onset of the skin le¬sions. In 25/32 children (78%) with
cleared-up AD the onset was before and in 12/24 children (50%)
with persisting AD after the 6th mo of life (p=0.023). There was a
significant relationship between AD outcome and the skin lesion
distribution at the first examination. 29/32 children with healing
(91%) had typical skin lesions at the first ex¬amination, while in
10/24 children (42%) with persisting AD the lesions were not
typical or widespread (p = 0.0001). A significant relationship
was found between AD out-come and the de¬velopment of food
tolerance. 95% of children with healing achieved a complete or
partial tolerance to the offending foods, while 50% with persisting
AD failed to lose FH (p=O.OO07).
Additional significant differences between the two groups were
found regarding association with respira¬tory allergy (p=0.0007), total (p=0.0001) and specific IgE (p=0.0001), the relationship
between development of tolerance and symptoms (p=0.0026)
and between tolerance and development of additional allergies
(p=0.035), while no difference was found for family history of
atopy, sex, AD severity score, and skin test responses. At the last
follow-up the children were divided into those with and without
respiratory al¬lergy. Both groups had a similar MA (6 yr+2/3mo).
There was a significant relationship between the respiratory
allergy prevalence at the last fol¬low-up and the positivity of skin
tests and/or IgE to in¬halant aller¬gens at the first exami¬nation.
11/18 children without respiratory allergy (39%) had positive
skin tests and/or IgE to inhalant allergens, while 19/26 children
(73%) with respiratory allergy at the last follow-up had posi¬tive
skin tests and/or IgE to inhalant allergens at the first examination
(p=0.023). In conclusion, several parameters were significantly
(0.023 =p=0.0001) associ¬ated with persisting skin lesions .
This confirms that few diseases like AD, although not being lethal,
are causes of invalu¬able physical and emotional suffering either
for children or their parents .