Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007570 (celiac disease)
13,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence for autoimmunity in diarrhoeal disease is reviewed. Firstly, coeliac disease (CD) is considered. The incidence of tissue-reactive autoantibodies in both adults and children with CD (68% and 65%, respectively) is higher than the incidence of these autoantibodies in controls (6% in normal adults, and 14% and 9% in disease controls drawn respectively from adult and child populations). The R1 antireticulin antibody, when present, was found to disappear after several weeks on a gluten-free diet, but in contrast, other autoantibodies persisted. Secondly, a case is argued for a new disease category, namely "autoimmune enteropathy." Seven cases are reviewed in which patients presented with protracted diarrhoea, a small intestinal enteropathy which failed to heal during periods of total parenteral nutrition, and evidence of a predisposition to autoimmunity (namely, the presence of high titre autoantibodies including one specific for gut epithelium, and/or the presence of associated diseases regarded to be autoimmune). Thirdly, evidence for autoimmunity in inflammatory bowel disease is reviewed and includes discussion of serum goblet cell antibodies and of circulating T cells which participate in antibody-dependent cellular cytotoxicity in vitro using colonic epithelial cells as targets. Finally, an unusual child is described who presented with chronic diarrhoea and a flat small intestinal mucosa, who responded to gluten withdrawal but who later relapsed spontaneously during a strict gluten-free diet. Her mucosa healed only after a period of total parenteral nutrition and treatment with oral steroids. This child's enteropathy was also associated with thyrotoxicosis and a microscopic colitis.
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PMID:Autoimmunity in diarrhoeal disease. 402 May 70

We studied a 47-year-old man with spinocerebellar degeneration and malabsorption due to celiac enteropathy; the serum vitamin E level was normal. The neurologic disorder initially deteriorated despite improvement of small bowel histology on a gluten-free diet and vitamin E therapy, but later stabilized. The etiology of the neurologic disorder in adult celiac disease has not been identified and does not appear to be vitamin E deficiency.
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PMID:Celiac disease and spinocerebellar degeneration with normal vitamin E status. 402 55

The mitotic activity of epithelial lymphocytes (expressed as percentage mitotic figures/3,000 lymphocytes/mucosal biopsy) was determined in a random sample of jejunal biopsies performed on 44 children with malabsorption, diarrhoea, or failure to thrive. The mitotic index (MI) exceeded 0.2% in 19 biopsies obtained from children with untreated celiac sprue (CS); there were no false positives. The remaining 25 biopsies (MI of less than 0.2%) were considered to be "nonceliac" in origin, among which were several with a severe degree of villous flattening. Conditions in this latter category excluded by a low MI included cow's milk protein enteropathy, selective immunoglobulin A deficiency, combined variable immunodeficiency, Crohn's jejunitis, and intractable diarrhoea of infancy. A high MI (greater than 0.2%) prospectively distinguishes mucosal lesions due to untreated CS from other causes of malabsorption, particularly those associated with villous flattening, but in which the MI is less than 0.2%. This index is therefore proposed as a simple, reliable, and prospective histological marker of CS, and one that could: reduce the need to perform multiple biopsies during a gluten-free diet; and avoid the necessity for follow-up "diagnostic" gluten challenges, especially in very young children.
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PMID:Studies of intestinal lymphoid tissue. VIII. Use of epithelial lymphocyte mitotic indices in differentiating untreated celiac sprue mucosa from other childhood enteropathies. 406 81

A monozygous female twin pair discordant for dermatitis herpetiformis and concordant for gluten-sensitive enteropathy is reported. The diagnosis of dermatitis herpetiformis was verified by demonstrating granular IgA deposits in the uninvolved skin. Gluten-sensitive enteropathy was confirmed according to the ESPGAN criteria. Monozygosity was proved by the standard genetic characteristics.
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PMID:Dermatitis herpetiformis in monozygous twins: discordance for dermatitis herpetiformis and concordance for gluten-sensitive enteropathy. 407 57

In comparison with proteins, peptides occur only in very small amounts in foods. An exception are peptides, which result from proteins to a higher or lower extent in the course of natural or microbial disintegration or ripening processes. Recently, proteinases are used for process optimization or quality improvement in the production or processing of foods. Usually, the protein degradation in these cases is only small, but functional properties may be improved. Peptides frequently show a bitter taste and may limit the sensory value of foods. Sources and possibilities to remove the bitter taste are discussed. In dietetics protein-free peptide diets are introduced for special indications. They contain oligopeptides which are produced by intensive hydrolysis of proteins. The intestinal absorption of small peptides is different from that of free amino acids. Finally, physiological effects of some dietary peptides are discussed (e.g. peptides as enzyme inhibitors, coeliac disease as a gliadine-peptide induced enteropathy, exorphines as neurotransmitters).
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PMID:[Importance of peptides from enzymatically degraded proteins as components of foodstuffs]. 407 71

Sera from 101 patients with adult coeliac disease, 46 patients with childhood coeliac disease, 50 patients with dermatitis herpetiformis, and 479 patients with various other diseases, including skin, gastrointestinal, haematological, and immunological disorders, have been tested for the presence of the antireticulin antibody. Positive sera were retested at higher dilutions. Antireticulin antibody was only found in a significant proportion of patients with three diseases, ie, coeliac disease, dermatitis herpetiformis, and Crohn's disease. Antireticulin antibody was present in 38 out of 101 patients (38%) with adult coeliac disease, 27 out of 46 patients (59%) with childhood coeliac disease, 11 out of 50 patients (22%) with dermatitis herpetiformis, and nine out of 38 patients (24%) with Crohn's disease. In the 434 other patients with various disorders the antireticulin antibody was present in only six 1.4%) (two patients were pregnant, one had vitiligo, one had tropical sprue, one had reticulum cell sarcoma, and one had pernicious anaemia). In patients with gluten-sensitive enteropathy, ie, coeliac disease and dermatitis herpetiformis, there was a significantly higher incidence in patients taking a normal diet compared with those on a gluten-free diet. The presence of antireticulin antibody would appear to be particularly helpful in diagnosing childhood coeliac disease as it was found in 22 out of 26 patients (85%) taking a normal diet.
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PMID:Antireticulin antibody: incidence and diagnostic significance. 457 3

A new method for the analysis of small-intestinal crypt-cell kinetics using routine peroral diagnostic biopsies is described. Untreated patients with childhood and adult coeliac disease and adults with the gluten-sensitive enteropathy of dermatitis herpetiformis were studied, together with groups of adult and childhood controls. In the classical flat avillous mucosae the increase in crypt size was found to be three-dimensional. The number of proliferating cells per crypt was shown to be markedly increased, and an even greater rise in the crypt-cell production rate was demonstrated. A significant increase in the mitotic index was also confirmed in the avillous mucosae. On the basis of these findings it is suggested that the characteristic crypt morphology in glutensensitive enteropathy can be explained as an adjustment to accommodate the expanded mass of proliferating and maturing cells necessary to support the augmented cell production rate. We may speculate that this in turn is a response to a pathologically rapid loss of cells from the mucosal surface.
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PMID:Cell kinetics in flat (avillous) mucosa of the human small intestine. 475 34

In the present study the relation between the gluten-sensitive intestinal lesion observed in dermatitis herpetiformis (DH) and in gluten-sensitive enteropathy (coeliac sprue) (GSE) was analyzed. Jejunal IgA synthesis in DH was estimated from the extent of incorporation of [(14)C]leucine into IgA in jejunal biopsy specimens during short-term in vitro culture. Patients with DH have significantly elevated incorporation values as compared to normal control individuals (18,880+/-13,614 vs. 5,830+/-3,190 cpm/mg tissue protein/ 90 min) (P < 0.02) and the degree of elevation correlates well with the degree of morphologic abnormality. Thus patients with DH are similar to patients with GSE where elevated local mucosal IgA synthesis has also been observed. By using both morphologic and immunologic criteria for evaluating intestinal status, patients with DH and intestinal disease were distinguished from patients with DH free of intestinal disease. Of the eight patients in the former group, seven carried HL-A8 (87.5%), an incidence which is strikingly similar to that observed in patients with GSE alone (88.5%). In contrast, of the seven patients in the latter group (without gastro-intestinal disease) two had HL-A8, an incidence (27%) not significantly different from that in the normal population (20%) (P > 0.1).Thus, both in respect to local mucosal increase in IgA synthetic rates and in respect to the association with HL-A8, the intestinal lesion of DH is similar to that of GSE.
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PMID:Dermatitis herpetiformis. Immunologic concomitants of small intestinal disease and relationship to histocompatibility antigen HL-A8. 483 85

Two patients who had had idiopathic steatorrhoea for several years developed typical eruptions of dermatitis herpetiformis. In each case the rash responded to treatment with dapsone.It is more usual for the rash to precede the enteropathy when the two occur together, but the association between coeliac disease and dermatitis herpetiformis is not yet clear.
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PMID:Dermatitis herpetiformis in two patients with idiopathic steatorrhoea (adult coeliac disease). 567 13

Cow's milk protein intolerance is a transient food intolerance of early infancy. Ingestion of cow's milk protein causes an enteropathy of variable degree. Clinical manifestations are primarily gastrointestinal, although dermal and respiratory symptoms add to the clinical syndrome. Three types are found: an acute anaphylactic reaction, a chronic mild form, and a chronic severe form which is of utmost practical importance in severe protracted diarrhoea of infancy. A graduated diagnostic procedure is proposed, taking into account clinical and morphological reactions to cow's milk proteins. Pathogenesis is immunologically mediated. A concept of transient food protein intolerance is developed which has to be separated from the permanent intolerance of gluten in coeliac disease. Prognosis of cow's milk protein intolerance is excellent after elimination of the offending agent. Breast feeding seems to be effective in prevention of the disease.
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PMID:[Cow's milk protein intolerance: clinical and pathogenic aspects (author's transl)]. 611 75


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