Budesonide for induction of remission in Crohn's disease

Guidelines for clinical practice are intended to suggest preferable approaches to particular medical problems as established by interpretation and collation of scientifi cally valid research, derived from extensive review of published literature. When data that will withstand objective scrutiny are not available, a recommendation may be made based on a consensus of experts. Guidelines are intended to apply to the clinical situation for all physicians without regard to specialty. Guidelines are intended to be fl exible, not necessarily indicating the only acceptable approach, and should be distinguished from standards of care that are infl exible and rarely violated. Given the wide range of choices in any health-care problem, the physician should select the course best suited to the individual patient and the clinical situation presented. These guidelines are developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee. Expert opinion is solicited from the outset for the document. The quality of evidence upon which a specifi c recommendation is based is as follows: Grade A: Homogeneous evidence from multiple well-designed randomized (therapeutic) or cohort (descriptive) controlled trials, each involving a number of participants to be of suffi cient statistical power. Grade B: Evidence from at least one large well-designed clinical trial with or without randomization, from cohort or case -control analytic studies, or well-designed meta-analysis. Grade C: Evidence based on clinical experience, descriptive studies, or reports of expert committees. The Committee reviews guidelines in depth, with participation from experienced clinicians and others in related fi elds. The fi nal recommendations are based on the data available at the time of the production of the document and may be updated with pertinent scientifi c developments at a later time.

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“…Controlled-release oral budesonide formulations at a dose of 9 mg daily have been demonstrated to be more e ective than placebo (114,115) …”

Section: Mild To Moderate Active Diseasementioning

confidence: 99%

Management of Crohn's Disease in Adults

2009

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“…Despite general agreement that treatment decisions for active Crohn's disease should be based on the site as well as the activity and behavior of the disease, the sample size is too small for statistically valid conclusions to be drawn from therapeutic trials when patients are stratified according to the site of disease [117] . For mildly active IBD, budesonide 9 mg/d is favored because it is superior to both placebo (OR = 2.85, 95%CI: 1.67-4.87) [118,119] and 5-ASA 4 g/d (OR = 2.8, 95%CI: 1.50-5.20) [120] , and it achieves remission in 51%-60% of individuals over 8-10 wk [119,[121][122][123] . Budesonide is preferred to prednisolone for mildly active CD because it is associated with fewer side effects, although a Cochrane systematic review has shown budesonide to be somewhat less effective than prednisolone (pooled OR for the five trials 0.69, 95%CI: 0.51-0.95) [119] .…”

Section: Filipovic Br Et Al Psychiatric Discomfort and Ibd Treatmentmentioning

confidence: 99%

“…For mildly active IBD, budesonide 9 mg/d is favored because it is superior to both placebo (OR = 2.85, 95%CI: 1.67-4.87) [118,119] and 5-ASA 4 g/d (OR = 2.8, 95%CI: 1.50-5.20) [120] , and it achieves remission in 51%-60% of individuals over 8-10 wk [119,[121][122][123] . Budesonide is preferred to prednisolone for mildly active CD because it is associated with fewer side effects, although a Cochrane systematic review has shown budesonide to be somewhat less effective than prednisolone (pooled OR for the five trials 0.69, 95%CI: 0.51-0.95) [119] . For corticosteroid-related adverse effects, budesonide showed no difference from the placebo (OR = 0.98, 95%CI: 0.58-1.67…”

Section: Filipovic Br Et Al Psychiatric Discomfort and Ibd Treatmentmentioning

confidence: 99%

Psychiatric comorbidity in the treatment of patients with inflammatory bowel disease

Filipović¹,

Filipović²

2014

WJG

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Ulcerative colitis and Crohn's disease, commonly known as inflammatory bowel disease (IBD), draw attention from specialists of various disorders, including gastroenterology, psychiatry, and radiology. The involvement of a cortical influence in the brain-gut axis as well as the interaction of the hypothalamic-pituitary-adrenal axis and the peripheral nervous system provide an initial explanation of the psychological symptoms associated with IBD. The involvement of structures the limbic system, such as the anterior cingulate cortex, the prefrontal cortex, and the amygdala, paves the way for the discovery of the mechanisms underlying depression depression, anxiety, alexithymia, personality traits, and other psychological impairments following the onset of IBD. Psychiatric therapy in IBD patients is almost as important as the gastroenterological approach and consists of pharmacological treatment and psychotherapy. Neither of the available psychiatric treatment methods is considered the golden standard because both methods have side effects, and psychotropic medication can provoke the worsening of IBD symptoms. Thus, both approaches must be applied with awareness of the possibility of side effects. We suggest that psychiatrists and gastroenterologists work together to reach a consensus on IBD therapy to ensure success and to reduce side effects and relapse to the lowest possible rates.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Inflammatory bowel disease; Psychiatry; Treatment; Personality traits; Depression; Anxiety Core tip: The involvement of a dysfunction of brain-gut interactions in the pathogenesis of inflammatory bowel disease (IBD) is represented by a dysfunction of the autonomic nervous system, an abnormal hypothalamicpituitary-adrenal axis and cholinergic anti-inflammatory pathway, a deleterious effect of stress and depression, an abnormal coupling of the prefrontal cortex-amygdaloid complex, and an abnormal relation between the microbiota and the brain as pro-inflammatory factors. New investigations have provided a critical link between forebrain changes and abdominal pain independent of active disease and drug treatment, providing a potential basis for an explanation of the psychological symptoms and brain influence in the pathogenesis of IBD.

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“…Budesonide in a dose of 9 mg/day has been indicated in terminal ileum and ileocecal CD with mild to moderate activity. Budesonide is rapidly metabolized in its passage through the liver, less effective in controlling inflammatory activity than prednisolone, and has fewer adverse effects because the slightest change in plasma cortisol (33) . The budesonide was compared to prednisolone in nine randomized trials (44) .…”

Section: Corticosteroidsmentioning

confidence: 99%