ABSTRACT
Cetiedil, [2-cyclohexyl-2-(3-thienyl)ethanoic acid 2-(hexahydro-1H-azepin-1-yl)ethyl ester], which blocks the intermediate calcium-activated potassium ion permeability (IK(Ca)) in red blood cells, was used as a lead for investigating structure-activity relationships with the aim of determining the pharmacophore and of synthesizing agents of greater potency. A series of compounds having structures related to cetiedil was made and tested on rabbit erythrocytes. Channel blocking activity within the series was found to correlate well with octanol-water partition coefficients but not with the specific chemical structure of the acid moiety. However, whereas log P for the compounds spans a range of values over 4 orders of magnitude, potency only increases by 2 orders. This suggests that hydrophobic interactions with an active site on the channel are probably not the main determinants of activity. It seems more likely that increased lipophilicity enhances access to the channel, probably from within the cell membrane. In keeping with this interpretation, cetiedil methoiodide was found to be inactive. Triphenylethanoic was found to be a more effective acid grouping than 2-cyclohexyl-2-(3-thienyl)ethanoic, and its 2-(hexahydro-1H-azepin-l-yl)ethyl ester (11) was approximately 3 times more potent than cetiedil. The 9-benzylfluoren-9-yl carboxylic acid ester (21) was found to be approximately 9 times more active than cetiedil, and replacing -CO(2)- in 21 by an ethynyl (-C identical to C-) linkage (compound 26, UCL 1608) increased potency by some 15-fold over that of cetiedil.
Subject(s)
Azepines/chemistry , Azepines/chemical synthesis , Calcium/metabolism , Erythrocytes/drug effects , Fluorenes/chemical synthesis , Potassium Channel Blockers , Potassium/metabolism , Animals , Azepines/pharmacology , Cell Membrane Permeability , Erythrocytes/metabolism , Fluorenes/chemistry , Fluorenes/pharmacology , In Vitro Techniques , Octanols , Rabbits , Solubility , Solvents , Structure-Activity Relationship , WaterABSTRACT
BACKGROUND: It has been known for many years that small intestinal maltase activities are reduced in malnourished infants and in other patients with villous atrophy. The recent availability of human maltase-glucoamylase cDNA provides the opportunity to test the hypothesis that villous atrophy accounts for the reduced maltase enzyme activity in malnourished infants. METHODS: Mucosal biopsy specimens obtained for clinical evaluation of malnourished infants with poor responses to refeeding were examined by quantitative methods for enzyme activity and mRNA levels. RESULTS: Maltase activity and maltase-glucoamylase mRNA were reduced (approximately 45% of normal). When maltase-glucoamylase message was normalized to villin message, a structural protein expressed only in enterocytes, a preservation of maltase messages in surviving enterocytes was documented. The luminal glucose transporter-villin message was also preserved. CONCLUSIONS: The loss of maltase-glucoamylase message paralleled the reduction in villin message and degree of villous atrophy. The reduced maltase-glucoamylase message also paralleled sucrase-isomaltase message, previously found to be decreased in proportion to villous atrophy of malnourished infants. The data directly demonstrate, for the first time, that the terminal steps of starch 1-4 starch digestion and sucrase-isomaltase 1-6 starch digestion are decreased in malnourished infants, secondary to villous atrophy. These data in prior and present reports suggest that mechanisms underlying the chronic villous atrophy of malnutrition should be a priority for investigations in malnourished infants with slower than expected weight gain during refeeding.
Subject(s)
Intestines/enzymology , Intestines/pathology , Nutrition Disorders/enzymology , Nutrition Disorders/pathology , alpha-Glucosidases/metabolism , Actins/genetics , Atrophy , Biopsy , Carrier Proteins/genetics , Child, Preschool , Female , Humans , Infant , Intestinal Mucosa/enzymology , Intestinal Mucosa/pathology , Male , Membrane Glycoproteins/genetics , Microfilament Proteins/genetics , Monosaccharide Transport Proteins/genetics , Nutritional Status , RNA, Messenger/metabolism , Sodium-Glucose Transporter 1 , alpha-Glucosidases/geneticsABSTRACT
Although popular, peer education is surrounded by considerable ambiguity. To encourage greater clarity an operational framework for defining and interpreting peer interventions is presented in this article. The author recommends that consideration should be given to what it is that constitutes "peerness", the aims and methods of an intervention and the way in which peer educators are involved. Reflecting a gap in the existing literature, particular attention is paid to the nature of peer involvement. A key distinction is posited between "peer development" and "peer delivery" and it is suggested that there is a "fit" between location, approach and client group.
Subject(s)
Peer Group , School Health Services , Substance-Related Disorders/prevention & control , Adolescent , Adult , England , Female , Health Plan Implementation , Humans , Male , Program EvaluationABSTRACT
1. The actions of some inhibitors of the Ca2+-activated K+ permeability in mammalian red cells have been compared. 2. Block of the permeability was assessed from the reduction in the net loss of K+ that followed the application of the Ca2+ ionophore A23187 (2 microM) to rabbit red cells suspended at a haematocrit of 1% in a low potassium solution ([K]0 0.12-0.17 mM) at 37 degrees C. Net movement of K+ was measured using a K+-sensitive electrode placed in the suspension. 3. The concentrations (microM +/- s.d.) of the compounds tested causing 50% inhibition of K+ loss were: quinine, 37 +/- 3; cetiedil, 26 +/- 1; the cetiedil congeners UCL 1269, UCL 1274 and UCL 1495, approximately 150, 8.2 +/- 0.1, 0.92 +/- 0.03 respectively; clotrimazole, 1.2 +/- 0.1; nitrendipine, 3.6 +/- 0.5 and charybdotoxin, 0.015 +/- 0.002. 4. The characteristics of the block suggested that compounds could be placed in two groups. For one set (quinine, cetiedil, and the UCL congeners), the concentration-inhibition curves were steeper (Hill coefficient, nH, > or = 2.7) than for the other (clotrimazole, nitrendipine, charybdotoxin) for which nH approximately 1. 5. Compounds in the first set alone became less active on raising the concentration of K+ in the external solution to 5.4 mM. 6. The rate of K+ loss induced by A23187 slowed in the presence of high concentrations of cetiedil and its analogues, suggesting a use-dependent component to the inhibitory action. This was not seen with clotrimazole. 7. The blocking action of the cetiedil analogue UCL 1274 could not be overcome by an increase in external Ca2+ and its potency was unaltered when K+ loss was induced by the application of Pb2+ (10 microM) rather than by A23187. 8. These results, taken with the findings of others, suggest that agents that block the red cell Ca2+-activated K+ permeability can be placed in two groups with different mechanisms of action. The differences can be explained by supposing that clotrimazole and charybdotoxin act at the outer face of the channel whereas cetiedil and its congeners may block within it, either at or near the K+ binding site that determines the flow of K+.
Subject(s)
Calcium/physiology , Cell Membrane Permeability/drug effects , Erythrocytes/drug effects , Potassium/metabolism , Analgesics, Non-Narcotic/pharmacology , Animals , Antisickling Agents/pharmacology , Azepines/pharmacology , Calcimycin/pharmacology , Calcium/pharmacology , Calcium Channel Blockers/pharmacology , Charybdotoxin/pharmacology , Clotrimazole/pharmacology , Dose-Response Relationship, Drug , Erythrocyte Membrane/drug effects , Erythrocyte Membrane/metabolism , Erythrocytes/cytology , Erythrocytes/metabolism , Growth Inhibitors/pharmacology , Ionophores/pharmacology , Lead/pharmacology , Mammals , Nitrendipine/pharmacology , Potassium/pharmacology , Potassium Channel Blockers , Quinine/pharmacology , Rabbits , Time FactorsABSTRACT
BACKGROUND: Programmed cell death refers to the genetically determined processes by which cells die in response to physiologic extracellular and intracellular signals, morphologically described as apoptosis. In physiologic and pathologic circumstances this process may involve effector and target cells. METHODS: To identify serine esterase granules in intraepithelial lymphocytes, fresh-frozen human small intestine mucosal sections from normal and celiac-affected mucosa were incubated with substrate-specific N-alpha-benzyloxy-carbonyl-L-lysine thiobenzyl (BLT) and a chromogen (4 Benzoylamino-2,5-diethoxybenzene-dazonium chloride hemi [zinc chloride] salt as capture agent and were examined by light microscopy. RESULTS: Normal mucosa showed an occasional intraepithelial lymphocyte with BLT-positive intracytoplasmic granules. Some large mononuclear cells of the lamina propria were similarly stained. Many more intraepithelial lymphocytes were BLT-positive among the surface enterocytes of untreated celiac mucosa. Lamina propria mononuclear cells close to the basal layer of crypt cells also appeared to be increased. CONCLUSIONS: The histochemical identification of BLT-positive esters within intraepithelial lymphocytes suggests their involvement in enterocyte death under physiologic conditions. The increased BLT-positive intraepithelial lymphocytes found in the celiac mucosa may be related to the known increase in cytotoxic intraepithelial lymphocytes in untreated celiac disease.
Subject(s)
Apoptosis , Celiac Disease/pathology , Cytoplasmic Granules/chemistry , Intestinal Mucosa/pathology , Lymphocytes/ultrastructure , Membrane Glycoproteins/analysis , Child , Granzymes , Histocytochemistry , Humans , Lymphocytes/physiology , Lysine/analogs & derivatives , Lysine/analysis , Perforin , Pore Forming Cytotoxic Proteins , Serine Endopeptidases/analysisABSTRACT
BACKGROUND: Concern over the adequacy of histologic diagnosis of endoscopic duodenal biopsies in children prompted this comparative study on the histologic quality of endoscopic versus capsule biopsies. We found this problem addressed in only six previous reports. METHODS: Blind examinations of the histologic sections of 48 duodenal biopsies obtained by gastrointestinal endoscopy in children aged 2-18 years were compared to 52 biopsies obtained by the small bowel suction method (from children aged 1-16 years). RESULTS: Although 87.5% of endoscopic biopsies and 94.2% of capsule biopsies were adequate for histologic diagnosis, fragmentation or squashing was seen in 83.3% of endoscopic biopsies and only in 25% of capsule biopsies. CONCLUSIONS: Biopsies obtained by suction are of better quality than those obtained by endoscopy. If endoscopy is preferred for technical reasons, the following conditions should be observed: the patients should be aged over 2 years, and a minimum of four biopsies should be obtained with forceps of a diameter greater than 2 mm. Adequate histologic criteria for diagnosis should include at least one full-thickness mucosal specimen more than 3 mm in length, vertically oriented, and not fragmented. In children under age 2, duodenal or jejunal capsule biopsies are preferred, since the specimens are usually larger and less fragmented. Endoscopy is technically more difficult in the very young patient.
Subject(s)
Biopsy/methods , Celiac Disease/pathology , Intestinal Mucosa/pathology , Intestine, Small/pathology , Adolescent , Child , Child, Preschool , Duodenum/pathology , Endoscopy, Gastrointestinal , Humans , Infant , Jejunum/pathology , SuctionABSTRACT
BACKGROUND & AIMS: Many malnourished infants have reduced lactase specific activity in the small intestine. The aim of this study was to test the hypothesis that the hypolactasia of malnourished infants results from transcriptional suppression of lactase expression. METHODS: Biopsy specimens were studied from two groups of infants: 29 with malnutrition and 10 normally nourished controls with normal morphology and lactase activity. RESULTS: In malnourished infants, lactase messenger RNA (mRNA) was reduced to 32% and sucrase to 61% of normal. Lactase and sucrase enzyme proteins and activities were lower in malnourished infants, and partial villus atrophy was present. The genotype of adult hypolactasia was not present. CONCLUSIONS: Because the hypolactasia of malnourished children was associated with much lower lactase than sucrase mRNA abundance and because the epigenetic suppression, which accounted for the reduction of sucrase mRNA, was inadequate to explain the greater reduction of lactase mRNA, this study concludes that malnutrition suppresses lactase gene transcription or mRNA stability in infants. The reductions of lactase mRNA, distinct from those found in adults with genetic hypolactasia, explain the low lactase activities commonly found in malnourished infants.
Subject(s)
Gene Expression Regulation, Enzymologic , Nutrition Disorders/enzymology , beta-Galactosidase/genetics , Female , Genotype , Humans , Infant , Infant, Newborn , Lactase , Male , RNA, Messenger/analysis , Sucrase/genetics , Sucrase/metabolism , beta-Galactosidase/metabolismABSTRACT
Cetiedil ((+/-)-2-cyclohexyl-2-(3-thienyl)ethanoic acid 2-(hexahydro-1 H-azepin-1-yl) ethyl ester) possesses anti-sickling and analgesic, antispasmodic, local anaesthetic and vasodilator activities. A total synthesis and circular dichroism spectra of the enantiomers of cetiedil is described, together with a comparison of their effectiveness as blockers of the Ca(2+)-activated K+ permeability of rabbit erythrocytes; the contractile response of intestinal smooth muscle to acetylcholine; the Ca(2+)-dependent contraction of depolarized intestinal muscle; and the cell volume-sensitive K+ permeability (Kvol) of liver cells. The enantiomers did not differ substantially in their ability to block the Ca(2+)-activated K+ permeability of rabbit red cells or in their effectiveness as blockers of the contractile response of depolarized smooth muscle to externally applied Ca2+. There was a clear difference in the muscarinic blocking activity of the enantiomers, as assessed by inhibition of the contractile response of intestinal smooth muscle to acetylcholine; (+)-cetiedil was 7.7 +/- 0.2 (s.d.) times more active than the (-) from. The enantiomers also differed in their potency as blockers of the increase in membrane conductance which occurs when liver cells swell. The concentration of (+)-cetiedil needed to reduce the conductance increase by 50% was 2.04 +/- 0.54 (s.d.) microM; (-)-cetiedil was 2.6 +/- 0.8 (s.d.) times less active (IC50 of 5.2 +/- 1.2 microM). Differences in the biological actions of the enantiomers of cetiedil indicate that a more extensive study could be rewarding in relation to the use of the enantiomers both in therapeutics and in the study of K+ channels.
Subject(s)
Antisickling Agents/pharmacology , Azepines/pharmacology , Potassium Channel Blockers , Animals , Antisickling Agents/chemical synthesis , Azepines/chemical synthesis , Dose-Response Relationship, Drug , Erythrocytes/drug effects , Erythrocytes/metabolism , Muscle Contraction/drug effects , Muscle, Smooth/drug effects , Muscle, Smooth/physiology , Rabbits , Rats , StereoisomerismABSTRACT
The chronic diarrhea observed in young malnourished infants that is sensitive to dietary glucose and other carbohydrates is associated with variable degrees of patchy mucosal villous atrophy. To explore intrinsic mucosal function in the pathogenesis of this alimentary intolerance, we have conducted an immunohistologic investigation of brush-border enzyme proteins of clinically obtained, mucosal biopsy samples. We used a group of monoclonal antibodies against human brush-border aminopeptidase, sucrase/isomaltase (SI), maltase, and lactase enzyme proteins. SI was strongly and uniformly expressed in crypts and villi of 11 of the 14 subjects; in 3 subjects, however, SI was expressed in a mosaic pattern. Maltase and lactase were occasionally absent, but more commonly were expressed in a mosaic distribution. The mosaic expression of brush-border enzyme proteins has been reported in congenital enzyme deficiencies associated with normal intestinal histology. We report the mosaic expression of brush-border enzyme proteins as a functional alteration associated with a pathological lesion of the mucosa in infants with chronic diarrhea. Our observation challenges the existing concept of ontogenic regulation of brush-border enzyme activity.
Subject(s)
Diarrhea, Infantile/enzymology , Microvilli/enzymology , Nutrition Disorders/enzymology , Aminopeptidases/analysis , CD13 Antigens , Chronic Disease , Diarrhea, Infantile/pathology , Female , Humans , Infant , Intestinal Mucosa/enzymology , Intestinal Mucosa/pathology , Jejunum/metabolism , Jejunum/ultrastructure , Male , Microscopy, Fluorescence , Nutrition Disorders/pathology , Oligo-1,6-Glucosidase/analysis , Sucrase/analysis , alpha-Glucosidases/analysisABSTRACT
In an effort to increase our understanding of the pathogenesis of chronic protracted diarrhea in infants, we examined 44 jejunal mucosal specimens. Only 3 of the 44 specimens showed a normal mucosa (grade 1). Partial villous atrophy was seen in 17 mucosal specimens (grade 2) with marked patchiness in all of the specimens. Subtotal or total villous atrophy (grade 3) was found in the remaining 24 mucosal biopsies. Plasma cells and macrophages were variably increased and intraepithelial lymphocytes were moderately increased in grades 2 and 3. Eight of ten mucosal biopsy specimens embedded in plastic material and cut at 1-2-mm thickness, showed bacteria of unidentified nature, situated either above the microvillous layer or on the mucosal surface. Both adherent and nonadherent bacteria could be identified in the same specimen. We concluded that severe pathological mucosal changes are common in young infants with protracted diarrhea and that the presence of bacteria may be more common than has previously been documented.
Subject(s)
Diarrhea, Infantile/pathology , Intestinal Mucosa/pathology , Jejunum/pathology , Atrophy , Biopsy , Chronic Disease , Gastrointestinal Diseases/pathology , Humans , Infant , Infant, Newborn , Microscopy, FluorescenceABSTRACT
Our electron microscopic study of biopsies taken from 10 infants with protracted diarrhea was conducted in an effort to determine the pathogenesis of the disorder. In this article, the ultrastructure of the jejunal mucosa of the infants is described in relation to overlying or adherent bacteria of unidentified type. In addition to the known changes on the enterocyte surface caused by adherent bacteria (cupping and effacement), other cytopathic changes, not previously reported, are documented. Included are widespread loss of enterocytes, including intraepithelial lymphocytes, into the bowel lumen; cytopathological changes within the enterocytes; and marked thickening of the basal laminae of the enterocytes and the endothelium of lamina propria blood vessels. In addition, we noted deposition of collagen fibrils in the lamina propria below the basal laminae, active phagolysis within macrophages, and lack of cisternal material (immunoglobulin) in the plasma-cell cytoplasm. Although these changes are nonspecific, they may be related in part to the presence of the nonadhering and adhering bacteria, and their identification may further our understanding of the "sick mucosa" that occurs in chronic diarrhea of infancy.
Subject(s)
Bacteria/cytology , Diarrhea, Infantile/microbiology , Intestinal Mucosa/microbiology , Jejunum/microbiology , Bacterial Adhesion , Biopsy , Chronic Disease , Diarrhea, Infantile/pathology , Humans , Infant , Infant, Newborn , Intestinal Mucosa/pathology , Intestinal Mucosa/ultrastructure , Jejunum/pathology , Jejunum/ultrastructure , Microscopy, Electron , Microvilli/microbiology , Microvilli/ultrastructureABSTRACT
Twenty five children with diarrhea were studied. Ten children without diarrhea or that had the last episodic one year before biopsy, represented the control group. Jejunal juice and biopsy specimens obtained from each patient were cultured, and bacteria obtained from these were tested against a further piece of mucosa and sample of pure juice from the same patient, to determine the presence within them of antibody against the small bowel bacteria. Duodenal mucosae antibody against non-pathogenic bacteria was demonstrated in 95% of children with diarrhea and only 25% of control group. The immunoglobulin classes involved, IgA and IgM, suggest a strong local immune system stimulation, although a systemic immune response can not be excluded since IgG was frequently found in the mucosa.
Subject(s)
Diarrhea/etiology , Immunoglobulins/analysis , Intestinal Mucosa/immunology , Intestinal Secretions/immunology , Intestine, Small/immunology , Child , Child, Preschool , Diarrhea, Infantile/etiology , Female , Fluorescent Antibody Technique , Humans , Infant , MaleABSTRACT
This article is an update on the importance of some gastrointestinal diseases such ulcerative colitis, coeliac disease and some types of diarrhoea, in preceding an autoimmune response. A correlation with autoimmune disease without digestive symptoms, is made (rheumatoid arthritis, Hashimoto's thyroiditis, ankylosing spondylitis, and so on). Recognising such interrelations should be followed by search of extradigestive symptoms of autoimmune gastrointestinal diseases, allowing a better understanding of the immunologic phenomena involved.
Subject(s)
Autoimmune Diseases , Celiac Disease/immunology , Colitis, Ulcerative/immunology , Antigen-Antibody Complex/immunology , Diarrhea/immunology , HumansABSTRACT
The small-intestinal mucosa of normal children and of celiac patients was studied using the Class II DP (SB) Ia-like monoclonal antibody ILR-1 and an immunoperoxidase technique. Positive staining of the Golgi region of the epithelial cells of villi and crypts, and of the brush border of villous epithelium, was seen in the histologically normal mucosa. In active celiac disease with "flat" mucosa, the surface epithelium showed poor staining, but the crypt epithelium stained strongly in the Golgi region. We suggest that the Ia-like antigens are a product of the epithelial cells themselves, arising most likely in the Golgi apparatus, and that this staining pattern is altered in active celiac disease.
Subject(s)
Celiac Disease/immunology , Histocompatibility Antigens Class II/analysis , Intestinal Mucosa/analysis , Child , Humans , Immunoenzyme Techniques , Intestine, Small/analysisABSTRACT
A patient with mast cell disease of the small bowel is described in whom clinical, histological, and ultrastructural studies served to delineate the characteristic features of the disease. Urticaria pigmentosa, steatorrhea, eosinophilia, absence of antireticulin antibodies, and submucosal nodularity seen on radiographic study of the duodenum were the clinical characteristics. The endoscopic appearance was that of severe exudative duodenitis. The histology of the small intestinal mucosa showed crypt cell destruction and villous atrophy. Marked infiltration of the lamina propria with mast cells, eosinophils, and neutrophils was also distinctive. The enterocytes retained their columnar epithelium, confirmed on electron microscopy. The fine structural abnormalities of the mast cells are demonstrated for the first time. Degranulated mast cells predominated within the lamina propria and none was seen among the epithelial layers. The mast cell nuclei were irregular, often binuclear, and showed loss of their normal heterochromatin pattern. In their cytoplasm only few granulated bodies were seen and even more rarely inclusions with whorls and scrolls. We conclude that the clinical, histopathological, and ultrastructural appearances in mast cell disease of the small bowel are distinctive and should be used as criteria for diagnosis. Care should be taken in the evaluation of the number of mast cells since the demonstration of these cells may be affected by various fixing and staining techniques.
Subject(s)
Jejunal Diseases/pathology , Jejunum/ultrastructure , Urticaria Pigmentosa/pathology , Adult , Female , Humans , Intestinal Mucosa/ultrastructure , Lymphocytes/ultrastructure , Macrophages/ultrastructure , Mast Cells/ultrastructure , Middle Aged , Plasma Cells/ultrastructureSubject(s)
Celiac Disease , Autoimmune Diseases/complications , Celiac Disease/complications , Celiac Disease/etiology , Celiac Disease/immunology , Dietary Proteins/metabolism , Glutens/metabolism , Histocompatibility Antigens Class II/immunology , Humans , Intestinal Absorption , Intestinal Mucosa/immunology , Intestinal Neoplasms/complications , Intestinal Neoplasms/immunology , Intestine, Small/immunology , Lymphoma/complications , T-Lymphocytes/immunologyABSTRACT
A direct immunofluorescent technique with fluorescein-labeled antigens was used to examine the jejunal mucosa for specific antibody reduction in 23 children aged 2--25 months referred for diagnostic biopsy. Plasma cells containing antibodies to beta-lactoglobulin (beta LG) or bovine serum albumin (BSA) were present in 11 of 16 biopsies from patients with cow's milk protein intolerance (CMPI) but only one of eight controls, all on a diet containing cow's milk. Antibody-containing cells (ACC) constituted approximately 0.5--5% of the total (IgA + IgM) plasma cell population. Their presence did not correlate with either histologic abnormality or IgA plasma cell count. Double immunofluorescence with rhodamine-labeled antigens and fluorescein-labeled class-specific anti-human immunoglobulin sera showed the ACC to be approximately 70% IgA cells and 30% IgE cells.
Subject(s)
Food Hypersensitivity/immunology , Intestinal Mucosa/immunology , Jejunum/immunology , Milk Proteins/immunology , Milk/adverse effects , Animals , Antibodies/analysis , Antibody Formation , Antibody Specificity , Biopsy , Cattle , Child, Preschool , Female , Fluorescent Antibody Technique , Humans , Infant , Lactoglobulins/immunology , Male , Plasma Cells/immunology , Serum Albumin, Bovine/immunologyABSTRACT
The infant acquires immunological competence in the neonatal period through the passage of antigens from the enteric lumen through gut-associated lymphoid tissues, principally the Peyer's patches and the appendix. Immune deficient mechanisms may be involved in several gastrointestinal diseases manifesting in the neonatal period as well as throughout childhood. Principally among these are neonatal necrotising enterocolitis, atopy and food intolerances, coeliac disease, cow's milk protein intolerance, diarrhoea associated with hypogammaglobulinaemia, malnutrition and inflammatory bowel disease. The mechanism whereby immune reactions are involved in the pathogenesis of these diseases is discussed.
Subject(s)
Celiac Disease/immunology , Enterocolitis, Pseudomembranous/immunology , Infant, Newborn, Diseases/immunology , Lactose Intolerance/immunology , B-Lymphocytes/analysis , Food Hypersensitivity/immunology , Humans , Immunity, Maternally-Acquired , Immunoglobulin A/analysis , Immunoglobulin M/analysis , Infant, Newborn , Nutrition Disorders/immunologyABSTRACT
Twenty-one children aged between 2 and 54 months, 14 with eczema and 7 with allergies in first-degree relatives, were referred for diagnostic jejunal mucosal biopsy for a variety of symptoms. A partial villous atrophy was found in 19 of the 21 biopsies obtained; the other 2 were normal. We report a highly significant (P less than 0.0001) lower IgA cell count in biopsies with partial villous atrophy compared with the results of our previous study of IgA and IgM plasma cells in the mucosal biopsies in children without eczema or a history of atopy matched for age and histological appearances. The IgM cell count was also lower.