Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five adults had inflammatory rheumatic disorders 6 to 20 years before the diagnosis of coeliac disease. It is known that joint inflammation occurs in certain patients with adult coeliac sprue who develop either a specific inflammatory rheumatic disease or an atypical progressive polyarthropathy, sometimes as the first manifestation of the intestinal disorder. The diagnosis of adult coeliac sprue should be entertained in these cases even in absence of major digestive disorders or malabsorption. IgA anti-reticulin antibodies and atrophy of the duodenojejunal villosities are the best indicators for diagnosis. There are two important reasons for making the diagnosis of "asymptomatic adult coeliac sprue". First a gluten-free diet can improve or even cure the inflammatory joint disease, a rare situation which emphasizes the causal relationship between these two diseases. Second, the risk of developing lymphoma (especially in the small bowel) is apparently lower in patients on gluten-free diet. Pathogenesis is unclear. Frequently the two autoimmune disorders simply appear to coincide in the same patient; more rarely, arthritis is a symptom of coeliac disease. The immunological mechanisms probably begin when antigens cross an excessively permeable intestinal mucosa.
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PMID:[Inflammatory rheumatism and celiac disease in adults. Coincidence or pathogenic relationship?]. 776 62

Coeliac disease occurs more commonly in children with insulin-dependent diabetes mellitus (IDDM) than in the general population, but the prevalence of coeliac disease in adults with diabetes is unknown. We therefore screened an adult hospital-based diabetic population using IgA antigliadin antibody (IgA-AGA) to identify those patients requiring intestinal biopsy. In 1 year, 1789 patients (43% IDDM, 57% NIDDM) were screened, and 73 had raised IgA-AGA. Of these patients, 49 agreed to duodenal biopsy and 13 (10 IDDM) had coeliac disease. Selective IgA deficiency was found in eight patients, one of whom had coeliac disease. Of these 14 patients with newly diagnosed coeliac disease, four had microcytic anaemia, nine a low serum ferritin, and four a low albumin-corrected calcium. Eight patients had symptoms which improved on gluten withdrawal. Dietary compliance was maintained in 6/8 symptomatic patients, but only in 1/6 without symptoms. Included in the 1789 patients were four (all IDDM) with known coeliac disease. The overall prevalence of coeliac disease in adult patients with IDDM was 1:50 compared with 1:340 in NIDDM. Coeliac disease is common in adults with IDDM and may cause malabsorption and ill health. It should be suspected in any IDDM patient with gastrointestinal symptoms or unexplained anaemia.
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PMID:The prevalence of coeliac disease in adult diabetes mellitus. 798 59

Eighty-three patients with autoimmune thyroid disorders were screened for coeliac disease. The screening was performed with IgA-class reticulin and endomysium antibody, IgA- and IgG-class gliadin antibody tests, and various biochemical tests for malabsorption. None of the tested subjects had selective IgA deficiency, which excludes the possibility of not detecting positives by an IgA-class test. Of the 83 patients, three asymptomatic coeliac patients were found, and one patient with coeliac disease previously diagnosed, an overall frequency of 4.8%. In addition, 25 patients with a solitary nodule of the thyroid gland were examined and one of them (4%) was found to have coeliac disease. By contrast, one (0.4%) out of 249 age- and sex-matched blood donors was found to have coeliac disease. All newly detected coeliac patients had IgA-class gliadin, reticulin and endomysium antibodies, but none of the patients had any gastrointestinal symptoms or abnormal biochemical findings suggesting coeliac disease. Treatment of thyroid disorders and coeliac disease was successful in these patients. The present results confirm that the frequency of subclinical coeliac disease is increased among patients with autoimmune thyroid disorders. IgA-class reticulin, endomysium or gliadin antibody tests are suitable screening methods for detecting these patients, as far as selective IgA-deficiency is excluded.
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PMID:Autoimmune thyroid disorders and coeliac disease. 813 Aug 87

Content of IgA, IgG, IgM, C3 and C4 components of complement, properdin factor B, acid glycoprotein, alpha 1-antitrypsin, transferrin and ceruloplasmin were studied using immunochemical procedures in blood serum, gastric and duodenal contents of healthy persons and of patients after stomach resection. In patients with symptoms of malabsorption concentration of IgA and IgG was drastically increased in gastric and duodenal contents by 51% and 188%, respectively, and by 53% and 371%, respectively. Local activation of the complement system was also observed, which involved an increase of C3 component in stomach and small intestine by 122% and 31%, respectively. As a result of postoperative anastomositis content of albumin and the properdin factor B was distinctly increased in the duodenum. The data obtained suggest that studies of various functional proteins in gastric and duodenal contents are recommended for evaluation of a disease genesis as well as for diagnosis of acute local inflammation.
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PMID:[The local humoral immune system in patients with malabsorption syndrome]. 816 Apr 29

The aim of this work was to establish the diagnostic and follow up value of IgA-class antiendomysium (IgA-EmA) and IgA-class antigliadin (IgA-AGA) antibodies in celiac disease. Correlation with the intestinal histology at the different stages of the disease was evaluated, as well as its therapeutic monitoring ability. Fifty six children, twenty seven girls and twenty nine boys, aged six months to twelve years old, were studied. Thirty nine celiac children were al different diagnostic stages of the disease. Seventeen children with malabsorption symptoms and with normal intestinal histology were used as controls. Sixty blood samples were obtained simultaneously with the small intestinal biopsy. IgA-AGA (ELISA method) and IgA-EmA (immunofluorescent test performed over lower third Rhesus monkey esophagus) were determined in every blood sample. In 34 serum samples from patients with total or subtotal villous atrophy, two were negative for IgA-AGA and only one was negative for IgA-EmA. In 26 samples from patients with normal intestinal histology, two were positive for IgA-AGA and four were positive for IgA-EmA. The results for IgA-EmA had sensitivity 97%, specificity 84.6%, positive predictive value 89.2% and negative predictive value 95%. In the case of IgA-AGA were: sensitivity 94.1%, specificity 92.3%, positive predictive value 94.1%, negative predictive value 92.3%. IgA-AGA and IgA-EmA showed a high correlation with intestinal histology and are in combination powerful tools for the diagnosis and follow up of celiac patients. Besides, they provide a useful aid in the indication of a jejunal biopsy and in close monitoring of the dietary treatment compliance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Correlation of IgA class antigliadin and antiendomysial antibodies (IgA-AGA-IgA-EMA) with intestinal histology in celiac disease]. 823 60

Immunoproliferative small intestinal disease (IPSID) is prevalent in the Mediterranean region and in many Third World countries but is rare in Southeast Asia. Between 1980-1990, 4 cases of IPSID were admitted to Ramathibodi Hospital, Bangkok. Three were males and the mean age was 32 +/- 20.2 years. All patients presented with chronic diarrhea of 7 months to 6 years duration, and weight loss of 15 to 31 kg. All were malnourished, three cachectic, and one patient showed growth retardation. Intestinal parasites were found in all cases: two had multiple infections and three had uncommon protozoal infections (coccidium, cryptosporidium). Barium radiographs revealed intestinal mucosal fold thickening with malabsorption pattern in all cases. Alpha chain IgA was detected in one patient. The remainder underwent exploratory laparotomy and the histological finding was of plasma lymphocytic infiltration of the small intestinal mucosa. All patients responded to oral tetracycline with complete remission occurring in one case. During the follow-up period, 3 cases had progressive retractable clinical courses but all died 2 to 5 years after the diagnosis. The causes of death in these patients were secondary bacterial infection (1 case), intestinal tuberculosis (1 case), fungal infection (1 case) and immunoblastic sarcoma in another case. The results of this study confirm the occurrence of IPSID in Thailand. IPSID responds to oral antibiotic therapy and complete remission may be achieved during the early reversible benign phase, thus an awareness of its occurrence is of clinical importance.
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PMID:Immunoproliferative small intestinal disease (IPSID) in Thailand. 836 83

One of the most common primary immunodeficiencies is the selective deficiency of IgA, which is present in very variable clinical conditions. This situation had conducted to different criteria with respect to the clinical meaning in a particular patient. The association of immunodeficiency of IgA and intestinal malabsorption is reported as statistically significant in the international literature. Nevertheless, the precise pathogenic connection between them is unknown. The relationship between bowel and immune system is reviewed here, and illustrated with the clinical case of a six-year old girl who presented with malabsorption and selective deficiency of IgA.
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PMID:[Selective IgA deficiency and malabsorption. Review of the literature apropos of a case]. 844 82

Celiac disease is characterized by small intestinal damage with loss of absorptive villi and hyperplasia of the crypts, typically leading to malabsorption. In addition to nutrient deficiencies, prolonged celiac disease is associated with an increased risk for malignancy, especially intestinal T-cell lymphoma. Celiac disease is precipitated by ingestion of the protein gliadin, a component of wheat gluten, and usually resolves on its withdrawal. Gliadin initiates mucosal damage which involves an immunological process in individuals with a genetic predisposition. However, the mechanism responsible for the small intestinal damage characteristic of celiac disease is still under debate. Small intestinal biopsy with the demonstration of a flat mucosa which is reversed on a gluten-free diet is considered the main approach for diagnosis of classical celiac disease. In addition, IgA antibodies against gliadin and endomysium, a structure of the smooth muscle connective tissue, are valuable tools for the detection of patients with celiac disease and for therapy control. Incidence rates of childhood celiac disease range from 1:300 in Western Ireland to 1:4700 in other European countries, and subclinical cases detected by serological screening revealed prevalences of 3.3 and 4 per 1000 in Italy and the USA, respectively. IgA antibodies to endomysium are particularly specific indicators of celiac disease, suggesting that this structure contains one or more target autoantigens that play a role in the pathogenesis of the disease. However, the identification of the endomysial autoantigen(s) has remained elusive. We identified tissue transglutaminase as the unknown endomysial autoantigen. Interestingly, gliadin is a preferred substrate for this enzyme, giving rise to novel antigenic epitopes.
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PMID:Identification of tissue transglutaminase as the autoantigen of celiac disease. 921 95

The aim of this study was to examine serum levels of beta-2-microglobulin (b-2-m) in 132 children at various stages for the evaluation of celiac disease (CD). Serum b-2-m was analyzed by a radio immunoassay (RIA) method, using a beta-2-micro RIA kit (Pharmacia, Uppsala, Sweden). The mean concentration of b-2-m in children with an established diagnosis of CD was 4.38 +/- 1.86 mg/l. In children receiving a gluten-free diet, the mean b-2-m concentration was 1.95 +/- 1.09 mg/l, and in children who received a gluten-containing diet, the concentration was 3.19 +/- 0.71 mg/l. In children with CD who were on a gluten-free diet and who presented no antibodies against EmA in class IgA serum, b-2-m concentration was within the normal range (1.86 +/- 0.55 mg/l). The concentration of b-2-m in children with secondary malabsorption syndrome was within the physiological range (1.77 +/- 0.64 mg/l). In children with IgA-EmA antibodies present in serum, the b-2-m concentration was significantly higher (3.5 +/- 1.23 mg/l; P < 0.001) than that in children with IgA-EmA in serum. We showed a linear dependence between the degree of villous atrophy in CD and concentrations of b-2-m in serum (r2 = 0.94). Determination of b-2-m concentration in sera of children with CD may be used to monitor treatment with a gluten-free diet and to differentiate secondary malabsorption syndrome from CD.
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PMID:Estimation of serum beta-2-microglobulin in children with malabsorption disorders syndrome. 921 43

In the rapidly increasing elderly population, diarrhoea as a result of drug therapy is an important consideration. The elderly consume a disproportionately large number of drugs for multiple acute and chronic diseases. Drugs can compromise both immune and nonimmune responses. Aging decreases the quality and proportion of T cells which in turn reduces the production of secretory IgA, the primary immune response of the gut. Acid production in the stomach decreases with increasing age and this compromise its vital 'self-sterilising' function, thus increasing the risk of diarrhoea due to viral, bacterial and protozoal pathogens. Other nonimmune defence mechanisms include the motility of the small intestine and the host-protective commensal bacteria of the colon. Drug induced hypomotility may result in bacterial overgrowth, deconjugation of bile salts and diarrhoea. Less commonly, diarrhoea may occur due to hypermotility because of a cholinergic-like syndrome. In the colon the host-protective commensal bacteria provide a powerful defence against pathogens. Disruption of this commensal population by antibiotic therapy may result in Clostridium difficile supra-infection which causes diarrhoea through toxin production. This is especially important in the elderly patient on chemotherapy for malignancy and those with multiple diseases. The organism responds to vancomycin, metronidazole and bacitracin. Metronidazole is the suggested drug of choice, with vancomycin reserved for relapses. Drugs also cause diarrhoea by interfering with normal physiological processes. Drugs impair fluid absorption by activating adenylate cyclase within the small intestinal enterocyte which increases the level of cyclic AMP. This causes active secretion of Cl- and HCO3-, passive efflux of Na+, K+ and water and inhibition of Na+ and Cl- into the enterocyte. Examples of these drugs (secretagogues) are bisacodyl, misoprostol and chenodeoxycholic acid (used to dissolve cholesterol gallstones). Drugs may also affect a second mechanism that regulates water and electrolyte transport, the Na+, K+ exchange pump. The energy for this pump is provided by the ATPase mediated breakdown of ATP. ATPase may be inhibited by digoxin, auranofin, colchicine and olsalazine. A number of drugs cause osmotic diarrhoea including antacids containing magnesium trisilicate or hydroxide. Lactulose is being used increasingly in compensated liver disease to increase protein tolerance and prevent hepatic encephalopathy. Sorbitol, an osmotic laxative agent also used in some liquid pharmaceutical preparations, induces diarrhoea by virtue of its osmotic potential. Another mechanism by which drugs cause diarrhoea is by mucosal damage of the small and large bowel. In the small intestine mucosal damage causes diarrhoea and fat malabsorption, as may occur with neomycin and colchicine. In the colon, for example, gold salts and penicillamine cause colitis of varying severity. Though the causes of diarrhoea are diverse, a drug-associated aetiology should always be considered and actively sought and addressed to prevent the complications of dehydration, electrolyte imbalance and undernutrition.
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PMID:Mechanisms of drug-induced diarrhoea in the elderly. 978 28


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