Specific Antibodies in Infants with Gastrointestinal Intolerance to Cow’s Milk Protein

Sp, Fälström; Ahlstedt, S.; La, Hank

doi:10.1159/000232011

Cited by 43 publications

(37 citation statements)

References 18 publications

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“…While the low numbers of late reactors in this study preclude definitive statisti cal analysis of antibody levels, it is of interest that the 3 patients who showed the highest levels of IgE milk antibodies for this group developed eczema after milk challenge. Our observation that elevated IgE antibod ies may appear in immediate and late forms of CMA suggests that Dannaeus and Johansson [2], who dem onstrated immediate skin reactions in acute CMA, and Fallstrom [9], who found elevated total IgE levels in late-onset CMA, were merely studying different aspects of the spectrum of milk allergy in childhood. A type 1 hypersensitivity response alone cannot ex plain the slow onset of clinical reaction in these latereacting patients.…”

Section: Discussionmentioning

confidence: 95%

“…Like Savilahti [3] and Fallstrom et al [9] we have identified a third group of late-reacting CMA patients who developed mainly gastrointestinal symptoms and/or eczematous lesions more than 20 h after com mencing milk ingestion [5]. While the low numbers of late reactors in this study preclude definitive statisti cal analysis of antibody levels, it is of interest that the 3 patients who showed the highest levels of IgE milk antibodies for this group developed eczema after milk challenge.…”

Section: Discussionmentioning

confidence: 99%

“…Patients with delayed-onset reactions did not demonstrate these associations. On the other hand, Fallstrom et al [9] reported that elevated levels of IgE and IgG milk antibodies were only found in patients with delayed-onset reactions.…”

Section: Introductionmentioning

confidence: 99%

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Humoral Immune Response to Cow’s Milk in Children with Cow’s Milk Allergy

Firer

Hoskings²,

Hill

1987

Int Arch Allergy Immunol

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In 47 infants and children aged 4–66 months with clinically proven cow’s milk allergy and in a group of age-matched controls, serum IgG, IgA and IgM cow’s milk-specific antibodies were determined with ELISA assays while IgE cow’s milk-specific antibodies were measured with Pharmacia RAST. The patients were divided into three separate groups according to the time of clinical response to a standardized cow’s milk challenge protocol. Immediate reactions ( < 45 min after challenge), which were mainly accompanied by urticarial skin eruptions, were associated with elevated IgE milk-specific antibody levels, indicating the involvement of an immediate hypersensitivity mechanism. Alternatively, intermediate reactions (1–20 h after challenge), which were mainly accompanied by vomiting and diarrhea, were not IgE-mediated. In the late reactions ( > 20 h after challenge) both eczematous and gastrointestinal reactions were seen. Patients with eczema-tous eruptions also showed elevated IgE milk-specific antibody levels. IgG milk-specific antibody levels were similar in each of the patient groups but all groups were significantly lower than in the controls. Levels of IgA and IgM milk-specific antibodies were similar in patients and controls. The results indicate that different im-munopathogenic mechanisms are operative in these subgroups of patients with cow’s milk allergy.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

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Humoral Immune Response to Cow’s Milk in Children with Cow’s Milk Allergy

Firer

Hoskings²,

Hill

1987

Int Arch Allergy Immunol

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“…However, later studies have not verified such changes in complement: no reduction in C3 took place during nine challenges in CMA with malabsorption (98); and in three other series with 43 similar positive challenges with CM the complement fractions measured were unchanged (28,79,116). In 13 children with AD and CMA complement fractions 3 and 4 were unchanged during the positive challenge test (86).…”

Section: Serum Complement Fractionsmentioning

confidence: 99%

Cow's Milk Allergy

Savilahti

1981

Allergy

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By the end of the last century prevention of waterborne infections by chlorination of water supplies, pasteurization of cow's milk (CM) and production of suitable, easily cleaned bottles and nipples for infants had made artificial infant feeding a relatively safe procedure. But in the early years of the present century unexplained difficulties were reported in infants fed with cow's milk; some of them had continuous diarrhoea and failed to thrive (103). It was speculated that such infants had difficulty in digesting foreign proteins, although they could readily assimilate those in breast milk. In the following years cases of anaphylactic shock caused by CM were described, one of them with a fatal outcome (29). Animal studies showed that one species produced precipitins to proteins of milk from another species, and this type of reaction to the foreign structure of CM proteins was presumed to account for the symptoms seen in infants (29). In 1906, precipitins to CM were found in blood from a marasmic infant fed with CM (80). A year later reports appeared describing successful desensitization: injections of small quantities of cow serum cured and prevented hypersensitivity to oral CM and its symptoms (102). This was not a solution to the problem, however, as treatment with serum caused severe reactions (95). The mechanism and components of C M causing these reactions were debated. Wernstedt suggested that the symptoms were due to altered reactivity to CM because of earlier contact with it, and proposed that it should be called allergy (119). Subsequently, the intestinal symptoms were shown to be caused by the whey fraction of CM (42). They were noted to vary in severity and disappeared with increasing age. A decade later (1921) urticaria was described as a symptom of CM hypersensitivity (104). By the 1930's and 40's however, CMA was considered a rare disease ( I 12), but the decrease in breast feeding in most developed countries has made cow's milk allergy (CMA) an important cause of infant morbidity and one of the best known and most frequently encountered problems in current infant feeding practices. DEFINITIONThe majority of infants can be reared on CM formulas without untoward effects. However, sensitive immunochemical methods show that they do react to the foreign proteins in CM. When the immunologic reactions to CM are associated with clinical symptoms, the child can be said to be allergic to CM (89). Obviously, the simplest and the most convincing way to verify cow's milk allergy (CMA) would be to demonstrate this either abnormally strong or qualitatively altered immune reaction to C M proteins. As yet, however, this cannot be done by any single test or combination of tests. Therefore the diagnosis of CMA has to be based on the clinical response to CM. In most cases it is enough to observe a favourable response to elimination of CM, reappearance of symptoms during one challenge test and their -disappearance on renewed elimination. When symptoms are severe it is unethical to perform more than one challenge.Ot...

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“…coeliac disease [5,6], cow's milk protein intolerance of delayed onset [7,8] and inflammatory bowel disease [9,10]. T cells are held to play a central role in these conditions.…”

Section: Introductionmentioning

confidence: 99%

Avidity progression of dietary antibodies in healthy and coeliac children

Saalman

Dahlgren

Fällström

et al. 2003

Clinical and Experimental Immunology

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SUMMARYIn most individuals minute amounts of food proteins pass undegraded across the intestinal mucosa and trigger antibody formation. Children with coeliac disease have enhanced antibody production against gliadin as well as other dietary antigens, e.g. b -lactoglobulin, in cow's milk. Antibody avidity, i.e. the binding strength between antibody and antigen, often increases during antibody responses and may be related to the biological effectiveness of antibodies. The aim of the present study was to determine the avidity of serum IgG antibodies against b -lactoglobulin and gliadin in healthy children during early childhood and compare these avidities to those found in children with coeliac disease. The average antibody avidity was analysed using a thiocyanate elution assay, whereas the antibody activity of the corresponding sera was assayed by ELISA. The avidity of serum IgG antibodies against b -lactoglobulin as well as gliadin increased with age in healthy children, even in the face of falling antibody titres to the same antigens. Children with untreated coeliac disease had IgG anti-b -lactoglobulin antibodies of significantly higher avidity than healthy children of the same age, and the same trend was observed for IgG antigliadin antibodies. The present data suggest that the avidities of antibodies against dietary antigens increase progressively during early childhood, and that this process seems to be accelerated during active coeliac disease.

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Specific Antibodies in Infants with Gastrointestinal Intolerance to Cow’s Milk Protein

Cited by 43 publications

References 18 publications

Humoral Immune Response to Cow’s Milk in Children with Cow’s Milk Allergy

Humoral Immune Response to Cow’s Milk in Children with Cow’s Milk Allergy

Cow's Milk Allergy

Avidity progression of dietary antibodies in healthy and coeliac children

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