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[Increased serum levels of soluble IL-2 receptor in food intolerance: possible mechanism of delayed immunity in milk intolerance].

The levels of soluble interleukin-2 receptor (sIL-2R) were measured in 35 serum samples from children with food intolerance; 19 had an IgE-mediated sensitization and were considered as atopic patients, skin tests and RAST were negative in the remaining 16 children and they were diagnosed as having cow milk intolerance (CMI) Forty-three coeliac patients were included as a positive control group and 18 normal children as the negative control group. The atopic group showed normal values of sIL-2R (1,183 +/- 468 u/ml); however, it was increased in children with CMI (1,453 +/- 469 u/ml, p < 0.05). The sIL-2R mean value was highest in patients with gastrointestinal symptoms (1,458 +/- 461 u/ml, p: 0.03) and the presence of atopic dermatitis was not relevant. The sIL-2R was also elevated in 8 children with igE-mediated sensitization against cow's milk (1,477 +/- 328 u/ml, p < 0.05). These results suggest that a delayed cellular mechanism occurred in CMI, similar to that present in coeliac disease, although it was less severe. In addition, there is an overlap of humoral and cellular immunological mechanisms in the IgE-mediated sensitization to cow's milk, but we did not find this coincidence in the allergy to remaining foods. From a pathogenic point of view, to separate CMI from IgE-mediated allergies to milk does not seem to be sufficiently justified at the present time. It is possible that the atopy against cow milk proteins in children has a different immunological mechanism than the atopy to other foods, which would explain its better prognosis.

Adolescent↗

Allergy to cow's milk in the first year of life and its prevention.

Cow's milk allergy in the first year of life is one of the most common problems faced by pediatricians. Both over and under diagnosis is seen. Cow's milk allergy, which is IgE-mediated should be differentiated from milk intolerance due to lactase deficiency or other causes. Cow's milk allergy may effect the gastrointestinal tract, respiratory tract, skin or blood. Anaphylaxis may occur. Diagnosis is made primarily on clinical grounds but skin tests and/or RAST are of value. Elimination and subsequent challenge confirms the diagnosis but challenge is not always necessary. Challenge should not be performed if there is evidence of anaphylaxis. Avoidance is the mainstay of treatment and breastfeeding is the optimal choice. Since antigenically intact cow's milk protein can pass into the breast milk, the mother should avoid excessive intake of milk products herself while breast feeding. Alternatives to breast milk such as soy formulas or hydrolysed casein or whey formulas may be used. Twenty-five percent of milk-sensitive infants are also allergic to soy protein. Hydrolysed casein formulas are more hypoallergenic but are expensive and less palatable. Hydrolysed whey formula, which is comparable in expense to soy formulas but is less allergenic, may prove of value in the management of the milk-allergic infant as well as for prophylaxis in infants from susceptible parents. Parents of infants born to families with bilateral atopic histories may be able to prevent milk allergy by using dietary manipulations which include decreased prenatal maternal milk intake and while breast feeding as well as careful avoidance of milk products in the infant's diet during the first year of life.

Antigens↗

Quantitative analysis of small intestinal mucosa in cow's milk-sensitive enteropathy.

The appearance of the small intestinal mucosa in cow's milk protein intolerance (CMPI) was studied using quantitative morphometry. The parameters under study were the numbers of eosinophil cells in the lamina propria and epithelium, villous height, crypt zone depth, villous height/crypt zone depth ratio, and total mucosal thickness. Tracings of whole sections were analysed using a suitably programmed minicomputer linked to a digitising table. Small bowel biopsy specimens from children with untreated CMPI, from children before and after clinical relapse on cow's milk challenges, and from children with resolved CMPI were compared to each other, to those from control infants, and to those from children with coeliac disease. No change of diagnostic significance could be found in the number of lamina propria eosinophil cells, but levels of intraepithelial eosinophils were significantly increased following cow's milk challenge. Quantification of mucosal dimensions confirmed the presence of a cow's milk-sensitive enteropathy and established the finding of a thin mucosa in CMPI regardless of clinical disease activity. Mucosal thickness was not different from control values following resolution of the disease. In coeliac disease mucosal thickness was significantly greater than in CMPI (apart from young children with untreated coeliac disease whose mucosa was not thicker than that of children with untreated CMPI) but not different from control values. It is suggested that in CMPI there is a limitation in the capacity of crypt cells to compensate for the loss of villous epithelium.

Biopsy↗

Specialized formulas and feedings for infants with malabsorption or formula intolerance.

The composition of specialized formulas for infants who experience malabsorption or formula intolerance is described in detail. The limited studies of efficacy, as well as a rationale for selecting an appropriate formula for infants with malabsorption or formula intolerance, are discussed. Infants with symptoms of diarrhea or emesis may have intolerance to milk lactose or milk protein. Soy formulas contain no lactose or cow's milk and should be the first choice of an alternative feeding because of cost and convenience. Some infants may be intolerant of soy as well as cow's milk protein. They benefit from formula containing neither cow's milk nor soy protein or from a specially processed milk-based formula containing hydrolyzed casein. A carbohydrate-free formula to which the desired type of carbohydrate is added may be helpful in the diagnosis and treatment of disaccharidase deficiencies and monosaccharide intolerances. Infants with extensive intestinal resections or intractable diarrhea may require specialized infant formulas with qualitative/quantitative modifications of fat, carbohydrate, and protein. Formulas with medium-chain triglycerides may be useful for infants with steatorrhea. "Preterm" formulas or milk from the infant's mother are preferred for preterm infants, since such feedings promote improved fat and carbohydrate absorption and better meet the infant's nutrient requirements.

Animals↗

Optic nerve in globoid leukodystrophy (Krabbe's disease). Ultrastructural changes.

Globoid leukodystrophy (Krabbe's disease) was diagnosed in an infant in whom a progressive neurological disorder and optic atrophy developed. At autopsy, ultrastructural examination of the optic nerves and cerebral white matter revealed characteristic tubular inclusions in globoid-epithelioid cells. Thinning of the nerve fiber and ganglion cell layers of the retina appeared to be due to retrograde degeneration of the optic nerve related to the abnormal metabolism of myelin. We discuss the pathogenesis of the clinical and pathological ocular findings, with regard to the inherited absence of the enzyme galactocerebroside beta-galactosidase and the accumulation in the optic nerve and brain of its substrates, galactocerebroside and psychosine.

Brain↗