Scandinavian journal of gastroenterology
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Scand. J. Gastroenterol. · Jan 2002
Hyperhomocysteinaemia, coagulation pathway activation and thrombophilia in patients with inflammatory bowel disease.
The 5,10-methylenetetrahydrofolate reductase (MTHFR) 677C-->T polymorphism encoding the thermolabile variant is, when present as homozygote type (TT variant), a known genetic cause of mild hyperhomocysteinaemia (HHCY). This polymorphism has been observed in increased numbers in patients with inflammatory bowel disease (IBD). Coagulation and fibrinolysis are activated in patients with active IBD, but it is not known whether raised plasma homocysteine (HCY) found in patients with IBD significantly contributes to this activation. The aim of this study was to investigate if HHCY or presence of the TT variant significantly induces a hypercoagulable state in IBD patients receiving anti-inflammatory therapy during active disease, and to study if genetic determinants for thromboembolic disease are more frequent in these patients. ⋯ This study found no correlation between the MTHFR TT variant or HHCY and a hypercoagulable state in IBD patients receiving anti-inflammatory treatment. This coagulation activity is high during exacerbations of disease, but a considerable reduction is seen in patients on anti-inflammatory therapy compared with non-treated patients. Coagulation activation in IBD is probably a consequence of the inflammatory nature of the disease. That thrombophilia could be a contributory or primary factor in the development of IBD is not supported by the present study, as the frequencies for the genetic determinants for thrombophilia are similar in IBD patients and controls.
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Scand. J. Gastroenterol. · Jan 2002
Not all HLA DR3 DQ2 haplotypes confer equal susceptibility to coeliac disease: transmission analysis in families.
HLA-DQ is the only established susceptibility factor for coeliac disease. We tested whether all HLA haplotypes with the known risk marker, HLA-DQ2, confer equal susceptibility to coeliac disease, i.e. whether haplotype transmission from DQ2 homozygous parents to patients is random. The random transmission would strengthen the importance of DQ2 as the only risk factor within the HLA region. ⋯ The results suggest that DQ2 is not the only HLA-linked genetic risk factor for coeliac disease but the conserved haplotype harbours at least one other risk gene.
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Scand. J. Gastroenterol. · Dec 2001
Link between Helicobacter pylori infection and iron-deficiency anaemia in patients with coeliac disease.
Iron-deficiency anaemia is a frequent finding in coeliac disease. Recent investigations have identified Helicobacter pylori infection as a factor responsible for iron deficiency. We investigated the potential relationship between H. pylori and iron-deficiency anaemia in patients with coeliac disease. ⋯ This study shows a significant association between H. pylori infection and iron-deficiency anaemia in patients with coeliac disease. The discovery of iron-deficiency anaemia in coeliac subjects may constitute another indication for the diagnosis and treatment of this worldwide infection.
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Scand. J. Gastroenterol. · Oct 2001
Cellular markers of systemic inflammation and immune suppression in patients with organ failure due to severe acute pancreatitis.
Few data are available on cellular markers of systemic inflammation and immune suppression in early acute pancreatitis. The aim of this study was to describe the cellular immune inflammatory status of patients with acute pancreatitis in relation to development of organ failure. ⋯ Immune suppression develops early, rapidly and unexpectedly in patients with acute pancreatitis. Monitoring immune inflammatory status may provide the means by which to identify patients who benefit from biological response modifier therapy.
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Scand. J. Gastroenterol. · Oct 2001
Functional dyspepsia symptoms, gastric emptying and satiety provocative test: analysis of relationships.
The correlation between symptoms and observed impaired function in functional dyspepsia is still inconsistent. The aims of the study were to obtain a measure of satiety by a meal test; to verify whether this compares with severity of symptoms assessed using a reproducible questionnaire; and to correlate the parameters of satiety test and gastric emptying with all the dyspeptic symptoms. ⋯ The satiety test gives a fine numerical measure of satiety and confirms the results of a symptoms questionnaire. Our study showed an indirect correlation between severity of early satiety--as measured by the satiety test, and gastric emptying rate, as well as an association between bloating and delayed gastric emptying.