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1.
Clin Ther ; 38(6): 1342-1358.e6, 2016 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-27091732

RESUMEN

PURPOSE: To compare the benefits and harms of anti-tumor necrosis factor (TNF)-α and anti-integrin agents as induction and maintenance therapy in adult patients with Crohn's disease. METHODS: We searched MEDLINE and the Cochrane Central Register of Controlled Trials from inception through July 2015 for randomized clinical trials in patients with Crohn's disease who reported response or remission with anti-TNF-α or anti-integrin agents administered as induction and/or maintenance therapy. Data on the study population, interventions, outcome measures, adverse events, and study methods were extracted independently by 2 authors. FINDINGS: Among 2503 citations identified, 23 met the eligibility criteria. Random-effects model meta-analyses and network meta-analyses were performed. No statistically significant difference was observed between anti-TNF-α and anti-integrin agents with respect to induction and maintenance of response (odds ratio [OR] = 1.20 [95% CI, 0.73-1.96] from 14 trials and OR = 1.23 [95% CI, 0.50-3.03] from 8 trials, respectively) or remission (OR = 1.13 [95% CI, 0.72-1.76] from 17 trials and OR = 1.18 [95% CI, 0.55-2.50] from 9 trials, respectively). No difference was observed in the indirect comparison of trials that reported results on the subgroup of anti-TNF-α naive patients. The proportions of patients with adverse events, infections, and treatment discontinuations were similar between the agents. IMPLICATIONS: Our indirect treatment comparisons did not find a statistically significant difference between anti-TNF-α and anti-integrin agents for induction or maintenance therapy. In the absence of head-to-head comparisons, it remains unclear which patient is more likely to respond better to any of these agents.


Asunto(s)
Enfermedad de Crohn/tratamiento farmacológico , Integrinas/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Anticuerpos Monoclonales/uso terapéutico , Anticuerpos Monoclonales Humanizados/uso terapéutico , Humanos , Quimioterapia de Inducción , Quimioterapia de Mantención , Metaanálisis en Red
2.
World J Gastrointest Pathophysiol ; 6(4): 219-27, 2015 Nov 15.
Artículo en Inglés | MEDLINE | ID: mdl-26600980

RESUMEN

Ulcerative colitis (UC) is a chronic lifelong condition characterized by alternating flare-ups and remission. There is no single known unifying cause, and the pathogenesis is multifactorial, with genetics, environmental factors, microbiota, and the immune system all playing roles. Current treatment modalities for UC include 5-aminosalicylates, corticosteroids, immunosuppressants (including purine antimetabolites, cyclosporine, and tacrolimus), and surgery. Therapeutic goals for UC are evolving. Medical treatment aims to induce remission and prevent relapse of disease activity. Infliximab, an anti-tumor necrosis factor (TNF)-α monoclonal antibody, is the first biological agent for the treatment of UC. Over the last decade, infliximab and adalimumab (anti-TNF-α agents) have been used for moderate to severe UC, and have been shown to be effective in inducing and maintaining remission. Recent studies have indicated that golimumab (another anti-TNF-α agent), tofacitinib (a Janus kinase inhibitor), and vedolizumab and etrolizumab (integrin antagonists), achieved good clinical remission and response rates in UC. Recently, golimumab and vedolizumab have been approved for UC by the United States Food and Drug Administration. Vedolizumab may be used as a first-line alternative to anti-TNF-α therapy in patients with an inadequate response to corticosteroids and/or immunosuppressants. Here, we provide updated information on various biological agents in the treatment of UC.

3.
Gastroenterol Rep (Oxf) ; 3(2): 103-9, 2015 May.
Artículo en Inglés | MEDLINE | ID: mdl-25344680

RESUMEN

Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD) worldwide. Better understanding of the pathogenesis of UC has led to the development of novel therapeutic agents that target specific mediators of the inflammatory cascade. A number of biological agents have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of UC and several more are currently in various phases of drug development. The commonly used agents include TNFα antagonists (e.g. infliximab, adalimumab, and golimumab) and anti-integrin agents (vedolizumab). These biological agents have profoundly influenced the management of UC patients, especially those with refractory disease. This paper reviews the currently available knowledge and evidence for the use of various biological agents in the treatment of UC.

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