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[Food allergy and other adverse reactions caused by food].

Adverse reactions to foods are not infrequent. They may be mediated by immunological mechanisms (food allergy) or non-immunologically (idiosyncrasy, pseudo-allergy, intolerance). Furthermore toxic effects of foods have to be clearly distinguished from food allergy as well as poorly defined conditions such as hyperkinesis or "tension-fatigue syndrome", the causal relation of which to foods is not well established. The diagnosis of food allergy includes convincing history, positive provocation and demonstration of immunological sensitization (mostly IgE, however other types of immune reactions may also be of importance. In the treatment of food allergy specific elimination diets as well as pharmacotherapy with the use of mast cell blocking agents are recommended. In single cases oral hyposensitization may be tried.

Diagnosis, Differential↗

Small intestinal permeability in pediatric clinical practice.

Passive permeability of small intestine to lactulose and mannitol was studied in children suspected of having intestinal disease, using a hypertonic differential sugar absorption test. Children with coeliac disease and cows' milk intolerance were shown to have an elevated urinary lactulose/mannitol recovery ratio when compared with controls, children with normal jejunal biopsy, or children in whom alternative explanations for failure to thrive had been demonstrated. The abnormality in permeability ratio principally reflects a reduced urinary recovery of mannitol following oral administration. This study demonstrates that a hypertonic sugar absorption test is well tolerated even by young children, is practicable in routine clinical pediatric practice, and is capable of demonstrating abnormal intestinal function in children with small intestinal disease.

Adolescent↗

Food allergy and food intolerance in childhood.

Food intolerance is a reproducible adverse reaction to a specific food ingredient that is not psychologically based. Food allergy is a form of food intolerance in which there is evidence that the response is caused by an immunological reaction to food. Other mechanisms of food intolerance include enzyme defects (e.g. lactase deficiency), pharmacological effects (e.g. histamine), toxic properties (e.g. haemagglutinating lectins) and irritants (e.g. spices). Food allergy in children is a highly contentious subject and there is often a striking lack of published evidence from which to base clinical decisions. The true prevalence of food allergy in children is unknown, although there is evidence of an increasing incidence of allergic reactions to some foods, especially peanuts. Our understanding of why some children are unable to tolerate certain foods (e.g. cow's milk, egg), or how they grow out of this intolerance, is very poor. Symptoms of food allergy in children are diverse and include vomiting, poor weight gain, abdominal pain, malabsorption, cough, wheeze, rhinitis, atopic eczema, urticaria and angioedema. Despite the lack of objective data to support the notion that food intolerance contributes to behaviour in children, this is a belief firmly held by many parents and some professionals. The gold standard for diagnosing food intolerance is the double-blind placebo-controlled food challenge (DBPCFC). There is often a poor correlation between the results of food provocation tests and those of skin prick tests of radioallergosorbent tests for specific food antibodies. For proven food allergy, elimination diets are the mainstay of management. In children these must be closely supervised to avoid nutritional deficiency and compromise of growth. Some children who have had severe (anaphylactic) reactions after food need to have a supply of self-injectable adrenaline made available to their parents and teachers and must also practice strict avoidance of the offending food.

Diet↗

The diagnosis and management of cow milk protein intolerance in the primary care setting.

Cow milk protein intolerance (CMPI) affects 3% of infants under the age of 12 months and is often misdiagnosed as GERD or colic, risking dangerous exposure to antigens. Most infants out grow CMPI by 12 months; however, those with IgE-mediated reactions usually continue to be intolerant to cow's milk proteins and also develop other allergens including environmental allergens that cause asthmatic symptoms. Clinical manifestations of CMPI include diarrhea, bloody stools, vomiting, feeding refusal, eczema, atopic dermatitis, urticaria, angioedema, allergic rhinitis, coughing, wheezing, failure to thrive, and anaphylaxis. The research and literature showed that CMPI is easily missed in the primary care setting and needs to be considered as a cause of infant distress and clinical symptoms. This article focuses on correctly diagnosing CMPI and managing it in the primary care setting.

Allergy and Immunology↗

Tolerance of a soy formula by infants and children.

For a minimum of one month (mean, 54 days), 287 infants and children less than 8 years of age were fed an isolated soy-protein formula. Prior to entry into the study, a cow's milk formula was being fed to 71%, a soy formula to 9%, and cow's milk or other formulas to 20%. Intolerance to cow's milk was reported in 35% of the patients, symptoms indicative of cow's milk intolerance in 23%, diarrhea or gastroenteritis in 18%, a family history of allergy in 13%, and insufficient weight gain, intolerance to other formulas, or constipation in 11%. The patients showed normal increases in weight and length during the study. A significant decrease in the following symptoms were reported in the patients from before to after treatment: abdominal cramps, bloating or gas, colic, diarrhea, fussiness, rashes or eczema, spitting up, waking up crying at night, wheezing, and vomiting. It is concluded that, while receiving soy formula, infants and children continued to thrive normally and that the formula was well tolerated. After receiving soy formula, the frequency of undesirable feeding-related symptoms was reduced in the majority of infants and children.

Body Height↗

[T lymphocyte populations of the intestinal mucosa in celiac disease in children. Immunohistochemical study].

In order to study the distribution of lymphocyte subpopulations in a pathologic intestinal mucosa, the authors, instead of using the classic method by counting the number of lymphocytes, present an original method permitting the exploitation of quantified data from labelled surface cells by texture analyser coupled with a computerized system. We investigated 25 children presenting with chronic diarrhea and villous atrophy and 5 control subjects. Fifteen of the 25 children had celiac disease (10 active with total villous atrophy and 5, celiac disease in remission with healing mucosa), 5 cow's milk protein intolerance with total or partial villous atrophy and 5, chronic diarrhea with partial villous atrophy. Immunohistochemical study with monoclonal antibodies was carried out on frozen sections using a three-step immunoperoxidase technique. Compared with the 5 controls, patients with food intolerance (celiac disease and cow's milk protein intolerance) showed a significant increase of T suppressor lymphocytes (p less than 0.01 and p less than 0.05) in the epithelium, whereas there were more T helper lymphocytes in the lamina propria (p less than 0.05 and p less than 0.01). Non-treated celiac disease was distinguished from treated celiac disease by a marked increase in intra-epithelial T cytotoxic-suppressors. These results suggest that T cytotoxic-suppressors may be the mediators of the lesions observed in celiac disease.

Adolescent↗

[Food allergies].

Food allergy in childhood presents with different clinical manifestations depending on the age of the affected child. Whereas toddlers and children with food allergy or pseudo-allergy present with similar symptoms as adults, two different forms have been identified in the newborn and infant period. One can occur as allergic colitis in breast or bottle fed infants. In breast fed infants the bloody mucoid stools are produced because of an allergic reaction of the colonic mucosa to foreign proteins which are delivered to the baby via breast milk. In bottle fed infants the given foreign protein itself can trigger the allergic reaction. The clinical, endoscopical and histological appearance is similar to that of ulcerative colitis. Elimination of foreign proteins from the diet of the mother or in bottle fed infants from the child is the therapy of choice. The second manifestation of food allergy in this age group is the cow's milk protein intolerance with predominantly gastrointestinal symptoms such as vomiting, diarrhea and failure to thrive. The diagnosis is based on the clinical picture alone. The usual laboratory tests don't discriminate enough and can therefore not confirm the diagnosis. Elimination of the affecting protein and replacement by a semi-elementary diet are recommended for therapy. The prevention of allergies by dietetic means has become of great importance since it was possible to identify newborns at risk for allergies. The prolonged breast feeding and the late introduction of solids later than the sixth month of life is the preventive measure. "Hypoallergenic" formulae are not recommended because not enough solid data are available to confirm their preventive effect.

Child↗

Bone lesions and dental caries after gastrectomy--evaluation of milk intolerance and operative procedure.

We investigated the development of bone lesions and dental caries in 350 patients who had undergone gastrectomy during the 11 year period from 1968 to 1978, on the basis of bone mineral content (BMC), decayed missing and filled (DMF) teeth and urinary c-AMP. We found that patients with low BMC and incidence of DMF teeth increased in number during the postoperative years; These abnormalities were, in comparison to the Billroth-I (B-I) and milk intake groups, significant in the Billroth-II (B-II) and non-milk intake groups. Among the gastrectomized patients, those with increased DMF teeth had significantly higher contents of urinary c-AMP. The possibility that secondary hyperparathyroidism resulting from gastrectomy contributes to the development and incidence of dental caries has to be given consideration.

Adolescent↗

Diagnostic value of a lymphocyte stimulation test in cow milk protein intolerance.

In order to evaluate the diagnostic value of a lymphocyte stimulation test with casein and beta lactoglobulin in cow milk intolerance (CMI), we studied 26 patients with a diagnosis of CMI and 25 age-matched controls with intestinal diseases other than CMI. Lymphocyte stimulation test to casein (P less than .001) and beta lactoglobulin (P less than .001) was significantly higher among CMI patients. Seventeen patients were RAST positive and nine negative for whole milk proteins. No differences were found in the lymphocyte stimulation test response between RAST-positive and RAST-negative subjects. These results suggest that lymphocyte stimulation test with highly purified antigens in optimal concentrations is specific and could be useful in the diagnosis of CMI.

Animals↗

Colitis, persistent diarrhea, and soy protein intolerance.

Four infants with suspected soy protein intolerance were studied prospectively. All had vomiting, diarrhea, hematochezia, and weight loss of more than 10%. Laboratory abnormalities included anemia (3), acidosis (3), hypoalbuminemia (3), hypernatremia (1), hyponatremia (3), and mild eosinophilia (2). Symptoms developed between three hours and five days after systematic testing with increasing volumes of soy formula. After challenge with soy protein formula, proctosigmoidoscopy and rectal biopsy were performed within 24 hours of developing stools with gross blood. Proctosigmoidoscopy showed both spontaneous and induced friability and loss of vascular pattern in mucosa. Rectal biopsy showed acute colitis with crypt abscesses, depletion of mucus from rectal glands, and polymorphonuclear leukocytes within the lamina propria. Soy protein-induced colitis should be suspected in those infants who present with persistent and bloody diarrhea after being fed soy formula.

Biopsy↗

Diagnosis and management of food allergy and intolerance in dogs and cats.

This paper reviews food allergy and intolerance in dogs and cats. Adverse reactions to ingested food components can affect many systems and can produce signs involving the skin, gastrointestinal tract, respiratory tract and central nervous system, and these clinical signs are reviewed. Most basic food ingredients have the potential to induce an allergic response, although most reactions are caused by proteins. In particular, dogs and cats can become sensitive to cow's milk, beef, fish or cereal. Food allergy and intolerance is rare in dogs and cats, although the incidence in practice is difficult to establish. Clinical signs are quite variable, depending on the individual response, although the major clinical sign is pruritus. Diagnosis can be difficult, as there is no single test available to help the clinician to confirm or refute the presence of food sensitivity. Diagnosis is based on dietary investigation in the form of elimination diets and test meals. Elimination diets for dogs include lamb, chicken, rabbit, horse meat and fish as sources of protein, with rice or potatoes. Successful elimination diets for cats include lamb, chicken, rabbit or venison, with rice. Improvement in clinical signs while on the elimination diet is suggestive of food allergy. The diagnosis should be confirmed by feeding the original diet, with the development of clinical signs within 7 to 14 days of feeding.

Animals↗

Enteric disease in early childhood inhibits microvillus expression by potential stem cells.

1. Enterocyte development of microvillus structure has been measured in intestinal biopsies obtained from children suffering from coeliac disease, cow's milk protein intolerance and microvillus atrophy, and the results compared with similar measurements carried out in control children. 2. All types of enteric disease caused a significant 30% reduction in the length of microvilli present on undifferentiated basal crypt enterocytes, here referred to as potential stem cells. 3. Microvillus growth measured in control enterocytes took place mainly over the basal third of the villus. There was then little further change in structure during subsequent enterocyte migration to the villus tip. 4. Microvillus length in diseased tissue remained more or less constant during enterocyte migration to the crypt-villus junction. Microvillus length then decreased slightly during subsequent enterocyte migration over stunted villi. 5. The present results are discussed in relation to the supposed properties of potential stem cells. Comparisons are also made between profiles of microvillus development measured in healthy children and mature adults.

Adult↗

Gastroesophageal reflux in children with recurrent abdominal pain.

In this study we investigated the presence of gastroesophageal reflux in children with recurrent abdominal pain and its possible relationship to food intolerance-associated duodenal inflammation. Twenty-four-hour intra-esophageal pH monitoring, an endoscopic duodenal biopsy and a small bowel 51Cr-EDTA permeability test were performed in 25 children with recurrent abdominal pain. In 14 cases (56%) the pH monitoring was abnormal, pointing to the presence of pathological gastroesophageal reflux. Treatment of gastroesophageal reflux in the latter patients resulted in resolution or improvement of abdominal pain in 10 cases (71%). Gastroesophageal reflux did not appear to be associated with either intestinal permeability to 51Cr-EDTA or duodenal biopsy findings. We conclude that pathological gastroesophageal reflex is a frequent finding in children with recurrent abdominal pain, that it is unrelated to duodenal inflammation and that there might be a causal relationship between pathological gastroesophageal reflux and recurrent abdominal pain in children.

Abdominal Pain↗

Evaluation of the intraepithelial lymphocyte count in the jejunum in childhood enteropathies.

Intraepithelial lymphocyte counts were evaluated in 131 jejunal mucosal biopsies taken from children with a small intestinal enteropathy arising from a variety of causes including coeliac disease, (untreated, after gluten withdrawal, and during subsequent challenge), giardiasis, cow's milk protein intolerance, and 'intractable diarrhoea'. The counts were compared with those from the biopsies of children referred for investigation but in whom no gastrointestinal disease was demonstrated and from healthy siblings of children with coeliac disease, investigated during a family study. Children with coeliac disease showed a raised count which fell after gluten withdrawal as has been demonstrated by others in adults. Lymphocytic infiltration of the epithelium increased rapidly during gluten challenge in such children, while no change was seen in those children proven ultimately not to have coeliac disease by the usually recognized criteria. In other enteropathies the range of counts was wide, overlapping with both normal and coeliac groups and indicating the nonspecificity of lymphocytic infiltration of the gut epithelium. The findings are discussed in relation to their significance and to further avenues of investigation to determine their possible diagnostic value in confirming the diagnosis of coeliac disease during gluten challenge.

Biopsy↗

[Immunological aspects of food intolerance in children during first years of life].

A study was made of the morphofunctional status and local defence of the gastrointestinal tract in 122 children aged 4 months to 6 years, suffering from food intolerance showed up by atopic dermatitis in 52 children and by chronic diarrhea in 70 children. Based on the allergological anamnesis, scarification cutaneous tests with food allergens, detection of antibodies to food antigens (RAST, HAIT) food allergy was revealed in all the children. Chronic gastroduodenitis was identified in all the children suffering from atopic dermatitis and in 95% of the children with chronic diarrhea. It should be mentioned that one-third of that group had a graver illness--diffuse duodenitis with sub-atrophy of the villi. The allergic genesis of the impairment of the gastroduodenal mucosa was confirmed. It was more remarkable in atopic dermatitis (tissue eosinophilia and high content of IgE-plasmacytes in the duodenal mucosa). The decrease of local immune defence of the mucous membrane, lactase deficiency, elevated growth of microorganisms in the duodenal contents promote the rise of intestinal barrier permeability for food antigens and enhancement of sensitization.

Age Factors↗

[Genogeographic primary hypolactasia in the Old World populations].

The geographic distribution of primary hypolactasia (i.e., the genetically determined (LAC*R), age-dependent decrease in lactase activity, which is phenotypically expressed as the intolerance to whole milk), was studied. Data on the distribution of primary hypolactasia and the LAC*R gene frequencies in populations of the Old World are analyzed, with special emphasis on LAC*R distribution in Russia. New data on populations of Kildin Saamis, Mordovian ethnic groups (Mokshas and Erzyas), Udmurtians, Komi-Permiaks, Komi-Zyrians (Komi-Izhem ethnographic group), Northern (Sos'va) Mansis, Northern Khantys, and Russians are described. Gene geographic maps of the LAC*R gene's distribution in populations of the Old World, Europe, and the Ural region were constructed. A map reflecting the amount of the original information on different regions and, therefore, the reliability of the gene geographic maps, is given. In Europe, the interpopulation diversity Gst of the LAC*R gene was significantly higher (0.169) than the average diversity of the European gene pool. The high variation was assumed to result from a potent differentiating selection that affects the gene for primary hypolactasia.

Africa↗

Cow's milk intolerance with melena.

The clinical features, the results of gastric secretory function tests, and the duodenojejunal morphology of six infants (aged 0.42-1.23 years) with anemia and melena considered to be due to latent cow's milk intolerance (LCMI) were compared with the findings in nine infants (aged 0.19-0.87 years) with cow's milk-induced malabsorption (CMI). The infants with LCMI had a short period of breast feeding, normal weight gain without symptoms of malabsorption, and no atopic history. The maximal acid secretion was decreased (p < 0.01) and the concentration of fasting serum gastrin raised (p < 0.01) compared with the controls. Gastric biopsy revealed epithelial degeneration in three and erosion in one out of four samples. The duodenojejunal biopsy revealed slight changes in two samples, the others being normal. The number of eosinophils was increased in four out of six biopsies. Although the number of intraepithelial lymphocytes was increased in LCMI the rise was not as significant as in children with CMI (p < 0.05). We conclude from our results that LCMI seems to be a seperate clinical entity. The determination of fasting serum gastrin, maximal gastric acid secretion and intraepithelial lymphocytes on duodenojejunal biopsy appear to be helpful in making the diagnosis.

Animals↗

Sleep characteristics in milk-intolerant infants.

We have shown that there is a relation between allergy to cow's milk and chronic sleeplessness in infants. In the present report we describe the sleep characteristics of children with allergy-related sleep disruption. We compared the polygraphic characteristics of nine infants studied before and after the exclusion of milk from the diet. The infants had a mean age of 18.3 +/- 13.3 and 25.4 +/- 12.7 weeks at the first and the second recording, respectively. Diagnosis of allergy was based on clinical observation. Sleep normalized after milk was withdrawn, deteriorated after a challenge with milk, and normalized again on a second trial of milk elimination. Before the change in diet, the infants' polygraphic recording showed frequent arousals (8-22), short sleep cycles, and a large amount of NREM1 sleep. Gastroesophageal reflux and sleep apnea were not responsible for the sleep fragmentation. After milk was excluded from the diet for 7 weeks, the infants showed striking changes in sleep quality. There was a significant decrease in number of arousals (-41.7%) and an increase in total sleep time (+22.7%) and in NREM2 and 3 sleep (+387.9%). NREM1 sleep decreased significantly (-42.1%). During the second recordings, these sleep values could not be distinguished from those of 40 age-matched controls studied in the same laboratory environments. We do not know if the observed modifications in sleep could reflect immunologic changes within the central nervous system.

Arousal↗