Thrombotic complications in inflammatory bowel diseases.

Inflammatory bowel disease (IBD), Crohn's Disease (CD) and Ulcerative Colitis (UC) are associated with an increased risk of arterial and venous thromboembolism. A 2 to 3 time fold increased risk of developing thromboembolic complications was reported for IBD patients compared to general population. A systematic literature search was conducted using PubMed, Medline, Scopus, Cochrane database. The key words were: "Inflammatory Bowell Disease", "Crohn's Disease and Thrombosis", "Ulcerative Colitis and Thrombosis", "Thrombosis" and "Inflammatory Bowel Diseases and Thrombosis". Full articles and abstracts were included. Studies such as case reports, letters and commentaries were excluded from the analysis if appropriate data could not be extracted. Although no randomized controlled trials (RCTs) have been established to evaluate the efficacy of thromboprophylaxis in patients with IBD due to the incidence of VTE and PE in such patients, it is highly recommended the adoption of thromboprophylactic measures. Available prophylaxis and treatment options include pharmacological anticoagulant therapy (LMWH-Low Molecular Weight Heparin, Fondaparinux and UH-Unfractionated Heparin) and mechanical prophylaxis. In case of acute VTE patient must be treated with fibrinolytic agents and in selected non-responsive cases vascular surgery. IBD patients have an increased risk of VTE complications. Prophylaxis for VTE should be recommended in all patients who do not show contraindications to treatment.

Eradication of Helicobacter pylori may reduce disease severity in rheumatoid arthritis.

BACKGROUND: A triggering infectious agent has long been postulated in rheumatoid arthritis. Data on the possible role of Helicobacter pylori infection are lacking. AIM: To assess the effect of H. pylori eradication in patients with rheumatoid arthritis. METHODS: Fifty-eight adult patients with established rheumatoid arthritis and dyspeptic symptoms were recruited - 28 were H. pylori-positive and 30 were H. pylori-negative on the basis of invasive tests. All infected patients were treated successfully. We evaluated the disease activity using clinical and laboratory parameters at baseline and every 4 months during 2 years, and compared the variations in the two subgroups. RESULTS: H. pylori-eradicated rheumatoid arthritis patients showed progressive improvement over time (P < 0.0001) of all clinical indices compared with baseline, whereas H. pylori-negative rheumatoid arthritis patients remained substantially unchanged. After 2 years, H. pylori-eradicated rheumatoid arthritis patients differed significantly (P < 0.04-0.0001) from patients without H. pylori infection in terms of improvement of all clinical parameters. At the same time point, several laboratory indices (erythrocyte sedimentation rate, fibrinogen, alpha2-globulins and antinuclear antibody) showed significantly lower values (P < 0.02-0.0003) in the H. pylori-eradicated subgroup compared to the H. pylori-negative subgroup. CONCLUSIONS: Our data suggest that H. pylori infection is implicated in the pathogenesis of rheumatoid arthritis, in that its eradication may induce a significant improvement of disease activity over 24 months. H. pylori eradication seems to be advantageous in infected rheumatoid arthritis patients, but controlled studies are needed.