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        <title>BMC Gastroenterology - Latest Articles</title>
        <link>http://www.biomedcentral.com/bmcgastroenterol/</link>
        <description>The latest research articles published by BMC Gastroenterology</description>
        <dc:date>2009-07-09T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-230X/9/52" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-230X/9/51" />
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        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/52">
        <title>Early effects of oral administration of lafutidine with mosapride compared with lafutidine alone on intragastric pH values</title>
        <description>Background:
The ideal medication for treatment of acid related diseases should have a rapid onset of action to promote hemostasis and resolution of symptoms. The aim of our study was to investigate the inhibitory effects on gastric acid secretion after a single oral administration of lafutidine, that is a newly synthesized histamine H2 receptor antagonist, with mosapride, that is a 5-hydroxytryptamine 4 receptor agonist and known to have prokinetic properties on the gastrointestinal tract, or lafutidine alone.
Methods:
Ten Helicobacter pylori negative male subjects participated in this randomized, two-way crossover study. Intragastric pH was monitored continuously for 4 hours after a single oral administration of lafutidine 10 mg or lafutidine 10 mg with mosapride 5 mg (the lafutidine being administrated one hour after the mosapride). Each administration was separated by a 7-day washout period.
Results:
The average pH during the 4-hour period after administration of lafutidine 10 mgwith mosapride 5 mg was higher than after lafutidine 10 mg alone (median: 5.25 versus 4.58, respectively; p = 0.0318). During the 3-4 hour study period, lafutidine 10 mg with mosapride 5 mg provided a higher pH, compared to lafutidine 10 mg alone (median: 7.28 versus 6.42; p = 0.0208).
Conclusions:
In H. pylori negative healthy male subjects, an oral dose of lafutidine 10 mg with mosapride 5 mg more rapidly increased intragastric pH than lafutidine 10 mg alone.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/52</link>
                <dc:creator>Hiroshi Iida</dc:creator>
                <dc:creator>Masahiko Inamori</dc:creator>
                <dc:creator>Yuichi Nozaki</dc:creator>
                <dc:creator>Hiroki Endo</dc:creator>
                <dc:creator>Kunihiro Hosono</dc:creator>
                <dc:creator>Tomoyuki Akiyama</dc:creator>
                <dc:creator>Yasunari Sakamoto</dc:creator>
                <dc:creator>Hirokazu Takahashi</dc:creator>
                <dc:creator>Tomoko Koide</dc:creator>
                <dc:creator>Chikako Tokoro</dc:creator>
                <dc:creator>Yasunobu Abe</dc:creator>
                <dc:creator>Atsushi Nakajima</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:52</dc:source>
        <dc:date>2009-07-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-52</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>52</prism:startingPage>
        <prism:publicationDate>2009-07-09T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/51">
        <title>Associations of a PTPN11 G/A polymorphism at intron 3 with Helicobactor pylori seropositivity, gastric atrophy and gastric cancer in Japanese</title>
        <description>Background:
Previous studies have revealed the significance of Helicobacter pylori (H. pylori) infection as a risk factor of gastric cancer. Cytotoxin-associated gene A (cagA) positivity has been demonstrated to determine the clinical outcome of H. pylori infection in the presence of SHP-2 (src homology 2 domain-containing protein tyrosine phosphatase-2). This study aimed to examine the formerly reported association of G/A PTPN11 (protein-tyrosine phosphatase, nonreceptor-type 11) polymorphism (rs2301756) with gastric atrophy, as well as the association with gastric cancer in a Japanese population using a large sample size.
Methods:
Study subjects were 583 histologically diagnosed patients with gastric cancer (429 males and 154 females) and age- and sex-frequency-matched 1,636 non-cancer outpatients (1,203 males and 433 females), who visited Aichi Cancer Center Hospital between 2001-2005. Serum anti- H. pylori IgG antibody and pepsinogens were measured to evaluate H. pylori infection and gastric atrophy, respectively. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by a logistic model.
Results:
Among H. pylori seropositive non-cancer outpatients, the age- and sex-adjusted OR of gastric atrophy was 0.82 (95% CI 0.62-1.10, P=0.194) for G/A, 0.84 (95% CI 0.39-1.81, P=0.650) for A/A, and 0.83 (95% CI 0.62-1.09, P=0.182) for G/A+A/A, relative to G/G genotype, and that of severe gastric atrophy was 0.70 (95% CI 0.47-1.04, P=0.079), 0.56 (95% CI 0.17-1.91, P=0.356), and 0.68 (95% CI 0.46-1.01, P=0.057), respectively. Among H. pylori infected subjects (H. pylori seropositive subjects and seronegative subjects with gastric atrophy), the adjusted OR of severe gastric atrophy was further reduced; 0.62 (95% CI 0.42-0.90, P=0.012) for G/A+A/A. The distribution of the genotype in patients with gastric cancer was not significantly different from that for H. pylori infected subjects without gastric atrophy.
Conclusion:
Our study results revealed that those with the A/A genotype of PTPN11 rs2301756 polymorphism are at lower risk of severe gastric atrophy, but are not associated with a decreased risk of gastric cancer, which partially supported our previous finding that the polymorphism in the PTPN11 gene encoding SHP-2 was associated with the gastric atrophy risk in H. pylori infected Japanese. The biological roles of this PTPN11 polymorphism require further investigation.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/51</link>
                <dc:creator>Asahi Hishida</dc:creator>
                <dc:creator>Keitaro Matsuo</dc:creator>
                <dc:creator>Yasuyuki Goto</dc:creator>
                <dc:creator>Mariko Naito</dc:creator>
                <dc:creator>Kenji Wakai</dc:creator>
                <dc:creator>Kazuo Tajima</dc:creator>
                <dc:creator>Nobuyuki Hamajima</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:51</dc:source>
        <dc:date>2009-07-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-51</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>51</prism:startingPage>
        <prism:publicationDate>2009-07-09T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/50">
        <title>The galactose elimination capacity and mortality in 781 Danish patients with newly-diagnosed liver cirrhosis: a cohort study</title>
        <description>Background:
Despite its biologic plausibility, the association between liver function and mortality of patients with chronic liver disease is not well supported by data. Therefore, we examined whether the galactose elimination capacity (GEC), a physiological measure of the total metabolic capacity of the liver, was associated with mortality in a large cohort of patients with newly-diagnosed cirrhosis.
Methods:
By combining data from a GEC database with data from healthcare registries we identified cirrhosis patients with a GEC test at the time of cirrhosis diagnosis in 1992-2005. We divided the patients into 10 equal-sized groups according to GEC and calculated all-cause mortality as well as cirrhosis-related and not cirrhosis-related mortality for each group. Cox regression was used to adjust the association between GEC and all-cause mortality for confounding by age, gender and comorbidity, measured by the Charlson comorbidity index.
Results:
We included 781 patients, and 454 (58%) of them died during 2,617 years of follow-up. Among the 75% of patients with a decreased GEC (&lt;1.75 mmol/min), GEC was a strong predictor of 30-day, 1-year, and 5-year mortality, and this could not be explained by confounding (crude hazard ratio for a 0.5 mmol/min GEC increase = 0.74, 95% CI 0.59-0.92; adjusted hazard ratio = 0.64, 95% CI 0.51-0.81). Further analyses showed that the association between GEC and mortality was identical for patients with alcoholic or non-alcoholic cirrhosis etiology, that it also existed among patients with comorbidity, and that GEC was only a predictor of cirrhosis-related mortality. Among the 25% of patients with a GEC in the normal range (1.75 mmol/min or higher), GEC was only weakly associated with mortality (crude hazard ratio = 0.79, 95% CI 0.59-1.05; adjusted hazard ratio = 0.80, 95% CI 0.60-1.08).
Conclusions:
Among patients with newly-diagnosed cirrhosis and a decreased GEC, the GEC was a strong predictor of short- and long-term all-cause and cirrhosis-related mortality. These findings support the expectation that loss of liver function increases mortality.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/50</link>
                <dc:creator>Peter Jepsen</dc:creator>
                <dc:creator>Hendrik Vilstrup</dc:creator>
                <dc:creator>Peter Ott</dc:creator>
                <dc:creator>Susanne Keiding</dc:creator>
                <dc:creator>Per Andersen</dc:creator>
                <dc:creator>Niels Tygstrup</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:50</dc:source>
        <dc:date>2009-06-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-50</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>50</prism:startingPage>
        <prism:publicationDate>2009-06-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/49">
        <title>Increasing prevalence and high incidence of celiac disease in elderly people: A population-based study</title>
        <description>Background:
Celiac disease may emerge at any age, but little is known of its appearance in elderly people. We evaluated the prevalence of the condition in individuals over 55 years of age, and determined the incidence of biopsy-proven celiac disease (CDb) and celiac disease including seropositive subjects for anti-tissue transglutaminase antibodies (CDb+s).
Methods:
The study based on prevalence figures in 2815 randomly selected subjects who had undergone a clinical examination and serologic screening for celiac disease in 2002. A second screening in the same population was carried out in 2005, comprising now 2216 individuals. Positive tissue transglutaminase antibodies were confirmed with small bowel biopsy.
Results:
Within three years the prevalence of CDb increased from 2.13 to 2.34%, and that of CDb+s from 2.45 to 2.70%. Five new cases were found among patients previously seronegative; two had minor abdominal symptoms and three were asymptomatic. The incidence of celiac disease in 2002-2005 was 0.23%, giving an annual incidence of 0.08% in this population.
Conclusions:
The prevalence of celiac disease was high in elderly people, but the symptoms were subtle. Repeated screening detected five biopsy-proven cases in three years, indicating that the disorder may develop even in the elderly. Increased alertness to the disorder is therefore warranted.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/49</link>
                <dc:creator>Anitta Vilppula</dc:creator>
                <dc:creator>Katri Kaukinen</dc:creator>
                <dc:creator>Liisa Luostarinen</dc:creator>
                <dc:creator>Ilkka Krekela</dc:creator>
                <dc:creator>Heikki Patrikainen</dc:creator>
                <dc:creator>Raisa Valve</dc:creator>
                <dc:creator>Markku Maki</dc:creator>
                <dc:creator>Pekka Collin</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:49</dc:source>
        <dc:date>2009-06-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-49</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>49</prism:startingPage>
        <prism:publicationDate>2009-06-29T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/48">
        <title>Assessment of safety and feasibility of a new technical variant of gastropexy for percutaneous endoscopic gastrostomy: an experience with 453 cases</title>
        <description>Background:
Percutaneous Endoscopic Gastrostomy (PEG) performed through the Introducer Technique is associated with lower risk of surgical infection when compared to the Pull Technique. Its use is less widespread as the fixation of the stomach to the abdominal wall is a stage of the procedure that is difficult to be performed. We present a new technical variant of gastropexy which is fast and easy to be performed. The aim of this study was to evaluate the safety and feasibility of a new technical variant of gastropexy in patients submitted to gastrostomy performed through the Introducer Technique.
Methods:
All the patients submitted to PEG through the Introducer Technique were evaluated using a new technical variant of gastropexy, which consists of two parallel stitches of trasfixation sutures involving the abdominal wall and the gastric wall, performed with a long curved needle.Prophylactic antibiotics were not used. Demographic aspects, initial diagnosis, indication, sedation doses, morbidity and surgical mortality were all analyzed.
Results:
Four hundred and thirty-five consecutive PEGs performed between June 2004 and May 2007 were studied. Nearly all the cases consisted of patients presenting malignant neoplasia, 79.5% of which sited in the head and neck. The main indication of PEG was dysphagia, found in 346 patients (79.5%). There were 12 complications (2.8%) in 11 patients, from which only one patient had peristomal infection (0.2%). There was one death related to the procedure.
Conclusions:
Gastropexy with the technical variant described here is easy to be performed and was feasible and safe in the present study. PEG performed by the Introducer Technique with this type of gastropexy was associated with low rates of wound infection even without the use of prophylactic antibiotics.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/48</link>
                <dc:creator>Paulo Campoli</dc:creator>
                <dc:creator>Daniela Cardoso</dc:creator>
                <dc:creator>Marilia Turchi</dc:creator>
                <dc:creator>Flavio Ejima</dc:creator>
                <dc:creator>Orlando Mota</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:48</dc:source>
        <dc:date>2009-06-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-48</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>48</prism:startingPage>
        <prism:publicationDate>2009-06-26T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/47">
        <title>Trends in esophageal cancer and body mass index by race and gender in the state of Michigan</title>
        <description>Background:
Adenocarcinoma of the esophagus has been increasing in incidence in the U.S. over the past several decades, particularly among white males. The factors driving the racial disparity in adenocarcinomas rates are not well understood.
Methods:
Here we examine trends in both esophageal cancer incidence and body mass index (BMI) in a geographically defined cohort by gender and race. Age-adjusted esophageal cancer incidence rates from 1985 to 2005 were calculated from data collected by the Michigan state cancer registry. Trends were analyzed along with trends in BMI data obtained from the Behavioral Risk Factor Survey administered by the Centers for Disease Control.
Results:
Overall, age adjusted incidence rates in esophageal carcinoma increased from 4.49 to 4.72 cases/100,000 persons per year in Michigan from 1985 to 2005. Among white males, the rate of adenocarcinomas increased by 0.21 cases/100,000 per year to a maximum of 6.40 cases/100,000 in 1999, after which these rates remained constant. There was a slight but non-significant increase in the rate of adenocarcinomas among African American males, for whom the average incidence rate was 8 times lower than that for white males (0.58 vs 4.72 cases/100,000 person years). While average BMI is rising in Michigan (from 26.68 in 1988 to 30.33 in 2005), average BMI was slightly higher among African Americans on average, and the rates of increase in BMI were not different between African American males and white males.
Conclusion:
The disparity between African American males and white males is not explained by ecological-level trends in BMI. Further research to identify the factors responsible for this disparity, possibly including anatomic fat distribution, are required.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/47</link>
                <dc:creator>Eric Kort</dc:creator>
                <dc:creator>Eric Sevensma</dc:creator>
                <dc:creator>Timothy Fitzgerald</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:47</dc:source>
        <dc:date>2009-06-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-47</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>47</prism:startingPage>
        <prism:publicationDate>2009-06-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/46">
        <title>Lipoprotein lipase activity and mass, apolipoprotein C-II mass and polymorphisms of apolipoproteins E and A5 in subjects with prior acute hypertriglyceridaemic pancreatitis</title>
        <description>Background:
Severe hypertriglyceridaemia due to chylomicronemia may trigger an acute pancreatitis. However, the basic underlying mechanism is usually not well understood. We decided to analyze some proteins involved in the catabolism of triglyceride-rich lipoproteins in patients with severe hypertriglyceridaemia.
Methods:
Twenty-four survivors of acute hypertriglyceridaemic pancreatitis (cases) and 31 patients with severe hypertriglyceridaemia (controls) were included. Clinical and anthropometrical data, chylomicronaemia, lipoprotein profile, postheparin lipoprotein lipase mass and activity, hepatic lipase activity, apolipoprotein C II and CIII mass, apo E and A5 polymorphisms were assessed.
Results:
Only five cases were found to have LPL mass and activity deficiency, all of them thin and having the first episode in childhood. No cases had apolipoprotein CII deficiency. No significant differences were found between the non-deficient LPL cases and the controls in terms of obesity, diabetes, alcohol consumption, drug therapy, gender distribution, evidence of fasting chylomicronaemia, lipid levels, LPL activity and mass, hepatic lipase activity, CII and CIII mass or apo E polymorphisms. However, the SNP S19W of apo A5 tended to be more prevalent in cases than controls (40% vs. 23%, NS).
Conclusion:
Primary defects in LPL and C-II are rare in survivors of acute hypertriglyceridaemic pancreatitis; lipase activity measurements should be restricted to those having their first episode during chilhood.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/46</link>
                <dc:creator>Inmaculada Coca-Prieto</dc:creator>
                <dc:creator>Pedro Valdivielso</dc:creator>
                <dc:creator>Gunilla Olivecrona</dc:creator>
                <dc:creator>Maria Jose Ariza</dc:creator>
                <dc:creator>Jose Rioja</dc:creator>
                <dc:creator>Pilar Font-Ugalde</dc:creator>
                <dc:creator>Carlota Garcia-Arias</dc:creator>
                <dc:creator>Pedro Gonzalez-Santos</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:46</dc:source>
        <dc:date>2009-06-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-46</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>46</prism:startingPage>
        <prism:publicationDate>2009-06-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/45">
        <title>Treatment of malignant gastric outlet obstruction with stents:  an evaluation of the reported variables for clinical outcome</title>
        <description>Background:
Malignant gastric outlet obstruction (GOO) is commonly seen in patients with advanced gastric-, pancreatic-, duodenal, hepatobiliary or metastatic malignancies. Ten to 25% of patients with pancreatic cancer will develop duodenal obstruction during the course of the disease. Duodenal stenting with self-expandable metal stents is an alternative treatment to surgical bypass procedures. Our aim was to review the published literature regarding treatment of malignant GOO with stents to reveal whether the information provided is sufficient to evaluate the clinical effects of this treatment
Methods:
A literature search from 2000 &#8211; 2007 was conducted in Pub Med, Embase, and Cochrane library, combining the following search terms: duodenal stent, malignant duodenal obstruction, gastric outlet obstruction, SEMS, and gastroenteroanastomosis.All publications presenting data with &#8805; 15 patients and only articles written in English were included and a review focusing on the following parameters were conducted: 1) The use of graded scoring systems evaluating clinical success; 2) Assessment of Quality of life (QoL) before and after treatment; 3) Information on stent-patency; 4) The use of objective criteria to evaluate the stent effect.
Results:
41 original papers in English were found; no RCT&apos;s. 16 out of 41 studies used some sort of graded scoring system. No studies had objectively evaluated QoL before or after stent treatment, using standardized QoL-questionnaires, 32/41 studies reported on stent patency and 9/41 performed an oral contrast examination after stent placement. Objective quantitative tests of gastric emptying had not been performed.
Conclusion:
Available reports do not provide sufficient relevant information of the clinical outcome of duodenal stenting. In future studies, these relevant issues should be addressed to allow improved evaluation of the effect of stent treatment.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/45</link>
                <dc:creator>Lene Larssen</dc:creator>
                <dc:creator>Asle Medhus</dc:creator>
                <dc:creator>Truls Hauge</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:45</dc:source>
        <dc:date>2009-06-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-45</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>45</prism:startingPage>
        <prism:publicationDate>2009-06-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/44">
        <title>Gluten sensitivity enteropathy in patients with recurrent aphthous stomatitis</title>
        <description>Background:
Gluten sensitive enteropathy (GSE) is an autoimmune enteropathy triggered by the ingestion of gluten-containing grains in susceptible individuals. Recurrent aphthous stomatitis (RAS) may be the sole manifestation of GSE. The aim of this study was to determine the prevalence of gluten sensitivity enteropathy (GSE) in a large group of patients with RAS and assess the efficacy of gluten free diet (GFD) on the improvement of aphthous lesions in those who were diagnosed with GSE.
Methods:
Two hundred and forty seven patients with RAS were included. The patients had at least three aphthous attacks per year. Patients were screened by IgA anti-endomysial antibody (EMA), IgA anti tissue transglutaminase (TTG) and serum IgA level. Those with a positive serology underwent endoscopic biopsies of the duodenal mucosa and patients with negative serology were excluded. The diagnosis of GSE was based on a positive serological test and abnormal duodenal histology. For patients with GSE, gluten free diet was recommended.
Results:
Six out of 247 RAS patients had positive TTG test alone, and one had positive EMA and TTG. All 7 patients with positive serologic tests underwent duodenal biopsies. Histological findings were compatible with GSE in all of them (Marsh I in four patients, Marsh II in two patients and Marsh IIIB in one another.). The mean age of GSE patients was 27.42 +/- 10.56 (range, 13 to 40) years old. They were suffering from RAS for an average duration of 4.5 years. All of the 7 GSE patients had not responded to the routine anti-aphthae medications, including topical corticosteroids, tetracycline and colchicine. Four patients who adhered to a strict gluten-free diet showed noticeable improvement in their aphthous lesions over a period of 6 months.
Conclusions:
A significant minority (e.g. 2.83%) of RAS patients have GSE. This could be compared with the 0.96% prevalence of GSE in the general population of Iran. This study suggests that evaluation for celiac disease is appropriate in patients with RAS. Additionally, the unresponsiveness to conventional anti-aphthae treatment could be an additional risk indicator.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/44</link>
                <dc:creator>Ramin Shakeri</dc:creator>
                <dc:creator>Farhad Zamani</dc:creator>
                <dc:creator>Rasoul Sotoudehmanesh</dc:creator>
                <dc:creator>Afsaneh Amiri</dc:creator>
                <dc:creator>Mehdi Mohamadnejad</dc:creator>
                <dc:creator>Fereydoun Davatchi</dc:creator>
                <dc:creator>Ali Mohammadi Karakani</dc:creator>
                <dc:creator>Reza Malekzadeh</dc:creator>
                <dc:creator>Farhad Shahram</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:44</dc:source>
        <dc:date>2009-06-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-44</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>44</prism:startingPage>
        <prism:publicationDate>2009-06-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/43">
        <title>The clinicopathologic observation, c-KIT gene mutation and clonal status of gastrointestinal stromal tumor in the sacrum </title>
        <description>Background:
It is very rare that gastrointestinal stromal tumor (GIST) occurs in the sacrum. Only one case of GIST occuring in the sacral region, with intracranial metastasis, has been reported in the literature. Moreover, only few cases have been published in literature about its clonal origin.Case presentationIn this report, we present a rare case of GIST occuring in the sacrum and describe its clinicopathologic features, c-KIT gene mutation and clonal status. Microscopically, the lesion was composed of spindle cells arranged in cords, knitted and whirlpool patterns. Trabecula of bone were found in the lesion. The cytoplasm of tumor cells were abundant, and the nuclei were fusiform. Mitotic figures were rare. Immunohistochemically, the tumor cells showed positive reactivity for CD117 and CD34. On mutation analysis, a c-KIT gene mutation was found in exon 11. The result of clonal analysis demonstrated that the GIST was monoclonal.
Conclusion:
In summary, we showed that tumor material, phenotypically identical with GISTs was found in the sacrum. It is difficult to differentiate GISTs from other spindle cell tumors, hence the need for immunohistochemistry, the examination of c-KIT gene amplification and sequencing.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/43</link>
                <dc:creator>Li Gong</dc:creator>
                <dc:creator>Yan-Hong Li</dc:creator>
                <dc:creator>Hua-Dong Zhao</dc:creator>
                <dc:creator>Jian-Ye Zhao</dc:creator>
                <dc:creator>Wei Zhang</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:43</dc:source>
        <dc:date>2009-06-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-43</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>43</prism:startingPage>
        <prism:publicationDate>2009-06-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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