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    ABSTRACT: Inflammatory bowel disease (IBD) is a chronic idiopathic inflammatory disease of the gastrointestinal (GI) tract. In the past decade a shift in the treatment paradigm of IBD has ensued. The availability of drugs capable of inducing mucosal healing, combined with the recognition that IBD is not an intermittent disease, but rather a progressive one causing bowel damage and disability, led us to a more stringent strategy. Tailored therapy with more aggressive treatment in high-risk patients, treating beyond symptoms, intervening early before damage occurs, optimizing therapeutic regimens, and actively pursuing sustained remission and sustained control of inflammation are strategies that are slowly being incorporated in our clinical practice. Furthermore, new drugs targeting different immunological pathways, such as vedolizumab, have recently been approved and therefore more therapeutic resources for patients failing anti-tumour necrosis factor alpha (anti-TNFα) agents will be available.
    Full-text · Article · May 2015
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    ABSTRACT: Ulcerative colitis (UC) is a chronic idiopathic inflammatory disease of the gastrointestinal tract that affects the mucosal lining of the colon. Recent epidemiological data show that its incidence and prevalence are increasing in many parts of the world, in parallel with altered lifestyles, improved access to health, improved sanitation and industrialisation rates. Current therapeutic strategies for treating UC have only been moderately successful. Despite major recent advances in inflammatory bowel disease therapeutic resources, a considerable proportion of patients are still refractory to conventional treatment. Less than half of all patients achieve long-term remission, many require colectomy, and the disease still has a major impact on patients' lives. Moreover, recent data point to slightly raised mortality. While these outcomes could be partly improved by optimising current therapeutic strategies, they clearly highlight the need to develop new therapies. Currently, a number of promising and innovative therapeutic approaches are being explored, some of which will hopefully survive to reach the clinic. Until such a time arrives, it is important that a better understanding of the clinical particularities of the disease, an improved knowledge of the host-microbiome negative interactions and of the environmental factors beyond disease development is achieved to obtain the final and desired outcome: to provide better treatment and quality of life for patients with this disabling disease.
    No preview · Article · Nov 2013 · Gut
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    ABSTRACT: We aimed to identify the clinical and genetic [IL23 receptor (IL23R) single nucleotide polymorphisms (SNPs)] predictors of response to therapy in patients with ulcerative colitis. A total of 174 patients with ulcerative colitis, 99 women and 75 men, were included. The mean age of the patients was 47±15 years and the mean disease duration was 11±9 years. The number of patients classified as responders (R) or nonresponders (NR) to several therapies was as follows: 110 R and 53 NR to mesalazine (5-ASA), 28 R and 20 NR to azathioprine (AZT), 18 R and 7 NR to infliximab. Clinical and demographic variables were recorded. A total of four SNPs were studied: IL23R G1142A, C2370A, G43045A, and G9T. Genotyping was performed by real-time PCR using Taqman probes. Older patients were more prone to respond to 5-ASA (P=0.004), whereas those with pancolitis were less likely to respond to such therapies (P=0.002). Patients with extraintestinal manifestations (EIMs) were less likely to respond to 5-ASA (P=0.001), AZT (P=0.03), and corticosteroids (P=0.06). Carriers of the mutant allele for IL23R SNPs had a significantly higher probability of developing EIMs (P<0.05), a higher probability of being refractory to 5-ASA (P<0.03), but a higher likelihood of responding to AZT (P=0.05). A significant synergism was observed between IL23R C2370A and EIMs with respect to nonresponse to 5-ASA (P=0.03). Besides extent of disease and age at disease onset, the presence of EIMs may be a marker of refractoriness to 5-ASA, corticosteroids, and AZT. IL23R SNPs are associated both with EIMs and with nonresponse to 5-ASA and corticosteroids.
    No preview · Article · Oct 2013 · European journal of gastroenterology & hepatology


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Journal of Crohn s and Colitis 09/2015; DOI:10.1093/ecco-jcc/jjv153
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Revista de neurologia 12/2014; 59(12):537-542.
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