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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The flat mucosal lesion of the small intestine is not pathognomonic of gluten-sensitive enteropathy (GSE). Frequently, the definitive diagnosis of this condition can only be established after three intestinal biopsies are performed: an initial one to show a flat mucosal lesion, one after a gluten-free diet to show morphological recovery, and one after a gluten challenge to show morphological deterioration. We used an organ culture model of GSE to determine the usefulness of this technique in establishing a diagnosis of GSE on the basis of the initial biopsy. Seventy-five patients with diarrhea, and/or malabsorption were evaluated prospectively; 40 had a flat mucosal lesion of variable degree; of these 26 were ultimately determined to have gluten-sensitive enteropathy by the above criteria. A rise in alkaline phosphatase activity of intestinal tissue from 22 of these 26 patients was inhibited when the tissue was cultured in gluten-containing medium as compared to enzyme activities of cultures in a gluten-free medium (108 +/- 69 versus 206 +/- 96, mean +/- SD, P less than 0.001). Mean enzyme values in the similarly cultured intestinal tissue from 13 of 14 patients ultimately shown not to have GSE were not affected by gluten (224 +/- 94 versus 201 +/- 109, P greater than 0.4). Examination of the data by stepwise discriminant analysis provided a function which correctly classified 35 of the 40 patients (88%). The false-positive and false-negative rate for establishing the diagnosis of GSE was 7% (1 of 14) and 15% (4 of 26), respectively. All patients with normal biopsies were classified correctly. The model can be used to establish prospectively the definitive diagnosis of GSE, obviate the need for additional diagnostic biopsies, and allow for the prompt pursuit of alternative diagnoses when gluten sensitivity is not shown.
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PMID:Definitive diagnosis of gluten-sensitive enteropathy. Use of an in vitro organ culture model. 71 Aug 38

We report coexistent collagenous colitis and collagenous sprue in a 62-year-old woman with diarrhea. Investigations suggested malabsorption, and small intestinal biopsies demonstrated a flattened mucosa with subepithelial collagen deposition. Colonic biopsies also showed a thickened subepithelial collagen band as well as a striking lamina propria inflammatory cell infiltrate. Symptomatic remission was induced with a gluten/lactose-free diet, oral prednisone, and sulfasalazine and has been maintained with gluten restriction alone. Repeat biopsies after 2 months demonstrated restoration of normal small intestinal and colonic collagen bands; only a chronic inflammatory cell infiltrate (consistent with microscopic/lymphocytic colitis) persisted in colonic biopsies. We propose that, in this instance, collagenous enterocolitis represented a diffuse manifestation of gluten sensitivity.
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PMID:Collagenous enterocolitis: a manifestation of gluten-sensitive enteropathy. 150 Jun 61

Adult coeliac disease has a broad clinical spectrum and remains undetected for years. Among subclinical deficiency states, attributable to coeliac enteropathy, combined iron and folic acid malabsorption is predominant. An unexplained recurrent iron anaemia is an indication for small intestinal biopsy. Gastro-intestinal disorders are present in only 50% of the cases. Coeliac disease is frequently associated with other major histocompatibility complex (MMC)-linked diseases which are mediated by immunological mechanisms: dermatitis herpetiformis, oral ulcerations, IgA nephropathy, rheumatoid arthritis, sarcoidosis. Dermatitis herpetiformis is a useful model for examination of the spectrum of mucosal changes that typify gluten sensitivity and subliminal lesions without villous atrophy. An increased interest is devoted to the intra-epithelial T-lymphocyte population, not only in the small intestine, but at the level of the stomach and the colon. A "rectal challenge" test has been proposed for detecting gluten sensitivity in coeliac patients. Such a test could be an original method of screening, reducing so the need of small intestinal biopsy. The preliminary results are to be confirmed. Until now, jejunoscopy remains mandatory for the diagnosis and the survey of intestinal lesions related to coeliac disease.
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PMID:[Celiac disease in adults: clinical aspects--role of endoscopy]. 163 35

A malabsorption syndrome was observed in a cynomolgus macaque. Clinical signs included weight loss despite increased appetite, and diarrhea, characterized by an increased volume of soft, tan, malodorous feces. Clinicopathologic findings included hypoalbuminemia, generalized dilation of bowel loops with a prolonged transit time, steatorrhea and markedly diminished absorption of D-xylose. Biopsies of the duodenum and jejunum had total villous atrophy, crypt hyperplasia and a plasmacytic-lymphocytic infiltrate of the lamina propria. The monkey's diet was changed to a semi-synthetic diet containing no grain products. Subsequently, stool characteristics, body weight and intestinal villous morphology returned to normal. This response to removal of grain products from the diet suggests a syndrome similar to gluten-sensitivity enteropathy in human beings.
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PMID:Gluten-sensitive enteropathy in a cynomolgus monkey. 319 52

Computerised image-analysis was used to quantitate small intestinal mucosae from celiac sprue and dermatitis herpetiformis patients, Gambian children with tropical-sprue-like malabsorption, first-degree celiac sprue relatives, and treated celiac sprue patients during challenge with a peptic-tryptic digest of gluten. A wide range of mucosal appearances was observed. Typically, 'flat' lesions (Type 2) revealed a reduced number of epithelial lymphocytes that were large and mitotically active. At the other extreme, mucosal architecture was relatively well preserved (Type 1) but surface epithelium contained an expanded population of small, non-mitotic lymphocytes, with or without crypt hyperplasia. Similar changes were observed in one-third of celiac relatives and following small dose gluten challenge. Larger dose challenges revealed a transition from Type 1 to Type 2 lesions over a 5-day period. Studies in a few patients over 2-4 years showed a similar type of progression. A major feature of this sequence was early appearance of crypt hypertrophy while villi persisted, indicating a role for factors other than increased loss of enterocytes from surface epithelium. These changes parallel the T lymphocyte-mediated events in graft-versus-host reactions in animals. It is thus concluded that the spectrum of immunopathologic changes observed in gluten sensitivity is fundamentally a cell-mediated effect, the degree of change being controlled by host genetic factors. In becoming flat, it appears obligatory for the mucosa to evolve through the earlier Type 1 lesion in which crypt hypertrophy is a prominent response.
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PMID:Studies of intestinal lymphoid tissue. XI--The immunopathology of cell-mediated reactions in gluten sensitivity and other enteropathies. 320 Dec 2

Several diseases of the small intestine, including gluten-sensitivity, present with malabsorption and a "flat" mucosa. Determination of the mitotic index of epithelial lymphocytes provides a simple, objective method of assessing, and thus of predicting, whether a flat mucosa is due to gluten-sensitivity (index greater than 0.2%), or not (index less than 0.2%). The use of this index in circumstances especially likely to cause diagnostic confusion--for example, intestinal lymphoma; Crohn's jejunitis of immunodeficiency--is illustrated in this paper. Of seven cases, five (two primary lymphoma, three immunodeficiency) had been treated with a gluten-free diet without benefit; a mitotic index performed on the initial biopsy in each of these patients could have predicted from the outset that none was gluten-sensitive. Of the remaining two cases, determination of the mitotic index on the biopsy initially obtained from a man with severe hypogammaglobulinaemia would have indicated that he was also gluten-sensitive. Empirical use of a gluten-free diet was avoided in the other patient (with flat small intestinal mucosa and low mitotic index) in whom the diagnosis was ultimately shown to be due to Crohn's disease of jejunum.
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PMID:Studies of intestinal lymphoid tissue. VI--Proliferative response of small intestinal epithelial lymphocytes distinguishes gluten- from non-gluten-induced enteropathy. 682 70

In recent years, there has been increasing recognition that the classical textbook presentation of celiac disease with a malabsorption syndrome and a flat jejunal mucosa is only part of a broad spectrum of clinical and histological features associated with gluten sensitivity. Diagnosis of this treatable condition is often delayed or missed because of a failure to appreciate that celiac disease can present at any age and that symptoms are often subtle and not clearly related to gastrointestinal disease. Nonspecific symptoms and nutritional deficiencies are especially common in older patients and may not always be investigated thoroughly. Use of serological screening tests has improved ease of detection of celiac disease in patients without classical symptoms.
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PMID:Celiac disease in older people. 1112 63

Celiac disease is a disorder caused by gluten-sensitivity which, when manifested in its classical digestive form, frequently presents a malabsorption syndrome. The aim of this study is to evaluate the faecal composition in celiac children with malabsorption syndrome at the moment of diagnosis by using near-infrared reflectance spectroscopy and to compare it with that of healthy children. Thirty children with biopsy-proven celiac disease and 86 age-matched control children were recruited in our study. Children collected 24 hour faecal specimens and the analyses of faeces, water, fat, nitrogen and sugar were performed using near-infrared reflectance spectroscopy. Results show that celiac children daily eliminate a significantly greater quantity of water, fat, nitrogen and sugar than those in the control group. This might be due to the higher weight of faeces eliminated in the celiac group and, of course, to their celiac condition. Of all the nutrients, faecal fat is the substance which undergoes the greatest change, indicating that this nutrient continues to be the best parameter for dealing with patients with malabsorption syndrome. Near-infrared reflectance spectroscopy appears to be a useful tool for assessing stool composition in celiac disease.
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PMID:[Measurement of stool composition in children with celiac disease using near-infrared reflectance spectroscopy]. 1288 98

The recent identification of tissue transglutaminase (tTG) as the autoantigen for celiac disease-associated anti-endomysial antibodies (EMA) has allowed the use of rapid immunoassay to detect the presence of autoantibodies, anti-tTG, in the serum of patients. In this study, we examined the prevalence of IgG or IgA anti-tTG in sera from patients with elevated levels of IgM rheumatoid factors, which are autoantibodies reactive with the Fc portion of IgG. We report here on four cases of anti-tTG positivity for patients with elevated IgM rheumatoid factor (RF) without evidence of celiac sprue. The study population consisted of 65 patients (26 men, 39 women; mean age, 49 years; range 4 - 92 years) with elevated RF (>20 U/ml ), and 23 healthy subjects (12 men, 11 women; mean age, 46 years; range, 21 - 54 years). IgG and IgA anti- tTG levels were detected using a commercially available ELISA kit (Immuno-Biological Laboratories, Germany). Out of 65 patients, one (1.5%) and three (4.6%) patients were positive for IgG and IgA anti-tTG antibodies, respectively, and this was a higher frequency than occurred in healthy subjects (0/23). The clinical features of the four cases positive for IgG or IgA anti-tTG were as follows: The first case (female, 63 yrs) positive for IgA anti-tTG antibody suffered from rheumatoid arthritis, type II diabetes mellitus, iron deficiency anemia and gastric indigestion without symptoms of malabsorption. She denied any gluten sensitivity on her diet. Her esophagogastroduodenoscopic biopsy showed mucosal atrophy with no elongated crypts or infiltration of inflammatory cells in the lamina propria. The remaining three cases positive for anti-tTG antibodies had interstitial pneumonia, a herniated lumbar disc, and mild scoliosis, respectively. They all denied any malabsorption symptoms or gluten sensitivity. Jejunal biopsy could not be performed in all four cases.
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PMID:Tissue transglutaminase autoantibodies in patients with IgM rheumatoid factors. 1551 14

Gluten sensitivity is an autoimmune disease that usually causes intestinal atrophy resulting in a malabsorption syndrome known as celiac disease. However, gluten sensitivity may involve several organs and is often associated with extraintestinal manifestations. Typically, patients with celiac disease have circulating anti-tissue transglutaminase and anti-gliadin antibodies. When patients with gluten sensitivity are affected by other autoimmune diseases, other autoantibodies may arise like anti-epidermal transglutaminase in dermatitis herpetiformis, anti-thyroid peroxidase antibodies in thyroiditis, and anti-islet cells antibodies in type 1 diabetes. The most common neurological manifestation of gluten sensitivity is ataxia, the so-called gluten ataxia (GA). In patients with GA we have demonstrated that anti-gliadin and anti-tissue transglutaminase antibodies cross-react with neurons but that additional anti-neural antibodies are present. The aim of the present article is to review the knowledge on animal models of gluten sensitivity, as well as reviewing the role of anti-neural antibodies in GA.
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PMID:Gluten ataxia: passive transfer in a mouse model. 1780 60


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