Gluten, major histocompatibility complex, and the small intestine: A molecular and immunobiologic approach to the spectrum of gluten sensitivity (‘celiac sprue’)

The acceptability of milk and milk products in populations with a high prevalence of lactose intolerance.

Non–IgE-mediated gastrointestinal food-induced allergic disorders (non-IgE-GI-FAs) account for an unknown proportion of food allergies and include food protein–induced enterocolitis syndrome (FPIES), food protein–induced allergic proctocolitis (FPIAP), and food protein–induced enteropathy (FPE). Non-IgE-GI-FAs are separate clinical entities but have many overlapping clinical and histologic features among themselves and with eosinophilic gastroenteropathies. Over the past decade, FPIES has emerged as the most actively studied non-IgE-GI-FA, potentially because of acute and distinct clinical features. FPIAP remains among the common causes of rectal bleeding in infants, while classic infantile FPE is rarely diagnosed. The overall most common allergens are cow's milk and soy; in patients with FPIES, rice and oat are also common. The most prominent clinical features of FPIES are repetitive emesis, pallor, and lethargy; chronic FPIES can lead to failure to thrive. FPIAP manifests with bloody stools in well-appearing young breast-fed or formula-fed infants. Features of FPE are nonbloody diarrhea, malabsorption, protein-losing enteropathy, hypoalbuminemia, and failure to thrive. Non-IgE-GI-FAs have a favorable prognosis; the majority resolve by 1 year in patients with FPIAP, 1 to 3 years in patients with FPE, and 1 to 5 years in patients with FPIES, with significant differences regarding specific foods. There is an urgent need to better define the natural history of FPIES and the pathophysiology of non-IgE-GI-FAs to develop biomarkers and novel therapies.

Non–IgE-mediated gastrointestinal food allergy

1 079 of 1 548 newborn infants were followed during their first year. 328 were prospectively contacted once a month. 751 were followed up at child welfare clinics. Altogether 20 were diagnosed as being cow's milk protein intolerant (1.9%). Symptoms from the gastrointestinal tract and the skin predominated. Only 2 had respiratory symptoms. Ten had their symptoms within one week after the introduction of cow's milk, 3 of them at their first cow's milk-containing meal. A further 4 already had symptoms when fed only human milk. The others (6 infants) showed symptoms after more than one week on a cow's milk containing diet. Before 2 years of age, 13 had recovered. Twelve of the cow's milk protein intolerant infants also showed adverse reactions to other foods, soy-protein intolerance being the most common (7 infants). A family history of allergy was found in 35% (116) of the 328 infants and in 70% (14) of those with cow's milk protein intolerance.

A prospective study of cow's milk protein intolerance in swedish infants

Background: Recent reports have suggested that gastroesophageal reflux in pediatric patients may be caused by food allergy. Objective: The aim of our study was to determine the frequency of the association of gastroesophageal reflux with cow's milk protein allergy in patients in the first year of life. Methods: We studied 204 consecutive patients (median age, 6.3 months) who had been diagnosed as having gastroesophageal reflux on the basis of 24-hour continuous pH monitoring and histologic examination of the esophageal mucosa. Results: Clinical history suggested diagnosis of cow's milk allergy in 19 infants, and 93 others had positive test results (serum IgE anti-lactoglobulin, prick tests, circulating or fecal or nasal mucus eosinophils) but did not have symptoms indicating cow's milk allergy. The cow's milk-free diet and two successive blind challenges confirmed the diagnosis of cow's milk allergy in 85 of the 204 patients with gastroesophageal reflux. The clinical presentations of the infants with gastroesophageal reflux alone were different, in view of the greater frequency of diarrhea (p Conclusions: Considering the frequency of this association, patients younger than 12 months old with symptoms of gastroesophageal reflux should be carefully examined to determine whether this disorder is primary or caused by cow's milk allergy.

Gastroesophageal reflux and cow's milk allergy in infants: A prospective study

Cows' milk protein enteropathy is recognised as a significant cause of persistent diarrhoea and malabsorption in young infants, but there are as yet no generally accepted diagnostic criteria A combined clinical and histological approach to the diagnosis of cows' milk protein-sensitive enteropathy has been used in 15 patients, and the following set of criteria are proposed (1) Clinical disease (diarrhoea with or without vomiting) while receiving cows' milk protein (2) Clinical improvement on a diet free of cows' milk protein (3) Normal or mildly abnormal histology of jejunal mucosa when taken 6-8 weeks after symptoms subside (4) Histological relapse, with or without clinical relapse, after re-exposure to cows' milk protein

https://adc.bmj.com/content/archdischild/53/1/20.full.pdf

Cows' milk protein-sensitive enteropathy. Combined clinical and histological criteria for diagnosis.

The effect of cows9 milk protein (CMP) on the mucosal disaccharidases was investigated in 23 infants with acute infective enteritis. Jejunal biopsies performed before and after cows9 milk provocation were subjected to histological examination and to mucosal disaccharidase enzyme (lactase, sucrase, and maltase) analyses. After milk challenge, changes in mucosal histology were observed in 18 infants, in 17 of them the levels of all 3 mucosal disaccharidases were much reduced. 10 of these infants developed diarrhoea and, in 6, the stools were positive for reducing sugar. It is concluded that CMP has a deleterious effect on the jejunal mucosa of young infants recovering from infective enteritis, so that in the management of young infants with sugar intolerance secondary to infective enteritis, CMP and lactose should be excluded from the diet.

https://adc.bmj.com/content/archdischild/54/1/39.full.pdf

Cows' milk protein-sensitive enteropathy: an important contributing cause of secondary sugar intolerance in young infants with acute infective enteritis.

The clinical and pathological details of an infant aged 1 year with progressive vaccinia are presented. Evidence of combined cellular and humoral deficiency was obtained in this infant during life. Despite therapy with hyperimmune gammaglobulin, N-methylisatin, B-thiosemicarbisone (methisazone), antibiotics and transfer factor, death occurred. Autopsy revealed thymic dysplasia and atrophy of lymphoid tissue within lymph nodes, spleen, tonsils and gastrointestinal tract. Recommendations regarding the management of progressive vaccinia are made.

A fatal case of progressive vaccinia--clinical and pathological studies.

entero- pathy hasbeenusedin15patients, andthefollowing setofcriteria areproposed. (1) Clinical disease (diarrhoea with orwithout vomiting) while receiving cows' milkprotein. (2)Clinical improvement on adiet free ofcows' milkprotein. (3)Normal ormildly abnormal histology ofjejunal mucosa when taken6-8weeksafter symptomssubside. (4)Histological relapse, withorwithout clinical relapse, after re-exposuretocows' milkprotein. Intolerance tocows' milk protein hasbeenreported inrecent years asacause ofpersistent diarrhoea and failure tothrive inCaucasian infants (Goldman etal., 1963; Gryboski, 1967; Freier etal., 1968; Kuitunen etal., 1975). Diagnosis hashitherto beenbased on certain clinical criteria described byGoldman etal. (1963). (1)Thedevelopment ofsymptoms which subside after dietary elimination ofmilk. (2)Symp- tomswhich recur within 48hours ofmilkchallenge. (3)Reactions tothree suchchallenges should be positive andhavea similar onset, duration, and clinical features. These criteria, while basically sound, arefrequently impractical andwebelieve leadtounderdiagnosis. Recently othercriteria havebeensuggested, the emphasis being placed onthedemonstration of intestinal mucosal damagebythetoxic effect of cows' milkprotein rather thanonclinical observa- tions (Walker-Smith, 1975; Shiner etal., 1975a, b). We haveusedbotha clinical andhistological approach tothediagnosis ofcows'milkprotein intolerance inaprospective study.

Cows'milkprotein-sensitiv e enteropathy Combined clinical andhistological criteria fordiagnosis

Iyngkaran, N., Robinson, M. J., Davis, K. A., Sumithran, E., Kumar, M. V., Ong, T. H., Yadav, M., Boey, C. G., Lam, S. K. and Puthucheary, S. D. (1979). Aust. Paediatr. J., 15, 266–270. Cow's milk protein sensitive enteropathy (CMPSE): an important cause of protracted diarrhoea in infancy. Twenty-six infants with protracted diarrhoea were studied, and 21 were found to have cow's milk protein sensitive enteropathy. Associated secondary sugar intolerance was present in the majority of these infants, but the symptoms did not improve with a lactose-free, cow's milk protein containing formula. Eleven infants tolerated and thrived well on a lactose and cow's milk protein-free formula. Ten infants required total parenteral nutrition for periods of 1 to 3 weeks before they tolerated a lactose and cow's milk protein-free formula orally. This limited study suggests that cow's milk protein sensitive enteropathy may be a major cause of protracted diarrhoea in infancy and that exclusion of cow's milk protein as well as lactose from the diet is essential in the nutritional rehabilitation of these infants. With careful manipulation of these special formulae the need for total parenteral nutrition may be obviated in many infants with protracted diarrhoea.

Cow's Milk Protein Sensitive Enteropathy (CMPSE): An Important Cause of Protracted Diarrhoea in Infancy

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