Oral Budesonide for Active Crohn's Disease

Gr, Greenberg; Bg, Feagan; Martin, François; Sutherland, L. R.; Ab, Thomson; Cn, Williams; Lg, Nilsson; Persson, Tore

doi:10.1056/nejm199409293311303

Cited by 511 publications

(186 citation statements)

References 18 publications

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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%

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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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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“…In the cells treated with free budesonide solution, we observed an immediate decrease of Il-8 production within the first 24 h of treatment. The effect did not last long, and the release rate rebounded and increased after the second day to fourth day, which fits with the in vivo dosing scheme of free budesonide that is renewed daily (Greenberg et al, 1994). Meanwhile, the PlGA-budesonide dispersion reduced the Il-8 release levels almost to the levels of the healthy control and maintained them throughout the experimental duration of 4 days (Fig.…”

Section: Discussionmentioning

confidence: 49%

“…the encapsulated drugs then are released upon the degradation of the nanocarrier in the desired areas (tabata et al, 1996). This passive targeting to the inflamed intestinal tissue using nanocarriers was successfully applied with different kinds of drugs (e.g., tacrolimus, rolipram, and 5-ASA) and different nanocarrier technologies by showing increased therapeutic efficacy and reduced adverse effects compared to free drug molecules (lamprecht et al, 2001c;Rutgeerts et al, 2009;Greenberg et al, 1994). Formulation development and testing in these studies was conducted in different rodent models of colitis based on the chemical induction of an acute inflammation by dextran sodium sulfate (DSS) or tri-nitrobenzene sulfonic acid (tNBS) (Hasani et al, 2009;lamprecht et al, 2001b).…”

Section: Introductionmentioning

confidence: 99%

Screening of budesonide nanoformulations for treatment of inflammatory bowel disease in an inflamed 3D cell-culture model

Leonard

Ali²,

Collnot

et al. 2012

ALTEX

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Summary Drug formulation screenings for treatment of inflammatory bowel disease (IBD) are mostly conducted in chemically induced rodent models that represent acute injury-caused inflammation instead of a chronic condition. To accurately screen drug formulations for chronic IBD, a relevant model that mimics the chronic condition in vitro is urgently needed. In an effort to reduce and potentially replace this scientifically and ethically questionable animal testing for IBD drugs, our laboratory has developed an in vitro model for the inflamed intestinal mucosa observed in chronic IBD, which allows high-throughput screening of anti-inflammatory drugs and their formulations. The in vitro model consists of intestinal epithelial cells, human blood-derived macrophages, and dendritic cells that are stimulated by the inflammatory cytokine interleukin-1β. In this study, the model was utilized for evaluation of the efficacy and deposition of budesonide, an anti-inflammatory drug, in three different pharmaceutical formulations: (1) a free drug solution, (2) encapsulated into PLGA nanoparticles, and (3) encapsulated into liposomes. The in vitro model of the inflamed intestinal mucosa demonstrated its ability to differentiate therapeutic efficacy among the formulations while maintaining the convenience of conventional in vitro studies and adequately representing the complex pathophysiological changes observed in vivo.

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“…When given in an oral controlled ileal release (CR) formulation to patients with active ileocaecal CD, budesonide was not significantly less effective than prednisolone in inducing remission in one study [14] and substantially better than placebo in another [15] . Side-effects were much fewer in patients given budesonide CR than prednisolone, as was adrenal suppression assessed by measurement of plasma cortisol levels [14] .…”

Section: New Formulations and Applications Of Existing Drugsmentioning

confidence: 99%

New treatments for inflammatory bowel disease

S¹

1998

WJG

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Oral Budesonide for Active Crohn's Disease

Abstract: In an eight-week trial, an oral controlled-release preparation of budesonide at an optimal daily dose of 9 mg was well tolerated and effective against active Crohn's disease of the ileum and proximal colon.

Cited by 511 publications

References 18 publications

Psychiatric comorbidity in the treatment of patients with inflammatory bowel disease

Psychiatric comorbidity in the treatment of patients with inflammatory bowel disease

Screening of budesonide nanoformulations for treatment of inflammatory bowel disease in an inflamed 3D cell-culture model

New treatments for inflammatory bowel disease

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