Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a case of a 42 year-old patient, female, already suffering in 1990 from pulmonary sarcoidosis at 0 radiological stage, together with uveitis and relapsing erythema nodosum, with dyspepsia and weight loss which benefited from corticosteroidal therapy, repeatedly applied at the relapses of Erythema Nodosum. This therapy induced clinical recovery and marked weight gain. After 3 years (in 1993), the appearance of chronic diarrhoea, weight loss, oedemas of the lower limbs and altered laboratory findings which suggested malabsorbtive syndrome, made us verify with clinical-instrumental examinations (serum AGA IgA and IgG, Xilose test, perendoscopic jejunal biopsy) the diagnosis of fully clinically expressed adult coeliac disease. The screening of close relatives, showed that the patient's brother, HLA like (HLA A1-B8), was suffering from a less expressive coeliac disease. After a wide review of the literature, authors emphasize particular aspects of both diseases, reporting clinical manifestations, possible morbid linkage and prognostic factors. They underline epidemiological, pathogenetic and genetic/immunological similarity. bound to support a possible non-causal linkage of the diseases, even within the family. The authors think this linkage to be underestimated, because it is not often searched for on identified.
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PMID:[Celiac disease (familial) associated with sarcoidosis. Clinical case and review of the literature]. 780 Jan 97

Adult celiac disease (CD) presents with very diverse symptoms that are clearly different from those typically seen in pediatric patients, including ferropenic anemia, dyspepsia, endocrine alterations and elevated transaminase concentration. We present the case of a 51-year-old overweight woman with altered basal blood glucose, hypercholesterolemia, hypertriglyceridemia and persisting elevated transaminase levels, who showed all the symptoms for a diagnosis of metabolic syndrome. Because she presented iron deficiency anemia, she was referred to the gastroenterology department and subsequently diagnosed with celiac disease after duodenal biopsies and detection of a compatible HLA haplotype. Gluten-free diet (GFD) was prescribed and after 6 mo the patient showed resolution of laboratory abnormalities (including recovering anemia and iron reserves, normalization of altered lipid and liver function parameters and decrease of glucose blood levels). No changes in weight or waist circumference were observed and no significant changes in diet were documented apart from the GFD. The present case study is the first reported description of an association between CD and metabolic syndrome, and invites investigation of the metabolic changes induced by gluten in celiac patients.
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PMID:Resolution of metabolic syndrome after following a gluten free diet in an adult woman diagnosed with celiac disease. 2186 Aug 36

Colonization of the human gastric mucosa by H. pylori may cause peptic and duodenal ulcers (DUs), gastric lymphomas, and gastric cancers. The cagL gene is a component of cag T4SS and is involved in cagA translocation into host. An association between the risk of gastric cancer and the type of HLA class II (DR and/or DQ) was suggested in different populations. The aim of this study was to investigate, the clinical association of the cagL gene with host HLA alleles in H. pylori strains that were isolated from patients with gastric cancer, DU, and non-ulcer dyspepsia (NUD) and to determine the HLA allele that confers susceptibility or resistance for the risk of gastric cancer and DU development in Turkish patients. A total of 94 patients (44 gastric cancer and 50 DU patients; 58 male, 36 female; mean age, 49.6 years), and 86 individuals (50 NUD patients and 36 persons with normal gastrointestinal system [NGIS]; 30 male, 56 female; mean age, 47.3 years) were included as the patient and the control groups, respectively. CagA and cagL were determined by PCR method. DNA from peripheral blood samples was obtained by EZ-DNA extraction kit. For HLA SSO typing, LIFECODES SSO Typing kits (HLA-A, HLA-B HLA-C, HLA-DRB1 and HLA-DQA1/B1 kits) were used. The CagL/CagA positivity distribution in the groups were as follows: 42 (95.4%) gastric cancer, 46 (92%) DU and, 34 (68%) NUD and no NGIS cases. The HLA-DQA1*01 (OR: 3.82) allele was significantly different, suggesting that these individuals with H. pylori strains harbouring the CagL/CagA positivity are susceptible to the risk of gastric cancer and DU, and the HLA-DQA1*05 (OR, 0.318) allele was suggested as a protective allele for the risk of gastric cancer and DU using univariate analyses. HLA-DQA1*01 (OR, 2.21), HLA-DQB1*06 (OR, 2.67), sex (male, OR, 2.27), and CagL/CagA/(<2) EPIYA C repeats (OR, 5.72) were detected independent risk factors that increased the risk of gastric cancer and DU using multivariate analyses. However, the HLA-DRB1*04 (OR, 0.28) allele was shown to be a protective allele, which decreased the risk of gastric cancer and DU. Gastric pathologies result from an interaction between bacterial virulence factors, host epigenetic and environmental factors, and H. pylori strain heterogeneity, such as genotypic variation among strains and variations in H. pylori populations within an individual host.
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PMID:Association between polymorphisms in HLA-A, HLA-B, HLA-DR, and DQ genes from gastric cancer and duodenal ulcer patients and cagL among cagA-positive Helicobacter pylori strains: The first study in a Turkish population. 3217 47