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        <title>BMC Gastroenterology - Most accessed articles</title>
        <link>http://www.biomedcentral.com/bmcgastroenterol/</link>
        <description>The most accessed research articles published by BMC Gastroenterology</description>
        <dc:date>2009-11-18T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-230X/9/82" />
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        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/82">
        <title>A comparison of diagnostic tests for lactose malabsorption - 
which one is the best?
</title>
        <description>Background:
Perceived milk intolerance is a common complaint, and tests for lactose malabsorption (LM) are unreliable. This study assesses the agreement between diagnostic tests for LM and describes the diagnostic properties of the tests.
Methods:
Patients above 18 years of age with suspected LM were included. After oral intake of 25 g lactose, a combined test with measurement of serum glucose (s-glucose) and hydrogen (H2) and methane (CH4) in expired air was performed and symptoms were recorded. In patients with discrepancies between the results, the combined test was repeated and a gene test for lactose non-persistence was added. The diagnosis of LM was based on an evaluation of all tests. The following tests were compared: Increase in H2, CH4, H2+CH4 and H2+CH4x2 in expired air, increase in s-glucose, and symptoms. The agreement was calculated and the diagnostic properties described.
Results:
Sixty patients were included, seven (12%) had LM. The agreement (kappa-values) between the methods varied from 0.25 to 0.91. The best test was the lactose breath test with measurement of the increase in H2 + CH4x2 in expired air. With a cut-off level &lt; 18 ppm, the area under the ROC-curve was 0.967 and sensitivity was 100%. This shows that measurement of CH4 in addition to H2 improves the diagnostic properties of the breath test.
Conclusion:
The agreement between commonly used methods for the diagnosis of LM was unsatisfactory. A lactose breath test with measurement of H2 + CH4x2 in expired air had the best diagnostic properties.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/82</link>
                <dc:creator>Oistein Hovde</dc:creator>
                <dc:creator>Per Farup</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:82</dc:source>
        <dc:date>2009-10-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-82</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>82</prism:startingPage>
        <prism:publicationDate>2009-10-31T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</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/9/79">
        <title>Investigation of innate immunity genes CARD4, CARD8 and CARD15 as germline susceptibility factors for colorectal cancer</title>
        <description>Background:
Variation in genes involved in the innate immune response may play a role in the predisposition to colorectal cancer (CRC). Several polymorphisms of the CARD15 gene (caspase activating recruitment domain, member 15) have been reported to be associated with an increased susceptibility to Crohn disease. Since the CARD15 gene product and other CARD proteins function in innate immunity, we investigated the impact of germline variation at the CARD4, CARD8 and CARD15 loci on the risk for sporadic CRC, using a large patient sample from Northern Germany.
Methods:
A total of 1044 patients who had been operated with sporadic colorectal carcinoma (median age at diagnosis: 59 years) were recruited and compared to 724 sex-matched, population-based control individuals (median age: 68 years). Genetic investigation was carried out following both a coding SNP and haplotype tagging approach. Subgroup analyses for N = 143 patients with early manifestation of CRC (&#8804;50 age at diagnosis) were performed for all CARD loci and subgroup analyses for diverse age strata were carried out for CARD15 mutations R702W, G908R and L1007fs. In addition, all SNPs were tested for association with disease presentation and family history of CRC.
Results:
No significant differences were observed between the patient and control allelic or haplotypic spectra of the three genes under study for the total cohort (N = 1044 patients). None of the analysed SNPs was significantly associated with either tumour location or yielded significant association in the familial or non-familial CRC patient subgroups. However, in a patient subgroup (&#8804;45 age at diagnosis) with early disease manifestation the mutant allele of CARD15 R702W was found to be significantly associated with disease susceptibility (9.7% in cases vs 4.6% in controls; Pallelic = 0.008, Pgenotypic = 0.0008, ORallelic = 2.22 (1.21-4.05) ORressessive = 21.9 (1.96-245.4).
Conclusion:
Variation in the innate immunity genes CARD4, CARD8 and CARD15 is unlikely to play a major role in the susceptibility to CRC in the German population. But, we report a significant disease contribution of CARD15 for CRC patients with very early disease manifestation, mainly driven by variant R702W.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/79</link>
                <dc:creator>Nikolaus Mockelmann</dc:creator>
                <dc:creator>Witigo von Schonfels</dc:creator>
                <dc:creator>Stephan Buch</dc:creator>
                <dc:creator>Oliver von Kampen</dc:creator>
                <dc:creator>Bence Sipos</dc:creator>
                <dc:creator>Jan Hendrik Egberts</dc:creator>
                <dc:creator>Philip Rosenstiel</dc:creator>
                <dc:creator>Andre Franke</dc:creator>
                <dc:creator>Mario Brosch</dc:creator>
                <dc:creator>Sebastian Hinz</dc:creator>
                <dc:creator>Christian Roder</dc:creator>
                <dc:creator>Holger Kalthoff</dc:creator>
                <dc:creator>Ulrich Folsch</dc:creator>
                <dc:creator>Michael Krawczak</dc:creator>
                <dc:creator>Stefan Schreiber</dc:creator>
                <dc:creator>Clemens Dieter Broring</dc:creator>
                <dc:creator>Jurgen Tepel</dc:creator>
                <dc:creator>Clemens Schafmayer</dc:creator>
                <dc:creator>Jochen Hampe</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:79</dc:source>
        <dc:date>2009-10-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-79</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>79</prism:startingPage>
        <prism:publicationDate>2009-10-20T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/81">
        <title>Liver fibrosis secondary to bile duct injury: correlation of Smad7 with TGF-beta and extracellular matrix proteins</title>
        <description>Background:
Liver fibrosis is the result of continuous liver injury stemming from different etiological factors. Bile duct injury induces an altered expression of TGF-&#946;, which has an important role in liver fibrosis because this cytokine induces the expression of target genes such as collagens, PAI-1, TIMPs, and others that lead to extracellular matrix deposition. Smad7 is the principal inhibitor that regulates the target gene transcription of the TGF-&#946; signaling. The aim of the study was to determine whether Smad7 mRNA expression correlates with the gene expression of TGF-&#946;, Col I, Col III, Col IV, or PAI-1 in liver fibrosis secondary to bile duct injury (BDI).
Results:
Serum TGF-&#946; concentration was higher in BDI patients (39 296 pg/ml) than in liver donors (9008 pg/ml). Morphometric analysis of liver sections showed 41.85% of tissue contained fibrotic deposits in BDI patients. mRNA expression of Smad7, Col I, and PAI-1 was also significantly higher (P &lt; 0.05) in patients with BDI than in controls. Smad7 mRNA expression correlated significantly with TGF-&#946; concentration, Col I and Col III expression, and the amount of fibrosis.
Conclusion:
We found augmented serum concentration of TGF-&#946; and an increase in the percentage of fibrotic tissue in the liver of BDI patients. Contrary to expected results, the 6-fold increase in Smad7 expression did not inhibit the expression of TGF-&#946;, collagens, and PAI-1. We also observed greater expression of Col I and Col III mRNA in BDI patients and significant correlations between their expression and TGF-&#946; concentration and Smad7 mRNA expression.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/81</link>
                <dc:creator>Maria del Pilar Alatorre-Carranza</dc:creator>
                <dc:creator>Alejandra Miranda-Diaz</dc:creator>
                <dc:creator>Irinea Yanez-Sanchez</dc:creator>
                <dc:creator>Oscar Pizano-Martinez</dc:creator>
                <dc:creator>Jose M Hermosillo-Sandoval</dc:creator>
                <dc:creator>Monica Vazquez-del Mercado</dc:creator>
                <dc:creator>Sebastian Hernandez-Hoyo</dc:creator>
                <dc:creator>Ricardo Abundis-Martinez</dc:creator>
                <dc:creator>Mary Fafutis-Morris</dc:creator>
                <dc:creator>Jorge Segura-Ortega</dc:creator>
                <dc:creator>Vidal Delgado-Rizo</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:81</dc:source>
        <dc:date>2009-10-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-81</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>81</prism:startingPage>
        <prism:publicationDate>2009-10-31T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-230X/9/15">
        <title>A Systematic Review and Meta-Analysis: Probiotics in the treatment of Irritable Bowel Syndrome </title>
        <description>Background:
Irritable Bowel Syndrome (IBS) is a common chronic gastrointestinal disorder and the evidence for efficacy of most drug therapies in the treatment of IBS is weak. A popular alternative is probiotics, which have been used in several conditions. including IBS. Probiotics are live microbial food supplements.The aim of this systematic review and meta-analysis of randomized trials study was to evaluate the efficacy of probiotics in alleviating symptoms in patients with irritable bowel syndrome. We searched Ovid versions of MEDLINE (1950&#8211;2007), EMBASE (1980&#8211;2007), CINAHL (1982&#8211;2007), AMED (1985&#8211;2007), the Cochrane library and hand searched retrieved papers.
Results:
We identified 14 randomized placebo controlled trials. Combined data suggested a modest improvement in overall symptoms after several weeks of treatment: for dichotomous data from seven trials the overall Odds Ratio (OR) was 1.6 (95% CI, 1.2 to 2.2); for continuous data from six trials the standardised mean difference (SMD) was 0.23 (95% CI, 0.07 to 0.38).For individual symptoms the results differed between the pooled dichotomous and pooled continuous data. Trials varied in relation to the length of treatment (4&#8211;26 weeks), dose, organisms and strengths of probiotics used.
Conclusion:
Probiotics may have a role in alleviating some of the symptoms of IBS, a condition for which currently evidence of efficacy of drug therapies is weak. However, as IBS is a condition that is chronic and usually intermittent longer term trials are recommended. Such research should focus on the type, optimal dose of probiotics and the subgroups of patients who are likely to benefit the most.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/15</link>
                <dc:creator>Nourieh Hoveyda</dc:creator>
                <dc:creator>Carl Heneghan</dc:creator>
                <dc:creator>Kamal Mahtani</dc:creator>
                <dc:creator>Rafael Perera</dc:creator>
                <dc:creator>Nia Roberts</dc:creator>
                <dc:creator>Paul Glasziou</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:15</dc:source>
        <dc:date>2009-02-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-15</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>15</prism:startingPage>
        <prism:publicationDate>2009-02-16T00:00:00Z</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/9/85">
        <title>A prospective, randomized, double-blind, placebo-controlled parallel-group dual site trial to evaluate the effects of a Bacillus coagulans-based product on functional intestinal gas symptom</title>
        <description>Background:
This randomized double blind placebo controlled dual site clinical trial compared a probiotic dietary supplement to placebo regarding effects on gastrointestinal symptoms in adults with post-prandial intestinal gas-related symptoms (abdominal pain, distention, flatulence) but no gastrointestinal (GI) diagnoses to explain the symptoms.
Methods:
Sixty-one adults were enrolled (age 36.5 &#177; 12.6 years; height 165.1 &#177; 9.2 cm; weight 75.4 &#177; 17.3 kg) and randomized to either Digestive Advantage&#8482; Gas Defense Formula - (GanedenBC30 Bacillus coagulans GBI-30, 6086): n = 30; or Placebo: n = 31. Study subjects were evaluated every two weeks over a four-week period using validated questionnaires and standard biochemical safety testing. Outcome criteria of interest included change from baseline in Gastrointestinal Symptom Rating Scale (GSRS) abdominal pain, abdominal distention, flatus, and the Severity of Dyspepsia Assessment (SODA) bloating and gas subscores over four weeks of product use.
Results:
Measured against the placebo, subjects in the probiotic group achieved significant improvements in GSRS abdominal pain subscore (p = 0.046) and the GSRS total score (p = 0.048), with a strong trend for improvement on the GSRS abdominal distension subscore (p = 0.061). A strong placebo effect was evident which could explain the lack of statistical significant differences between the groups for many of the efficacy variables.
Conclusion:
In conclusion, the Bacillus coagulans-based product was effective in improving the quality of life and reducing gastrointestinal symptoms in adults with post prandial intestinal gas-related symptoms and no GI diagnoses.Trial RegistrationClinicalTrials.gov Identifier: NCT00881322</description>
        <link>http://www.biomedcentral.com/1471-230X/9/85</link>
                <dc:creator>Douglas Kalman</dc:creator>
                <dc:creator>Howard Schwartz</dc:creator>
                <dc:creator>Patricia Alvarez</dc:creator>
                <dc:creator>Samantha Feldman</dc:creator>
                <dc:creator>John Pezzullo</dc:creator>
                <dc:creator>Diane Krieger</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:85</dc:source>
        <dc:date>2009-11-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-85</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>85</prism:startingPage>
        <prism:publicationDate>2009-11-18T00:00:00Z</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/9/78">
        <title>Importance of duodenal bulb biopsies in children for diagnosis of celiac disease in clinical practice  </title>
        <description>Background:
The patchy nature of villous lesion in celiac disease is increasingly being recognized. Current guidelines recommend four endoscopic duodenal mucosal biopsies from the second or more distal part of the duodenum to confirm the diagnosis of celiac disease. The purpose of the study was to investigate the usefulness of duodenal bulb mucosal biopsies in confirming the diagnosis of celiac disease in everyday clinical practice.
Methods:
All patients with a positive tissue-transglutaminase antibody requiring biopsy-confirmation of celiac disease over a two-year period were studied. Two endoscopic biopsies were taken from the duodenal bulb and four biopsies from the second (or distal) part of the duodenum.
Results:
Thirty-five patients were included, mean age 8.1 (&#177; 4.7) years. Thirty-one (88.6%) patients had abnormal distal duodenal biopsies, one had Marsh type 1, one had Marsh type 2 and twenty-nine had Marsh type 3 lesion. All but two patients with abnormal distal duodenal biopsies also had abnormal bulb biopsies. Four (11.4%) patients had normal distal duodenal biopsies but abnormal bulb biopsies. Of these, one patient had Marsh type 2 and three had Marsh type 3 lesion. The distal duodenum was also grossly normal in these four patients. The histological diagnosis of celiac disease would not have been possible in these four cases with distal duodenal biopsies only.
Conclusion:
The lesion in celiac disease in children can be patchy with duodenal bulb mucosa being the only area showing histological changes. The recommendations regarding the site of biopsies should be revised to include biopsies not only from distal duodenum but also from bulb to improve the diagnostic yield.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/78</link>
                <dc:creator>Mohsin Rashid</dc:creator>
                <dc:creator>Andrea MacDonald</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:78</dc:source>
        <dc:date>2009-10-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-78</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>78</prism:startingPage>
        <prism:publicationDate>2009-10-16T00:00:00Z</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/9/83">
        <title>The effect of psychological stress on iron absorption in rats</title>
        <description>Background:
Psychological stress (PS) is recognized as an important pathogenic factor which leads to metabolism disorder in many diseases. Previous studies have shown that systemic iron homeostasis in mammalians was changed under specific stress conditions.
Methods:
In present study, we used communication box to create psychological stress model and investigated the iron apparent absorption, iron accumulation in the apical poles of villous enterocytes and protein expressions of ferroportin 1 (FPN1), ferritin, divalent metal transporter 1 (DMT1).
Results:
Our study showed that iron apparent absorption decreased and iron significantly accumulated in the apical poles of villous enterocytes in 3 d and 7 d PS groups. The expression of intestinal FPN1 in 3 d and 7 d PS groups was lower than that of control, while the change of intestinal ferritin was opposite. However, the expression of DMT1 did not change.
Conclusion:
These results demonstrate that PS can decrease iron absorption in rats, which might be related to regulation expression of iron transporters.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/83</link>
                <dc:creator>Jianbo Chen</dc:creator>
                <dc:creator>Hui Shen</dc:creator>
                <dc:creator>Chengjie Chen</dc:creator>
                <dc:creator>Wanyin Wang</dc:creator>
                <dc:creator>Siyu Yu</dc:creator>
                <dc:creator>Min Zhao</dc:creator>
                <dc:creator>Min Li</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:83</dc:source>
        <dc:date>2009-11-13T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-83</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>83</prism:startingPage>
        <prism:publicationDate>2009-11-13T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</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/9/74">
        <title>Vitamin C supplement use may protect against gallstones: an observational study on a randomly selected population</title>
        <description>Background:
Animal experiments have shown a protective effect of vitamin C on the formation of gallstones. Few data in humans suggest an association between reduced vitamin C intake and increased prevalence of gallstone disease. The aim of this study was to assess the possible association of regular vitamin C supplementation with gallstone prevalence.
Methods:
An observational, population-based study of 2129 subjects aged 18-65 years randomly selected from the general population in southern Germany was conducted. Abdominal ultrasound examination, completion of a standardized questionnaire, compilation of anthropometric data and blood tests were used. Data were collected in November and December 2002. Data analysis was conducted between December 2005 and January 2006.
Results:
Prevalence of gallstones in the study population was 7.8% (167/2129). Subjects reporting vitamin C supplementation showed a prevalence of 4.7% (11/232), whereas in subjects not reporting regular vitamin C supplementation, the prevalence was 8.2% (156/1897). Female gender, hereditary predisposition, increasing age and body-mass index (BMI) were associated with increased prevalence of gallstones. Logistic regression with backward elimination adjusted for these factors showed reduced gallstone prevalence for vitamin C supplementation (odds ratio, OR 0.34; 95% confidence interval, CI 0.14 to 0.81; P = 0.01), increased physical activity (OR 0.62; 95% CI, 0.42 to 0.94; P = 0.02), and higher total cholesterol (OR 0.65; 95% CI, 0.52 to 0.79; P &lt; 0.001).
Conclusion:
Regular vitamin C supplementation and, to a lesser extent, increased physical activity and total cholesterol levels are associated with a reduced prevalence of gallstones. Regular vitamin C supplementation might exert a protective effect on the development of gallstones.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/74</link>
                <dc:creator>Thomas Walcher</dc:creator>
                <dc:creator>Mark Haenle</dc:creator>
                <dc:creator>Martina Kron</dc:creator>
                <dc:creator>Birgit Hay</dc:creator>
                <dc:creator>Richard Mason</dc:creator>
                <dc:creator>Daniel Walcher</dc:creator>
                <dc:creator>Gerald Steinbach</dc:creator>
                <dc:creator>Peter Kern</dc:creator>
                <dc:creator>Isolde Piechotowski</dc:creator>
                <dc:creator>Guido Adler</dc:creator>
                <dc:creator>Bernhard Boehm</dc:creator>
                <dc:creator>Wolfgang Koenig</dc:creator>
                <dc:creator>Wolfgang Kratzer</dc:creator>
                <dc:creator>Emil Study group</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:74</dc:source>
        <dc:date>2009-10-08T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-74</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>74</prism:startingPage>
        <prism:publicationDate>2009-10-08T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</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/7/34">
        <title>Portal vein thrombosis; risk factors, clinical presentation and treatment</title>
        <description>Background:
Portal vein thrombosis (PVT) is increasingly frequently being diagnosed, but systematic descriptions of the natural history and clinical handling of the condition are sparse. The aim of this retrospective study was to describe risk factors, clinical presentation, complications and treatment of portal vein thrombosis in a single-centre.
Methods:
Sixty-seven patients were identified in the electronic records from 1992 to 2005. All data were obtained from the patient records.
Results:
One or more risk factors (e.g. prothrombotic disorder or abdominal inflammation) were present in 87%. Symptoms were abdominalia, splenomegaly, fever, ascites, haematemesis, and weight loss. Abdominalia and fever occurred more frequently in patients with acute PVT. Frequent complications were splenomegaly, oesophageal- and gastric varices with or without bleeding, portal hypertensive gastropathy and ascites. Varices and bleeding were more frequent in patients with chronic PVT. Patients who received anticoagulant therapy more frequently achieved partial/complete recanalization. Patients with varices who were treated endoscopically in combination with &#946;-blockade had regression of the varices. The overall mortality was 13% in one year, and was dependent on underlying causes.
Conclusion:
Most patients had a combination of local and systemic risk factors for PVT. We observed that partial/complete recanalization was more frequent in patients treated with anticoagulation therapy, and that regression of varices was more pronounced in patients who where treated with active endoscopy combined with pharmacological treatment.</description>
        <link>http://www.biomedcentral.com/1471-230X/7/34</link>
                <dc:creator>Kirstine Sogaard</dc:creator>
                <dc:creator>Lone Astrup</dc:creator>
                <dc:creator>Hendrik Vilstrup</dc:creator>
                <dc:creator>Henning Gronbaek</dc:creator>
                <dc:source>BMC Gastroenterology 2007, 7:34</dc:source>
        <dc:date>2007-08-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-7-34</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>34</prism:startingPage>
        <prism:publicationDate>2007-08-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</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/9/21">
        <title>Blood ammonia levels in liver cirrhosis: a clue for the presence of esophageal varices.</title>
        <description>Background:
Portal hypertension leads to the formation of portosystemic collateral veins in liver cirrhosis. The resulting shunting is responsible for the development of portosystemic encephalopathy. Although ammonia plays a certain role in determining portosystemic encephalopathy, the venous ammonia level has not been found to correlate with the presence or severity of this entity. So, it has become partially obsolete. Realizing the need for non-invasive markers mirroring the presence of esophageal varices in order to reduce the number of endoscopy screening, we came back to determine whether there was a correlation between blood ammonia concentrations and the detection of portosystemic collateral veins, also evaluating splenomegaly, hypersplenism (thrombocytopenia) and the severity of liver cirrhosis.
Methods:
One hundred and fifty three consecutive patients with hepatic cirrhosis of various etiologies were recruited to participate in endoscopic and ultrasonography screening for the presence of portosystemic collaterals mostly esophageal varices, but also portal hypertensive gastropathy and large spontaneous shunts.
Results:
Based on Child-Pugh classification, the median level of blood ammonia was 45 mcM/L in 64 patients belonging to class A, 66 mcM/L in 66 patients of class B and 108 mcM/L in 23 patients of class C respectively (p &lt; 0.001).The grade of esophageal varices was concordant with venous ammonia levels (rho 0.43, p &lt; 0.001). The best area under the curve was given by ammonia concentrations, i, e., 0.78, when comparing areas of ammonia levels, platelet count and spleen longitudinal diameter at ultrasonography. Ammonia levels predicted hepatic decompensation and ascites presence (Odds Ratio 1.018, p &lt; 0.001).
Conclusion:
Identifying cirrhotic patients with high blood ammonia concentrations could be clinically useful, as high levels would lead to suspicion of being in presence of collaterals, in clinical practice of esophageal varices, and pinpoint those patients requiring closer follow-up and endoscopic screening.</description>
        <link>http://www.biomedcentral.com/1471-230X/9/21</link>
                <dc:creator>Giovanni Tarantino</dc:creator>
                <dc:creator>Vincenzo Citro</dc:creator>
                <dc:creator>Pasquale Esposito</dc:creator>
                <dc:creator>Sabrina Giaquinto</dc:creator>
                <dc:creator>Annalisa de Leone</dc:creator>
                <dc:creator>Graziella Milan</dc:creator>
                <dc:creator>Francesca Tripodi</dc:creator>
                <dc:creator>Michele Cirillo</dc:creator>
                <dc:creator>Roberto Lobello</dc:creator>
                <dc:source>BMC Gastroenterology 2009, 9:21</dc:source>
        <dc:date>2009-03-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-230X-9-21</dc:identifier>
        <prism:publicationName>BMC Gastroenterology</prism:publicationName>
        <prism:issn>1471-230X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>21</prism:startingPage>
        <prism:publicationDate>2009-03-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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