Gastrointestinal permeability in children with cow's milk allergy: effect of milk challenge and sodium cromoglycate as assessed with polyethyleneglycols (PEG 400 and PEG 1000)

Abstract

Abstract. Sixteen children with immediate‐type cow's milk allergy were challenged with increasing amounts of cow's milk. Gastrointestinal permeability was investigated before and after challenge by the 6‐hr urinary recovery of a mixture of different‐sized polyethyleneglycols (PEG 400 and PEG 1000). The results were related to clinical symptoms in the individual patients. The majority of the children displayed changed permeability characteristics after the challenge, both with respect to the maximum uptake of a small test molecule (usually 370 dalton PEG) and/or a large molecule (1074 dalton PFG), and to size‐dependent exclusion of probe molecules. When corrected for the dose of milk taken, the children showing the most severe immediate‐type symptoms also displayed the greatest alteration of permeability. Treatment with sodium cromoglycate (SCG) before the challenge diminished the effect on the uptake of probe molecules, usually decreased the severity of elicited symptoms, allowing about a tenfold increase in the milk dose. Cow's milk challenge in healthy children caused only minor permeability changes, whereas challenge in the sensitized subjects significantly changed (increased or decreased) the recovery of a large test molecule. The difference between healthy and allergic subjects was most obvious when correcting for dose of milk ingested. We conclude that (i) oral challenge with cow's milk in allergic subjects affects the mucosal barrier, and (ii) peroral treatment with SCG moderates immediate hypersensitivity reactions with respect to both tolerated antigen dose and intestinal permeability properties.

Antigen Absorption by the Jejunal Epithelium of Children with Cow's Milk Allergy

“…Increased absorption of PEG 4000 was reported in patients with eczema and food allergy (3), but no changes in permeability to PEG 400 or 1000 were recorded in allergic children on an elimination diet compared to healthy children (I). Increased intestinal permeability was only noted after milk challenge (2). In children with egg sensitivity, no significantly increased absorption of ovalbumin was demonstrated compared to control values, but reduced permeability was observed with sodium cromoglycate.…”

Increased Intestinal Permeability to Differently Sized Polyethylene Glycols in Uremic Rats: Effects of Low- and High-Protein Diets

“…The proposal that there is increased permeability of larger molecules is supported by the increased recovery ratios in (1) the uremic groups, (2) the uremic group on the high-protein diet compared to the control group on the high-protein diet, (3) the uremic group on the low-protein diet compared to the control group on the low-protein diet, and (4) the control group on the high-protein diet as compared to the control group on the low-protein diet. Increased recovery ratios or increased passage of larger molecules in relation to the smaller molecules indicate mucosal damage [20], Altered permeability of larger PEGs has been seen in Crohn's disease [21] and in children with cow's milk allergy challenged with milk [22], Inflammations and ulcerations as seen in Crohn's disease and in allergic gastrointestinal disorders have not been demonstrated in uremic rats [6,9]. Intestinal bacteria, enterotoxin from Escherichia coliand synthetic peptides which mimic bac terial peptides have all been demonstrated to increase the intestinal permeability towards dextran 3000 [23,24].…”

Supplementation with β-carotene or vitamin E protects against increase in anaphylactic response in β-lactoglobulin-sensitized Balb/c mice: ex vivo study

“…Local hypersensitivity reactions at mucosal surfaces play an important role in the pathophysiology of allergic diseases. Early clinical studies in children with cow's milk allergy (CMA) demonstrated intestinal permeability rise after, but not before, allergen challenge [3][4][5]. Experimental models indicate that the breach of epithelial barrier may be a consequence of Th2 switching or may possibly reflect exaggerated responses and viscous cycles caused by mast cell activation [6].…”