Symptoms of food allergies

In the process of evolution of food allergy symptoms, 3 stages can be distinguished:

1. A clear connection between the clinical picture and food provocation and a clear (until the complete disappearance of symptoms) effect of elimination measures.
2. Chronic course of the disease with food addiction: the severity of clinical manifestations is associated with the allergenicity of the diet, but it is no longer possible to achieve a stable state of remission even with long-term elimination.
3. Complete food independence. The formed chronic disease continues to develop based on the inclusion of secondary pathogenetic chains.

Clinical manifestations of gastrointestinal tract damage in food allergies depend on the localization of the process and the age of the child. For young children, the process is characterized by acuteness and generalization. Clinically expressed gastrointestinal syndrome is recorded in 1.9% of children in the first year of life. The most common are diarrhea, vomiting, abdominal pain, colitis, and loss of red blood cells with feces.

At the age of over one year, subacute and chronic course with more distinct localization of the lesion is more often noted. Abdominal pain is a frequent manifestation of food allergy in children of any age. It can proceed as colic associated with dyskinetic phenomena, be of a short-term nature with localization in the navel area. The appearance of pain in the epigastric region is often caused by a hyperacid state developing under the influence of released histamine. The causes of abdominal pain in food allergy are acute and chronic allergic lesions of the gastrointestinal tract (gastritis, duodenitis, enteritis, etc.).

The importance of food allergy in the development of ulcerative lesions of the gastrointestinal tract has been proven. Allergic inflammation of the intestinal mucosa leads to significant changes in the parietal microbial landscape (the number of bifidobacteria decreases and the content of E. coli and enterococcus increases). Long-term course of the disease can lead to the formation of secondary enzymatic deficiency with the development of lactose malabsorption syndrome, cereal gliadin (secondary celiac disease), exudative enteropathy. Cholecystopathy, hepatocholecystopathy, hypofermentia often develop, primarily with pancreatic enzyme deficiency, which is accompanied by increased absorption of protein antigens.

One of the first symptoms of a food allergy may be a picky appetite.

The frequency and severity of skin lesions in food allergies largely depend on the age of the child. The first half of life is characterized by infantile eczema, limited atopic dermatitis, which occur against the background of breastfeeding or the introduction of supplementary feeding, complementary feeding and food correction.

Characteristic symptoms of food allergies include Quincke's edema and urticaria. Among local forms of skin lesions, perioral allergy syndrome should be noted, which often develops to plant products that have cross-allergenicity with plant pollen.

One of the types of food allergy, in which the participation of IgE is not proven, is herpetiform dermatitis. It manifests itself as an itchy rash in combination with signs of gluten enteropathy. Children aged 2-7 years are most often ill. The appearance of erythematous polymorphic rashes with predominant localization in the area of the knees, elbows, shoulders, buttocks, and scalp is characteristic. In the area of the palms and soles, the rash can be hemorrhagic. Skin and intestinal manifestations of the disease react to the abolition of gluten, but the dynamics of skin recovery lags behind the normalization of intestinal functioning.

Respiratory system damage due to food allergies often manifests itself as allergic rhinitis and rhinosinusitis. Most often, allergic rhinitis in children under one year of age is caused by a reaction to cow's milk and vegetable juices. At an older age, cereals become more important.

A manifestation of IIA in young children may be acute subglottic laryngitis, developing several minutes after the consumption of a causative food allergen. Hyperplasia of lymphoid tissue in IIA may lead to the formation of adenoiditis and chronic tonsillitis.

Bronchial asthma of food etiology develops relatively rarely. I. M. Vorontsov proposed the term "second target asthma", since in this case an asthma attack develops when an allergen is ingested and depends on the remote action of biologically active substances. Aerosol contact with an allergen can occur due to the smell of fish, inhalation of an allergen from nuts. Food allergens play a significant role in the development of exogenous allergic alveolitis.

Heiner's syndrome is a rare form of primary pulmonary hemosiderosis caused by hypersensitivity to cow's milk. The disease occurs in young children and is characterized by wheezing, dyspnea, chronic cough, intermittent pulmonary infiltrates, hypochromic microcytic anemia, and growth retardation. Hemosiderin-laden macrophages (siderophages) can be found in sputum and gastric aspirate. The patient's condition improves after eliminating cow's milk from the diet.

Food allergies are associated with vegetative disorders that increase with age, behavioral features, and learning difficulties at school. Food allergies can be the cause of severe generalized allergic reactions: anaphylactic and anaphylactoid shock, hemorrhagic and other generalized vasculitis. In the literature, some cases of sudden death syndrome are associated with an allergic reaction to cow's milk.

Microscopy of mucus from feces can reveal a large number of eosinophils. The diagnosis is aided by eliminating the allergen from food - an elimination test , and vice versa, by prescribing an allergen - a provocative test and the reappearance of clinical manifestations. The reaction of the peripheral blood in the form of leukopenia and eosinophilia is also important.

The diagnosis can be confirmed by determining antibodies in the blood serum using the indirect enzyme-linked immunosorbent assay (ELISA) method, and by determining specific IgE antibodies using the radioimmunosorbent test.

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