Neurological deficits in patients with celiac disease.
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Celiac Disease↗
Biomedical subjects
Rami Eliakim
Publications and source records attributed to Rami Eliakim.
Chronic nicotine administration differentially alters jejunal and colonic inflammation in interleukin-10 deficient mice.
BACKGROUND: Cigarette smoking alters the course of inflammatory bowel disease, is associated with protection against ulcerative colitis, but aggravates or has no effect on Crohn's disease. While the aetiology of this discrepancy remains unclear, differences between location of involvement in ulcerative colitis and Crohn's disease have not been examined in these studies. AIM: To examine the effects of nicotine administration on the course of jejunitis and colitis in interleukin-10 deficient mice. METHODS: Male C57/BL10 IL-10 -/- and wild type mice were given nicotine (12.5 microg/ml) in their drinking water at age 12-14 weeks when they had developed clinical signs of inflammatory bowel disease. Gender and age matched control mice received tap water alone. All mice were killed after 2 weeks of treatment. Whole tissue sections of jejunum, proximal and distal colon were separated and examined by macroscopic and histological score. Northern blots were examined for somatostatin, intestinal trefoil factor and mucin-2. RESULTS: At 14-16 weeks, when the mice were killed, IL-10 -/- untreated control mice developed jejunitis (macroscopic score 1.4 +/- 0.5, microscopic score 2.0 +/- 0.2) and colitis (2.0 +/- 0.2 and 5.9 +/- 0.9, respectively). IL-10 -/- mice treated for 2 weeks with nicotine had significantly reduced colonic scores (1.4 +/- 0.6 and 2.2 +/- 0.15, respectively). In contrast, the jejunum was more severely damaged (2.6 +/- 0.4 and 4.0 +/- 0.3; P = 0.01, respectively). Nicotine significantly increased both somatostatin and intestinal trefoil factor mRNA expression in the colon but not in the jejunum; no effect was noted on mucin-2 or beta-actin mRNA expression. CONCLUSIONS: (1) Two weeks of nicotine administration leads to contrasting effects on jejunal and colonic inflammation in IL-10 -/- mice. (2) Nicotine ameliorated inflammation in the colon, which was associated with enhanced expression of two protective peptides.
Actins↗
Variable response to probiotics in two models of experimental colitis in rats.
BACKGROUND AND AIM: Clinical and experimental data suggest an important role for intestinal microflora in the pathogenesis of inflammatory bowel disease, and probiotics have been shown to ameliorate pouchitis. We evaluated the effect of different preparations of probiotic bacteria on experimental colitis in rats. METHODS: Rats were treated daily intragastrically with two probiotic preparations, VSL#3 or strain GG (LGG), 7 days before induction of colitis and for another week thereafter. Colitis was induced by intracolonic administration of either dinitrobenzene sulfonic acid (DNBS) or iodoacetamide. Rats were killed 7 days after induction of colitis, the colon isolated, washed, weighed, lesion area measured, and mucosa processed for determination of myeloperoxidase (MPO) and nitric oxide synthase (NOS) activities and prostaglandin E2 (PGE2) generation. RESULTS: In rats cotreated with VSL#3 or LGG and iodoacetamide, there was a significant decrease in the lesion area, 98 +/- 37 mm and 142 +/- 43 mm, respectively, as compared with 342 +/- 66 mm in the control group. Colonic wet weight significantly decreased to 1.3 +/- 0.1 g/10 cm and 1.4 +/- 0.1 g/10 cm, respectively, as compared with 1.7 +/- 0.1 g/10 cm. There was also a significant decrease in PGE2 generation, MPO, and NOS activities in the VSL#3 and LGG treatment groups. Presence of VSL#3 bacteria in the rat's colon was confirmed by culture and polymerase chain reaction (PCR) amplification. Neither probiotic preparation had an effect on the extent of colonic damage in DNBS-induced colitis. CONCLUSION: Both VSL#3 and LGG significantly ameliorated colitis induced by the sulfhydryl-blocker iodoacetamide, but had no effect on the immune-mediated DNBS-induced colitis. The results suggest a possible role for sulfhydryl compounds in the protective effect of probiotic bacteria, and support their use in patients with inflammatory bowel disease.
Alkylating Agents↗
The use of a single serological marker underestimates the prevalence of celiac disease in Israel: a study of blood donors.
OBJECTIVES: Recent studies suggest that celiac disease was previously underdiagnosed. To find out whether antiendomysial antibodies underestimate the prevalence of celiac disease, we elected to use a strategy combining multiple serological markers to explore the prevalence of celiac disease in Israel and the usefulness of the various antibodies in screening for celiac disease. METHODS: Serum samples from 1571 healthy blood donors were tested. A small intestinal biopsy was offered to all patients who tested positive for either human tissue transglutaminase antibodies, an ELISA kit based on antiendomysium (EMA-ELISA), immunoglobulin A antigliadin verified by antiendomysial immunofluorescence antibodies, and to patients who were IgA deficient with elevated antigliadin IgG. RESULTS: A total of 59 subjects (3.8% of study population) were offered an intestinal biopsy based on serological findings, and 30 of 59 patients agreed to undergo intestinal biopsy (1.9% of study population). Celiac disease was diagnosed in 10 patients, establishing a prevalence of at least 1:157 in the general population (0.6%, CI = 0.3-1.1%). Using any serological marker alone would have underestimated the prevalence of celiac disease, as it was diagnosed in only two patients who tested positive for endomysial immunofluorescence antibodies (prevalence of 1:786, 0.1%, CI = 0.02-0.5%), six patients positive for tissue transglutaminase (prevalence of 1:262, 0.4%, CI = 0.1-0.9%), and seven patients positive for ELISA-EMA (prevalence of 1:224, 0.45%, CI = 0.2-0.9%). CONCLUSIONS: The prevalence of celiac disease in Israel is at least 1:157 in the general population, confirming its underdiagnosis in previous studies. The disparity between the various serological markers suggest that the use of one serological marker is insufficient for establishing the true prevalence of celiac disease.
Adolescent↗
Large mesenteric lipoma ultrasonographically mimicking a mature cystic teratoma during pregnancy.
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Adult↗
[The medical treatment of upper gastrointestinal bleeding in the new millennium].
Treatment is advocated for patients manifesting upper gastrointestinal bleeding. The medical arsenal consists of H2-receptor blockers and proton pump inhibitors. Studies which were performed to test the efficacy of H2-blockers for bleeding did not present consistent conclusions. In vitro studies proved that H2-blockers given parenterally lose their efficacy after 24 hours, and the pH-drops back to near pretreatment level (pH 2.7). Omeprazole, the oldest pump inhibitor on the market, when given parenterally affects pH-within 30 minutes and does not lose its efficacy in the forthcoming days. In a few studies, when given enterally/parenterally Omeprazole lowered rates of recurrent bleeding, surgery and the number and rate of blood units transfused. On the whole it seems that H2-blockers have little or no role in the treatment of patients with upper gastrointestinal bleeding, while a proton pump inhibitor is of probable therapeutic value. There is no definite answer as to whether the drug should be given enterally or parenterally. It seems logical to start treatment of high-risk patients parenterally and the rest of the patients enterally (orally or via a nasogastric tube).
Anti-Ulcer Agents↗
Probiotics--scope and promise in inflammatory bowel disease.
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Humans↗
ELISA of anti-endomysial antibodies in the diagnosis of celiac disease: comparison with immunofluorescence assay of anti-endomysial antibodies and tissue transglutaminase antibodies.
BACKGROUND: Celiac disease is common in both children and adults. Small intestinal biopsy is mandatory for establishing a diagnosis. Anti-endomysial antibodies, detected by immunofluorescence, have a sensitivity and specificity close to 100% in the diagnosis of CD. Recently, tissue transglutaminase has been identified as the target autoantigen of antibodies against endomysium, and TTG antibodies are comparable to EMA-IMF in the diagnosis of CD. OBJECTIVE: To evaluate a new enzyme-linked immunosorbent assay kit for EMA, compared to EMA-IMF and TTG antibodies in the diagnosis of CD. METHODS: Our study population included all subjects with positive EMA-IMF who underwent intestinal biopsy (n = 21). From the same sera, TTG antibodies and EMA-ELISA were determined, and all antibody results were compared to the biopsy findings. RESULTS: EMA-IMF was able to predict biopsy findings of CD in 19 of 21 cases (90.5%). When patients with biopsy findings compatible with CD and positive EMA-IMF (n = 19) were tested for EMA-ELISA and TTG antibodies, 18 of the 19 were positive for both EMA-ELISA and TTG antibodies. A significant correlation was found between EMA-ELISA and TTG antibody titers (r = 0.74, P < 0.001). CONCLUSIONS: Our study demonstrates that EMA-ELISA is comparable to TTG antibodies in the diagnosis of CD, and supports the use of EMA-ELISA as a serologic marker for this disease.
Autoantibodies↗
Genetics of inflammatory bowel disease.
The etiology of inflammatory bowel diseases, Crohn's disease and ulcerative colitis, is uncertain. Studies of specific environmental factors and immune dysfunction have provided limited insight into disease pathogenesis. There is ample evidence that these diseases are in part the result of genetic predisposition. The early search for candidate genes focused on genes involved in the regulation of immune function. Recent genome-wide searches reported several susceptibility loci for Crohn's disease and ulcerative colitis. The recent identification of the IBD1 gene (NOD2) with mutations that are associated with susceptibility to Crohn's disease will have a major impact on the understanding of the genetics of this disease.
Australia↗