One hundred and twenty-five small intestinal biopsies from children with coeliac disease (CD), cow's milk protein intolerance (CMPI) and controls were compared by morphometric analysis, by counting intraepithelial lymphocytes (IEL) and by quantitative evaluation of immunoglobulin-containing cells of lamina propria. The double-stain immunofluorescent technique of Brandtzaeg and Baklien [2] was used, based on defined mucosal tissue units. A patchy enteropathy was found in 60% of CMPI, and in 14% of nonspecific changes, but never in CD. There was a significant difference in crypt depth between CD (360 +/- 80 microns) and CMPI (217 +/- 92 microns), even when lesions of equal grade were compared (P less than 0.015). IEL counts per 1000 epithelial cells showed even better discrimination between the groups (CD: 793 +/- 173, CMPI: 320 +/- 143, P less than 0.001). In CD, there was a relatively greater increase of IgM-cells (X 4.9) and of IgG-cells (X 4.2) than of IgA-cells (X 2.6). Ig-cell changes outlasted the morphological lesion in CD on a gluten-free diet. In CMPI, IgM-cells (X 2.3), IgG-cells (X 2.5), and IgA-cells (X 1.7) were proportionately increased, compared to controls. A special increase of IgE-cells in CMPI could not be substantiated. By computerized stepwise discriminant analysis based upon crypt depth, villus/crypt-ratio, IEL-count, and counts of IgM-, IgG-, IgA-containing cells of lamina propria, accurate classification of patient groups was accomplished, even when only the initial biopsy data were analysed.
Abstract. One hundred twenty-five small intestinal biopsies of coeliac children and controls were investigated prospectively for gliadin binding by specific immunofluorescent staining of lamina propria cells, using a TRITC rabbit IgG antigliadinconjugate. In parallel, sera were investigated for serum gliadin antibodies by a red cell immunosorbent fluorescence test (RIFT). There was no epithelial or reticulin staining found with antigliadin. Exclusively in coeliac disease, i.e. in all active coeliacs, and in 71% of coeliacs on a gluten-free diet, gliadinand immunoglobulin-containing cells were detected. Among these, there was a relatively higher proportion of IgM-and IgGcontaining cells, compared to IdA. They are possibly involved in a local B-cell reaction to gliadin. Their absolute numbers per mucosal tissue unit were small. There was no correlation found between serum gliadin antibody titres of different immunoglobulin classes, and the respective local gliadin-and immunoglobulin-containing cells. It is concluded that lamina propria cells are not a main source of serum gliadin antibodies. Pathogenetic and diagnostic consequences of these data await further clarification.
Use of Intratect® for immunoglobulin substitution in primary and secondary immunodeficiency under real-life conditions is associated with a low rate of suspected ADRs. Serious ADRs are rare and manageable.
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