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)

A morphometric study of intraepithelial (IE) lymphocytes per 100 epithelial cells, villous heights (VH), crypt depths (CrD), and epithelial cell heights (ECH) was made on jejunal specimens of 17 patients with cow's-milk allergy (CMA), 52 with celiac disease (CD), seven with congenital lactase deficiency (CLD), four with acrodermatitis enteropathica (AE), four with giardiasis, and four with dermatitis herpetiformis (DH). The aim of this study was to investigate how the morphometric parameters correlate with each other. All cases with CMA, CD, and DH had villous atrophy with hyperplasia of the crypts, both signs being more severe in cases with CD and DH than with CMA. IE lymphocyte infiltration was more intense in specimens of patients with CD and DH (mean 76.0), than those with CMA (mean 62.5). The ECH were equally reduced in patients with CD and CMA. In a follow-up specimen at 1 year and 10 months for CD patients and 11 months for CMA patients the inflammation was reduced, and the VH were increased but still differed from the controls. In CLD cases the morphology of the villi and crypts of the jejunum was quite normal, with no IE lymphocyte infiltration; ECH were reduced. Minor morphological changes were seen in the specimens of patients with AE and giardiasis. In the whole study group there was a significant linear correlation, either positive or negative, between all variables measured (IE lymphocytes, VH, CrD, and ECH).
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PMID:Morphometric study of the jejunal mucosa in various childhood enteropathies with special reference to intraepithelial lymphocytes. 718 67

Duodenal mucosa showed normal morphology, interepithelial lymphocytes, alkaline phosphatase, and sucrase in a girl with growth retardation and iron deficiency, but normal absorption of lactose and xylose after two years of abnormal stools. Mucosal lactase was low. Fourteen months later mucosal damage consistent with coeliac disease was evident, and gluten intolerance was subsequently confirmed by gluten challenge. It is probable that, in some children, the mucosal lesion occurs very gradually, so that at an early stage with normal morphology, suppression of lactase activity and possibly interference with iron absorption may be the only abnormalities.
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PMID:Early or pre-coeliac mucosa: development of gluten enteropathy. 746 78

Application of strict diagnostic criteria to celiac disease has led to the realization that there is a wide clinical spectrum within this disease. Normally there are immune reactions to dietary proteins, particularly secretory antibodies of IgA class, low titers of serum antibody and specific down-regulation of IgE and T cell reactivity (oral tolerance). From time to time, abnormal immunity to foods, either as inappropriately high titers of antibodies or qualitatively altered responses, produce disease. Lactase deficiency, with dose-related lactose and milk-intolerance, occurs in 50-90% of most populations. White, western Europeans are the exception.
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PMID:Mechanisms in adverse reactions to food. The gastrointestinal tract. 774 Dec

The prevalence of lactose maldigestion is lowest in Scandinavia and Northwest Europe (3-8%) and close to 100% in most of Southeast Asia. In Europe the frequency increases in the southern and eastern directions, reaching 70% in southern Italy and Turkey. There is also a high prevalence of lactose maldigestion in the people of Africa with the exception of cattle-raising nomads. Lactose maldigestion causes uncharacteristic abdominal symptoms such as bloating, borborygmus, colic, flatulence, and diarrhea. The degree of discomfort depends on the amount of lactose consumed, but also on an individual sensitivity to lactose. The symptoms of irritable bowel syndrome (IBS) and lactose maldigestion are similar. Consequently, most investigations indicate an increased frequency of lactose maldigestion in patients suffering from IBS. Recurrent abdominal pain (RAP) in children corresponds to IBS in adults. Lactose maldigestion is a frequent cause of RAP in regions with a high prevalence of lactose maldigestion in early childhood. Diffuse small-intestinal damage in celiac disease or kwashiorkor leads to a proportional decrease of all disaccharidase activities, with the most pronounced being decrease of lactase. The consumption of milk may then cause abdominal discomfort and increased diarrhea. Several investigations have indicated an increased frequency of lactose maldigestion in patients with osteoporosis. A connection between lactose maldigestion and decreased absorption of calcium has not been proven, however. The increased tendency toward osteoporosis is more likely caused by a lower calcium intake because of milk intolerance. Milk and dairy products with reduced lactose content are better tolerated by patients with lactose maldigestion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical significance of disaccharide maldigestion. 811 58

Recent antigliadin antibody (AGA) determination has become an important diagnostic tool in coeliac disease (CD). Although this test has high sensibility for the disease, it is less specific, especially for IgG class, because of its having been found in some acute and chronic common intestinal childhood diseases. We studied the behaviour of AGA, IgA and IgG, in 234 children affected by various gastrointestinal diseases, comparing the results with those obtained in 125 coeliac children and 788 normal children. The intestinal diseases were as follows: irritable bowel syndrome, cow's milk protein intolerance, acute infectious diarrhoea, parasitosis, lactase deficiency, recurrent abdominal pain, cystic fibrosis, chronic constipation, gastroesophageal reflux, intestinal lymphangiectasia, chronic intractable diarrhoea and nodular lymphoid hyperplasia. Our results showed that while AGA-IgA were absent in all children studied, with the exception of 3 cases of acute diarrhoea, a moderate percentage of AGA-IgG was observed in subjects with cow's milk protein intolerance, acute diarrhoea, irritable bowel syndrome, lactase deficiency, chronic intractable diarrhoea and in a low percentage of children with parasitosis, intestinal lymphangiectasia and nodular lymphoid hyperplasia. There was no antibody movement in subjects with cystic fibrosis, gastroesophageal reflux, recurrent abdominal pains and chronic constipation. The different behaviour of the two antibody classes could be explained by the fact that AGA-IgG were detected in diseases where scattered areas of mucosal damage could allow the permeability of the macromolecules inducing passage of gliadin through the mucosal barrier and immune system-induced antibody stimulation.
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PMID:[The predictive value of antigliadin antibodies (AGA) in the diagnosis of non-celiac gastrointestinal disease in children]. 834 Dec 33

Among 228 relatives of 101 gluten-sensitive patients, 13 anti-endomysium antibody (EmA) positive persons (7 children and 6 adults) were identified. In 12/13 cases jejunal biopsy confirmed severe villous atrophy consistent with celiac disease. In the single EmA positive sibling without villous atrophy the histology is thought to be influenced by a steroid treatment because of pulmonary disease. By routine EmA-testing 12 unexpected EmA positive patients were found out of 756 children with complaints and laboratory results otherwise not justifying jejunal biopsy at the first evaluation. Their initial diagnoses were: proteinuria, colitis, Crohn's disease, rickets, recurrent vomiting, resolved postinfectious lactase deficiency, "previously excluded" celiac disease. Severe villous atrophy could be demonstrated in all EmA positive patients subsequently. In further 204 EmA negative children the biopsy showed no atrophy. EmA positivity may reveal clinically not apparent severe villous atrophy emphasizing the role of a new non invasive and highly specific serological screening method for celiac disease.
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PMID:[New cases of celiac disease detected by anti-endomysial antibody test in families of gluten-sensitive patients and among children examined for non-specific gastrointestinal complaints]. 841 43

Interest in imported tropical diseases has increased with the rising number of travellers to the tropics. This is especially true in the case of tropical gastroenterologic disorders. The causative organisms of chronic diarrhoea are different from those causing acute diarrhoea. Bacteria are relatively unusual; parasites, e.g. Entamoeba histolytica or Giardia lamblia or an opportunistic parasitic infestation associated with an HIV infection are more likely. Furthermore, non-infectious causes, such as postinfective tropical malabsorption, lactase deficiency or coeliac disease have to be considered. Today, elderly people often undertake a journey to the tropics; in these cases the diarrhoea may be associated not only with an increased susceptibility to tropical bowel infections but also with causes previously present, such as diverticulosis, carcinoma or inflammatory bowel disease. The classification of chronic diarrhoea following a visit to the tropics is essentially the same as that for acute diarrhoea: diarrhoea with and without fever and with and without blood. In addition, malabsorption is an important feature of chronic diarrhoea.
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PMID:'The tropics in our bathroom': chronic diarrhoea after return from the tropics. 857 32

Coeliac disease is a human, genetically linked, disorder which develops in gluten-sensitive persons. The aim of this study was to investigate the effect of prolonged feeding of gliadin, a major fraction of gluten, on enzyme activities of enterocyte brush border membrane enzymes in rats, mice and pigs. Brush-border membranes were isolated from mucosal scrapings of the small intestine of 21-d-old rat pups hand-fed with formula milk diet, two-month-old nu/nu and +/+ BALB/c mice and two-month-old piglets fed three times a week starting at birth with high doses of gliadin. Activities of lactase, sucrase and dipeptidyl peptidase IV (DPP IV) were determined. Individual animal models differed in their response to gliadin feeding. In comparison with albumin fed controls the activities of DPP IV and lactase were decreased in rat pups, nu/nu BALB/c mice and piglets. DPP IV activity was mostly affected in the ileum of rats and piglets fed with gliadin starting at birth. On the other hand, lactase and sucrase activities of nu/nu BALB/c mice and piglets decreased to the largest extent in jejunum.
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PMID:Brush border enzyme activities in the small intestine after long-term gliadin feeding in animal models of human coeliac disease. 982 9

The present study aimed to describe the clinical manifestations of celiac sprue related to malnutrition and to analyze the associations between celiac sprue and other diagnoses. A case-control study compared the occurrence of comorbid diagnoses in case and control subjects with and without celiac sprue, respectively. All patients with a primary or secondary diagnosis of celiac sprue (ICD-579.0) who were discharged from hospitals of the Department of Veterans Affairs between 1986 and 1995 were selected as case subjects. In a multivariate logistic regression analysis, the occurrence of celiac disease served as outcome variable, while age, gender, ethnicity, and the comorbid occurrences of other diagnoses served as predictor variables. A total of 458 individual patients with celiac sprue were identified. The data confirmed the known associations of celiac sprue with dermatitis herpetiformis, lactase deficiency, enlargement of lymph nodes, and lymphoma. Celiac sprue was also found to be statistically significantly associated with pancreatic insufficiency, Crohn's disease, functional bowel symptoms, chronic nonalcoholic hepatitis, and pulmonary eosinophilia. The nutritional manifestations associated with celiac disease included nutritional marasmus, cachexia, weight loss, hypocalcemia, osteoporosis, vitamin B-complex deficiency, and various types of iron- and vitamin-deficiency anemias. The large variety of complex associations clearly indicates that celiac sprue is a systemic disease that involves multiple organs and exceeds an isolated nutritional intolerance to gluten.
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PMID:Celiac sprue among US military veterans: associated disorders and clinical manifestations. 1023 5

Trehalose is a disaccharide, the main dietary source being mushrooms. It has been approved as an additive in the preparation of dried food. Isolated intestinal trehalase deficiency is found in 8% of Greenlanders, but is rare elsewhere. The normal range of trehalase activity and the incidence of isolated trehalase deficiency in the UK have not been reported. Patients (n 400) were investigated for suspected malabsorption. Endoscopic distal duodenal biopsies were taken for histological assessment and maltase, sucrase, lactase and trehalase estimation. Disaccharidase activities were determined by Dahlqvist's technique (Dahlqvist, 1968). Most patients (n 369) had normal duodenal histology. In these, square root transformation of trehalase activity produced a normal distribution. The normal range (mean +/- 2 SD) was 4.79-37.12 U/g protein. One patient had an isolated borderline trehalase deficiency. The thirty-one patients with villous atrophy had significantly reduced disaccharidase activities. With ingestion of a gluten-free diet, maltase, sucrase and trehalase activities recovered to normal in most patients, whereas lactase activity did not. The normal range and very low incidence of isolated enzyme deficiency is comparable with that described in populations from the USA and mainland Europe. Activity is significantly reduced in untreated coeliac disease and recovers with treatment with a gluten-free diet. There is no place for routine determination of trehalase activity in the UK population and there should be no concern over the introduction of trehalose-containing dried foods.
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PMID:Intestinal trehalase activity in a UK population: establishing a normal range and the effect of disease. 1088 12


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