FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2255357183> ?p ?o ?g. }

• W2255357183 endingPage "987" @default.
• W2255357183 startingPage "940" @default.
• W2255357183 abstract "See CME Quiz on page 932.The disorders collectively known as inflammatory bowel disease (IBD) include Crohn's disease (CD) and ulcerative colitis (UC). CD, initially credited as having been described in 1932 by Drs Burrill Crohn, Gordon Oppenheimer, and Leon Ginzburg,1Crohn B. Ginzburg L. Oppenheimer G.R. Regional ileitis A pathologic and clinical entity.JAMA. 1932; 99: 1323-1329Crossref Google Scholar is an idiopathic transmural chronic inflammatory disorder affecting the gastrointestinal tract. UC, on the other hand, is credited to have been described by Drs Wilks and Moxon in 1875.2Wilks S, Moxon W. Lectures on pathological anatomy. 2nd ed. Philadelphia, PA: Lindsay and Blakiston, 1875.Google ScholarThese disorders spare no socioeconomic class, age, sex, or country of origin. These disorders are relatively common in the United States, accounting for disease in approximately 1 million individuals, with similar numbers in Europe. These complex disorders may have varied presentations and complications that ensue during their course, as has been evidenced by wide variations in clinical practice. This position statement reviews the evidence-based medicine and current practice patterns for the treatment of IBD in adults with 3 classes of drugs: corticosteroids, immunomodulators, and infliximab. The intent of this position statement is to bring consistency to patient care, but this should not necessarily be viewed as the standard of care for all patients. Individual care of patients should be managed on the basis of all clinical data available for that particular case. Patient preferences should be sought in an effort to make decisions in a partnership between patients and health care professionals.Development of Position StatementAn exhaustive review of the literature was performed using electronic databases (MEDLINE, PubMed, and Ovid; key words included “inflammatory bowel disease,” “ulcerative colitis,” and “Crohn's disease”). Standard textbooks with chapters on inflammatory bowel disease were evaluated, and the reference lists were also compiled for all articles to obtain references before a preliminary document was drafted. The preliminary draft was then reviewed by the Clinical Practice and Economics Committee of the American Gastroenterological Association.Grading of RecommendationsThis position statement conforms to the American Gastroenterological Association guidelines for evidence-based position statement development. The grading of each recommendation is dependent on the category of evidence supporting it.The quality of evidence on which a 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 sufficient statistical power.Grade B: Evidence from at least 1 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.General Principles of Medical Therapy for IBDThe treatment of patients with CD and UC is dependent on several distinct factors, including disease location (eg, ileocecal vs colonic or proctitis vs pancolitis), severity (mild, moderate, or severe), and complications. The treatment of patients should be individualized based on the patient's prior symptomatic response and tolerance to specific medical therapies. Therapy is sequential to treat acute disease and then to maintain remission. Surgery is appropriate for obstructing stenoses, cancerous or precancerous lesions, suppurative complications, or medically refractory disease. The use of narcotic analgesics should be avoided except for the treatment of patients in the perioperative setting, given the potential for tolerance and abuse in the setting of chronic disease.Medications Used for the Treatment of Patients With IBDThe current status of therapy for IBD is rapidly evolving, with many new biologic agents under investigation. In the forthcoming sections, the data that support the use of immunomodulators in IBD are reviewed. The use of corticosteroids, azathioprine (AZA), 6-mercaptopurine (6-MP), methotrexate, mycophenolate mofetil (MMF), cyclosporine, tacrolimus, and infliximab in particular are reviewed in both UC and CD. Aminosalicylates and antibiotics are not discussed.CorticosteroidsCorticosteroids include parenteral, oral, and topical agents. Examples of oral corticosteroids include prednisolone, prednisone, and budesonide, whereas parenteral agents include intravenous (IV) hydrocortisone, adrenocorticotropic hormone, and methylprednisolone. Corticosteroids, when used orally or parenterally, are potent anti-inflammatory agents for the acute treatment of patients with moderate to severe relapses of IBD. Budesonide (Entocort; AstraZeneca Pharmaceuticals, Wayne, PA) is a highly potent corticosteroid with limited systemic bioavailability due to extensive first-pass hepatic metabolism. Enteric preparations with distal small intestinal and proximal colonic release can produce therapeutic benefit with reduced systemic toxicity in ileocecal CD. Topical agents in the form of suppositories or foam have been used to treat patients with proctitis, whereas enemas are effective in patients with disease up to the splenic flexure. The mechanism of action of corticosteroids is not discussed here in detail given recent reviews of these data.3Amsterdam A. Tajima K. Sasson R. Cell-specific regulation of apoptosis by glucocorticoids: implication to their anti-inflammatory action.Biochem Pharmacol. 2002; 64: 843-850Crossref PubMed Scopus (105) Google Scholar, 4Clark A.R. Lasa M. Crosstalk between glucocorticoids and mitogen-activated protein kinase signaling pathways.Curr Opin Pharmacol. 2003; 3: 404-411Crossref PubMed Scopus (76) Google Scholar, 5Kagoshima M. Ito K. Cosio B. Adcock I.M. Glucocorticoid suppression of nuclear factor-kappa B: a role for histone modifications.Biochem Soc Trans. 2003; 31: 60-65Crossref PubMed Google Scholar, 6De Bosscher K. Vanden Berghe W. Haegeman G. The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression.Endocr Rev. 2003; 24: 488-522Crossref PubMed Scopus (493) Google Scholar, 7Hayashi R. Wada H. Ito K. Adcock I.M. Effects of glucocorticoids on gene transcription.Eur J Pharmacol. 2004; 500: 51-62Crossref PubMed Scopus (147) Google Scholar, 8Goulding N.J. The molecular complexity of glucocorticoid actions in inflammation—a four-ring circus.Curr Opin Pharmacol. 2004; 4: 629-636Crossref PubMed Scopus (65) Google Scholar, 9Buttgereit F. Saag K.G. Cutolo M. da Silva J.A. Bijlsma J.W. The molecular basis for the effectiveness, toxicity, and resistance to glucocorticoids: focus on the treatment of rheumatoid arthritis.Scand J Rheumatol. 2005; 34: 14-21Crossref PubMed Scopus (75) Google Scholar The use of corticosteroids in patients with IBD is intended to reduce inflammatory mediators through binding of the glucocorticoid receptor expressed by immune cells. Binding of glucocorticoids to their receptors results in the trans-repression of proinflammatory transcription factors such as nuclear factor κB and apoptosis of target inflammatory cells and activated lymphocytes.10Scheinman R.I. Cogswell P.C. Lofquist A.K. Baldwin Jr, A.S. Role of transcriptional activation of I kappa B alpha in mediation of immunosuppression by glucocorticoids.Science. 1995; 270: 283-286Crossref PubMed Google Scholar, 11Tao Y. Williams-Skipp C. Scheinman R.I. Mapping of glucocorticoid receptor DNA binding domain surfaces contributing to transrepression of NF-kappa B and induction of apoptosis.J Biol Chem. 2001; 276: 2329-2332Crossref PubMed Scopus (70) Google Scholar Choice of corticosteroid should be based on which has the greatest glucocorticoid activity compared with its mineralocorticoid activity.Mild to moderate IBDThe use of conventional corticosteroids such as prednisone is generally reserved for patients with moderate to severe disease. An exception would be patients who have failed to respond to first-line therapies for IBD such as mesalamine for UC or antibiotics for CD in whom corticosteroids are used because of the absence of effective, less toxic medications. Controlled ileal release (CIR) budesonide (Entocort) is indicated for the treatment of patients with mild to moderate ileal and right-sided colonic CD. Enteric-coated budesonide has not been shown to be more effective than placebo in patients with distal UC.12Lofberg R. Danielsson A. Suhr O. Suhr O. Nilsson A. Schioler R. Nyberg A. Hultcrantz R. Kollberg B. Gillberg R. Willen R. Persson T. Salde L. Oral budesonide versus prednisolone in patients with active extensive and left-sided ulcerative colitis.Gastroenterology. 1996; 110: 1713-1718Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar Indeed, even patients with CD who have distal colon or rectal involvement respond less well to enteric-coated budesonide than to conventional prednisone (remission, 47% vs 62.5%), suggesting this therapy is most efficacious in those with ileal and right-sided colonic involvement.13Bar-Meir S. Chowers Y. Lavy A. Lavy A. Abramovitch D. Sternberg A. Leichtmann G. Reshef R. Odes S. Moshkovitz M. Bruck R. Eliakim R. Maoz E. Mittmann U. Budesonide versus prednisone in the treatment of active Crohn's disease The Israeli Budesonide Study Group.Gastroenterology. 1998; 115: 835-840Abstract Full Text Full Text PDF PubMed Scopus (153) Google ScholarBudesonide is a topically active glucocorticoid structurally related to 16-hydroxyprednisolone.14Dahlberg E. Thalen A. Brattsand R. Brattsand R. Gustafsson J.A. Johansson U. Roempke K. Saartok T. Correlation between chemical structure, receptor binding, and biological activity of some novel, highly active, 16 alpha, 17 alpha-acetal-substituted glucocorticoids.Mol Pharmacol. 1984; 25: 70-78PubMed Google Scholar, 15Spencer C.M. McTavish D. Budesonide A review of its pharmacological properties and therapeutic efficacy in inflammatory bowel disease.Drugs. 1995; 50: 854-872Crossref PubMed Google Scholar Budesonide has a very high affinity for the glucocorticoid receptor (15 times that of prednisolone and 195 times that of hydrocortisone). The majority of the drug is converted by the cytochrome P-450 system in the liver to inactive metabolites, with only 10%–15% of the drug reaching the systemic circulation. The current preparation of budesonide (Entocort) available in the United States is formulated to allow the slow release of the drug, mainly in the ileum and the right side of the colon.16Miller-Larsson A. Gustafson B. Persson C.G. Brattsand R. Gut mucosal uptake and retention characteristics contribute to the high intestinal selectivity of budesonide compared with prednisolone in the rat.Aliment Pharmacol Ther. 2001; 15: 2019-2025Crossref PubMed Scopus (8) Google Scholar, 17Edsbacker S. Bengtsson B. Larsson P. Larsson P. Lundin P. Nilsson A. Ulmius J. Wollmer P. A pharmacoscintigraphic evaluation of oral budesonide given as controlled-release (Entocort) capsules.Aliment Pharmacol Ther. 2003; 17: 525-536Crossref PubMed Scopus (45) Google Scholar, 18Lundin P.D. Edsbacker S. Bergstrand M. Bergstrand M. Ejderhamn J. Linander H. Hogberg L. Persson T. Escher J.C. Lindquist B. Pharmacokinetics of budesonide controlled ileal release capsules in children and adults with active Crohn's disease.Aliment Pharmacol Ther. 2003; 17: 85-92Crossref PubMed Scopus (30) Google Scholar The Entocort capsule contains microcapsules made of an inner sugar core surrounded by budesonide in ethylcellulose and an outer acrylic-based resin coating (Eudragit; Rohm America, Piscataway, NJ) that dissolves at a pH of ≥5.5. Fifty-two percent to 70% of the CIR budesonide formulation is absorbed in the ileocolonic region, with a mean absorption time of 6.4 hours and a systemic bioavailability of 9% in healthy volunteers. The improved toxicity profile (discussed in the following text) of this agent compared with conventional corticosteroids relates to its low systemic bioavailability.Level A evidence supports the use of CIR budesonide for induction of remission of ileocolonic CD. First, CIR budesonide at a dosage of 9 mg/day is more effective than placebo at inducing remission (51% vs 20%) at 8 weeks (Table 1).19Greenberg G.R. Feagan B.G. Martin F. Martin F. Sutherland L.R. Thomson A.B. Williams C.N. Nilsson L.G. Persson T. Oral budesonide for active Crohn's disease Canadian Inflammatory Bowel Disease Study Group.N Engl J Med. 1994; 331: 836-841Crossref PubMed Scopus (420) Google Scholar CIR budesonide at a dosage of 9 mg/day is also more effective than mesalamine (Pentasa; Shire Pharmaceuticals, Wayne, PA) at a dosage of 4 g/day (69% vs 45% at 8 weeks).20Thomsen O.O. Cortot A. Jewel D. Wright J.P. Winter T. Veloso F.T. Vatn M. Persson T. Pettersson E. A comparison of budesonide and mesalamine for active Crohn's disease International Budesonide-Mesalamine Study Group.N Engl J Med. 1998; 339: 370-374Crossref PubMed Scopus (233) Google Scholar The time to onset of action with CIR budesonide is approximately 2 weeks. Trials comparing oral budesonide with prednisolone show comparable efficacy for inducing remission in active CD.13Bar-Meir S. Chowers Y. Lavy A. Lavy A. Abramovitch D. Sternberg A. Leichtmann G. Reshef R. Odes S. Moshkovitz M. Bruck R. Eliakim R. Maoz E. Mittmann U. Budesonide versus prednisone in the treatment of active Crohn's disease The Israeli Budesonide Study Group.Gastroenterology. 1998; 115: 835-840Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar, 21Rutgeerts P. Lofberg R. Malchow H. Lamers C. Olaison G. Jewell D. Danielsson A. Goebell H. Thomsen O.O. Lorenz-Meyer H. Hodgson H. Persson T. Seidegard C. A comparison of budesonide with prednisolone for active Crohn's disease.N Engl J Med. 1994; 331: 842-845Crossref PubMed Scopus (451) Google Scholar, 22Gross V. Andus T. Caesar I. Bischoff S.C. Lochs H. Tromm A. Schulz H.J. Bar U. Weber A. Gierend M. Ewe K. Scholmerich J. Oral pH-modified release budesonide versus 6-methylprednisolone in active Crohn's disease German/Austrian Budesonide Study Group.Eur J Gastroenterol Hepatol. 1996; 8: 905-909PubMed Google Scholar, 23Campieri M. Ferguson A. Doe W. Persson T. Nilsson L.G. Oral budesonide is as effective as oral prednisolone in active Crohn's disease The Global Budesonide Study Group.Gut. 1997; 41: 209-214Crossref PubMed Google Scholar In a meta-analysis comparing CIR budesonide with prednisolone, patients with moderate to severe disease (Crohn's Disease Activity Index [CDAI] scores >300) were less likely to respond to CIR budesonide.24Kane S.V. Schoenfeld P. Sandborn W.J. Tremaine W. Hofer T. Feagan B.G. The effectiveness of budesonide therapy for Crohn's disease.Aliment Pharmacol Ther. 2002; 16: 1509-1517Crossref PubMed Scopus (85) Google Scholar Because the side effect profile is superior to that of conventional corticosteroids (discussed in the following text), CIR budesonide may be considered first-line therapy for patients with mild to moderate ileal and right-sided colonic disease.Table 1Short-term Efficacy of Corticosteroids in IBDType of IBDnInterventions testedResponse/remissionPeriod of studyP valueReferencesMild to moderate active IBD CD (ileocecal)67Bud 3 mg dailyRemission33%8 wk<.001 (9 mg vs placebo)Greenberg et al, 199419Greenberg G.R. Feagan B.G. Martin F. Martin F. Sutherland L.R. Thomson A.B. Williams C.N. Nilsson L.G. Persson T. Oral budesonide for active Crohn's disease Canadian Inflammatory Bowel Disease Study Group.N Engl J Med. 1994; 331: 836-841Crossref PubMed Scopus (420) Google Scholar61Bud 9 mg daily51%64Bud 15 mg daily43%66Placebo20% CD (ileocecal)80Bud 9 mg dailyRemission48%8 wk<.05 (Bud groups vs placebo)Tremaine et al, 2002313Tremaine W.J. Hanauer S.B. Katz S. Winston B.D. Levine J.G. Persson T. Persson A. Budesonide CIR United States Study GroupBudesonide CIR capsules (once or twice daily divided-dose) in active Crohn's disease: a randomized placebo-controlled study in the United States.Am J Gastroenterol. 2002; 97: 1748-1754Crossref PubMed Google Scholar79Bud 4.5 mg BID53%41Placebo33% CD (ileocecal)91Bud 9 mg dailyRemission69%16 wk (primary end point, 8 wk).001Thomsen et al, 199820Thomsen O.O. Cortot A. Jewel D. Wright J.P. Winter T. Veloso F.T. Vatn M. Persson T. Pettersson E. A comparison of budesonide and mesalamine for active Crohn's disease International Budesonide-Mesalamine Study Group.N Engl J Med. 1998; 339: 370-374Crossref PubMed Scopus (233) Google Scholar83Mesalamine 2 g BID45% CD (ileocecal)88Bud 9 mg dailyRemission52%8 wkNSRutgeerts et al, 199421Rutgeerts P. Lofberg R. Malchow H. Lamers C. Olaison G. Jewell D. Danielsson A. Goebell H. Thomsen O.O. Lorenz-Meyer H. Hodgson H. Persson T. Seidegard C. A comparison of budesonide with prednisolone for active Crohn's disease.N Engl J Med. 1994; 331: 842-845Crossref PubMed Scopus (451) Google Scholar88Prednisolone 40 mg daily then tapered65% CD (ileocecal)58Bud 9 mg dailyRemission60%8 wkNSCampieri et al, 199723Campieri M. Ferguson A. Doe W. Persson T. Nilsson L.G. Oral budesonide is as effective as oral prednisolone in active Crohn's disease The Global Budesonide Study Group.Gut. 1997; 41: 209-214Crossref PubMed Google Scholar61Bud 4.5 mg BID42%58Prednisolone 40 mg daily then tapered60% CD (ileocecal)34Bud 3 mg TIDRemission56%8 wkNSGross et al, 199622Gross V. Andus T. Caesar I. Bischoff S.C. Lochs H. Tromm A. Schulz H.J. Bar U. Weber A. Gierend M. Ewe K. Scholmerich J. Oral pH-modified release budesonide versus 6-methylprednisolone in active Crohn's disease German/Austrian Budesonide Study Group.Eur J Gastroenterol Hepatol. 1996; 8: 905-909PubMed Google Scholar33Prednisolone 48 mg daily then tapered72.7% CD (ileocecal)100Bud 3 mg TIDRemission51%8 wkNSBar-Meir et al, 199813Bar-Meir S. Chowers Y. Lavy A. Lavy A. Abramovitch D. Sternberg A. Leichtmann G. Reshef R. Odes S. Moshkovitz M. Bruck R. Eliakim R. Maoz E. Mittmann U. Budesonide versus prednisone in the treatment of active Crohn's disease The Israeli Budesonide Study Group.Gastroenterology. 1998; 115: 835-840Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar101Prednisone 40 mg daily then tapered52.5%Moderate to severe CD85Prednisone 0.5–0.75 mg · kg−1 · day−1Remission60%17 wk.0001 (prednisone vs placebo)Summers et al (NCCDS), 197936Summers R.W. Switz D.M. Sessions Jr, J.T. Becktel J.M. Best W.R. Kern Jr, F. Singleton J.W. National Cooperative Crohn's Disease Study: results of drug treatment.Gastroenterology. 1979; 77: 847-869PubMed Google Scholar77Placebo30%59AZA 2.5 mg/kg40%74Sulfasalazine 1 g/15 kg43% CD47Methylprednisolone 48 mg/day (tapered by 8 mg/wk)Remission83%18 wk<.001 for prednisolone, <.05 for sulfasalazine, <.001 for combination compared with placeboMalchow et al (ECCDS), 198437Malchow H. Ewe K. Brandes J.W. Goebell H. Ehms H. Sommer H. Jesdinsky H. European Cooperative Crohn's Disease Study (ECCDS): results of drug treatment.Gastroenterology. 1984; 86: 249-266Abstract Full Text PDF PubMed Google Scholar54Sulfasalazine 3 g/day50%56Methylprednisolone + 3 g/day Sulfasalazine78%58 (active disease group)Placebo38% CDaCorticosteroid dosing was prednisolone 1 mg/kg body wt per day, reduced within weeks to a maintenance dose of 10–15 mg and kept at that level for 3–5 months.109Population-based Prednisolone 1 mg · kg−1 · day−1Complete remission, 48%Partial response, 32%No response, 20% 30 daysN/AMunkholm et al, 199441Munkholm P. Langholz E. Davidsen M. Binder V. Frequency of glucocorticoid resistance and dependency in Crohn's disease.Gut. 1994; 35: 360-362Crossref PubMed Google Scholar CDbThe initial dosages of prednisone ranged from 40 to 60 mg/day, and individual treating physicians attempted prednisone taper over a variable period of 3–6 months. Short-term 30-day responses for both studies were defined as follows. Complete remission: total regression of clinical symptoms declining to ≤2 bowel movements/day; no blood, pus, or mucus in feces; no abdominal pain, fever, weight loss, and extraintestinal symptoms. Partial remission: regression of clinical symptoms declining to ≤4 stools/day; blood, pus, mucus in feces; or abdominal pain or all 4 less than daily and no systemic symptoms as fever and weight loss. No response: no regression of clinical symptoms.173Population-based Prednisone 40–60 mg/dayComplete remission, 58%Partial response, 26%No response, 16%30 daysN/AFaubion et al, 200140Faubion Jr, W.A. Loftus Jr, E.V. Harmsen W.S. Zinsmeister A.R. Sandborn W.J. The natural history of corticosteroid therapy for inflammatory bowel disease: a population-based study.Gastroenterology. 2001; 121: 255-260Abstract Full Text Full Text PDF PubMed Google Scholar UCcFor UC studies by Truelove et al, remission was defined as 1–2 stools/day, no blood, no fever, no tachycardia, hemoglobin normal or returning toward normal, erythrocyte sedimentation rate normal or returning toward normal, and gaining weight. Partial remission was defined as intermediate between remission and no response.109Cortisone 100 mg/dayRemission, 41.3%Partial response, 27.5% 6 wk<.001Truelove and Witts, 1954, 195542Truelove S.C. Witts L.J. Cortisone in ulcerative colitis; preliminary report on a therapeutic trial.Br Med J. 1954; 4884: 375-378Crossref Google Scholar, 43Truelove S.C. Witts L.J. Cortisone in ulcerative colitis; final report on a therapeutic trial.Br Med J. 1955; 4947: 1041-1048Crossref Google Scholar101PlaceboRemission, 15.8%Partial response, 24.8% UCcFor UC studies by Truelove et al, remission was defined as 1–2 stools/day, no blood, no fever, no tachycardia, hemoglobin normal or returning toward normal, erythrocyte sedimentation rate normal or returning toward normal, and gaining weight. Partial remission was defined as intermediate between remission and no response.58Prednisolone 5 mg 4 times daily + hydrocortisone enema 100 mgRemission76%2 wk<.05Truelove et al, 196244Truelove S.C. Watkinson G. Draper G. Comparison of corticosteroid and sulphasalazine therapy in ulcerative colitis.Br Med J. 1962; 5321: 1708-1711Crossref Google Scholar60Sulfasalazine 2 g 4 times daily for first wk, 1 g 4 times daily second wk52% UC20Prednisone 60 mgRemission, 13/20 (65%)Partial response, 6/20 (30%) 5 wk<.01 for 2 higher doses compared with 20 mg/dayBaron et al, 196266Baron J.H. Connell A.M. Kanaghinis T.G. Lennard-Jones J.E. Jones A.F. Out-patient treatment of ulcerative colitis Comparison between three doses of oral prednisone.Br Med J. 1962; 5302: 441-443Crossref Google Scholar20Prednisone 40 mgRemission, 13/20 (65%)Partial response, 1/20 (5%) 20Prednisone 20 mg (all doses divided TID or 4 times daily)Remission, 6/20 (30%)Partial response, 3/20 (15%) UCbThe initial dosages of prednisone ranged from 40 to 60 mg/day, and individual treating physicians attempted prednisone taper over a variable period of 3–6 months. Short-term 30-day responses for both studies were defined as follows. Complete remission: total regression of clinical symptoms declining to ≤2 bowel movements/day; no blood, pus, or mucus in feces; no abdominal pain, fever, weight loss, and extraintestinal symptoms. Partial remission: regression of clinical symptoms declining to ≤4 stools/day; blood, pus, mucus in feces; or abdominal pain or all 4 less than daily and no systemic symptoms as fever and weight loss. No response: no regression of clinical symptoms.185Population-based Prednisone 40–60 mg/dayComplete remission, 54%Partial response, 30%No response, 16% 30 daysN/AFaubion et al, 200140Faubion Jr, W.A. Loftus Jr, E.V. Harmsen W.S. Zinsmeister A.R. Sandborn W.J. The natural history of corticosteroid therapy for inflammatory bowel disease: a population-based study.Gastroenterology. 2001; 121: 255-260Abstract Full Text Full Text PDF PubMed Google ScholarSevere UCcFor UC studies by Truelove et al, remission was defined as 1–2 stools/day, no blood, no fever, no tachycardia, hemoglobin normal or returning toward normal, erythrocyte sedimentation rate normal or returning toward normal, and gaining weight. Partial remission was defined as intermediate between remission and no response.149Prednisolone 60 mg/day IV + hydrocortisone 100 mg rectallyRemission, 64%Partial response, 13%No response, 23% 5 daysN/ATruelove et al, 1974, 197846Truelove S.C. Willoughby C.P. Lee E.G. Kettlewell M.G. Further experience in the treatment of severe attacks of ulcerative colitis.Lancet. 1978; 2: 1086-1088Abstract PubMed Scopus (170) Google Scholar, 47Truelove S.C. Jewell D.P. Intensive intravenous regimen for severe attacks of ulcerative colitis.Lancet. 1974; 1: 1067-1070Abstract PubMed Scopus (295) Google Scholar UCdTherapeutic success was defined as the absence of all symptoms and the reduction of the frequency of bowel movements to <2 per day. All other cases were classified as therapeutic failures. Also, if after the fourth day of treatment there was continuous fever of ≥37.5°C or colonic dilation on radiography, the study period was terminated early and the study treatment recorded as a failure.32Corticotropin (ACTH) 120 U/dayOverall remission 42%10 days.025Meyers et al, 198348Meyers S. Sachar D.B. Goldberg J.D. Janowitz H.D. Corticotropin versus hydrocortisone in the intravenous treatment of ulcerative colitis A prospective, randomized, double-blind clinical trial.Gastroenterology. 1983; 85: 351-357PubMed Google Scholar34Hydrocortisone 300 mg/day IVNo prior corticosteroids:ACTH, 63%Hydrocortisone, 28%Prior corticosteroids:ACTH, 25%Hydrocortisone, 53% .05 CD44ACTH 120 U/day IVACTH, 82%10 daysNSChun et al, 199853Chun A. Chadi R.M. Korelitz B.I. Colonna T. Felder J.B. Jackson M.H. Morgenstern E.H. Rubin S.D. Sacknoff A.G. Gleim G.M. Intravenous corticotrophin vs. hydrocortisone in the treatment of hospitalized patients with Crohn's disease: a randomized double-blind study and follow-up.Inflamm Bowel Dis. 1998; 4: 177-181Crossref PubMed Google Scholar44Hydrocortisone 300 mg/day IVHydrocortisone, 93%NOTE. Unless otherwise stated, remission for CD is defined as a CDAI score <150 and response is defined as a decrease in CDAI of >70 points.Bud, budesonide; BID, twice daily; TID, 3 times daily.a Corticosteroid dosing was prednisolone 1 mg/kg body wt per day, reduced within weeks to a maintenance dose of 10–15 mg and kept at that level for 3–5 months.b The initial dosages of prednisone ranged from 40 to 60 mg/day, and individual treating physicians attempted prednisone taper over a variable period of 3–6 months. Short-term 30-day responses for both studies were defined as follows. Complete remission: total regression of clinical symptoms declining to ≤2 bowel movements/day; no blood, pus, or mucus in feces; no abdominal pain, fever, weight loss, and extraintestinal symptoms. Partial remission: regression of clinical symptoms declining to ≤4 stools/day; blood, pus, mucus in feces; or abdominal pain or all 4 less than daily and no systemic symptoms as fever and weight loss. No response: no regression of clinical symptoms.c For UC studies by Truelove et al, remission was defined as 1–2 stools/day, no blood, no fever, no tachycardia, hemoglobin normal or returning toward normal, erythrocyte sedimentation rate normal or returning toward normal, and gaining weight. Partial remission was defined as intermediate between remission and no response.d Therapeutic success was defined as the absence of all symptoms and the reduction of the frequency of bowel movements to <2 per day. All other cases were classified as therapeutic failures. Also, if after the fourth day of treatment there was continuous fever of ≥37.5°C or colonic dilation on radiography, the study period was terminated early and the study treatment recorded as a failure. Open table in a new tab Topical therapy with either conventional corticosteroids or budesonide is effective for distal colonic inflammation. In 2 meta-analyses, topical corticosteroids were found to be less effective than topical mesalamine for inducing remission of distal UC.25Marshall J.K. Irvine E.J. Rectal corticosteroids versus alternative treatments in ulcerative colitis: a meta-analysis.Gut. 1997; 40: 775-781Crossref PubMed Google Scholar, 26Cohen R.D. Woseth D.M. Thisted R.A. Hanauer S.B. A meta-analysis and overview of the literature on treatment options for left-sided ulcerative colitis and ulcerative proctitis.Am J Gastroenterol. 2000; 95: 1263-1276Crossref PubMed Google Scholar In placebo-controlled trials, mesalamine enemas achieve remission rates between 60% and 70% at dosages between 1 and 4 g/day at 4 weeks of treatment. By contrast, 4-week remission data for corticosteroid enema preparations range between 30% and 40%.26Cohen R.D. Woseth D.M. Thisted R.A. Hanauer S.B. A meta-analysis and overview of the literature on treatment options for left-sided ulcerative colitis and ulcerative proctitis.Am J Gastroenterol. 2000; 95: 1263-1276Crossref PubMed Google Scholar However, the combination of topical corticosteroids with topical mesalamine is often more efficacious than either alone in the short-term treatment of patients with distal UC.27Mulder C.J. Fockens P. Meijer J.W. van der Heide H. Wiltink E.H. Tytgat G.N. Beclomethasone dipropionate (3 mg) versus 5-aminosalicylic acid (2 g) versus the combination of both (3 mg/2 g) as retention enemas in active ulcerative proctitis.Eur J Gastroenterol Hepatol. 1996; 8: 549-553Crossref PubMed Google Scholar Foam preparations are often better tolerated by patients and may be easier to retain.28Somerville K.W. Langman M.J. Kane S.P. MacGilchrist A.J. Watkinson G. Salmon P. Effect of treatment on symptoms and quality of life in patients with ulcerative colitis: comparative trial of hydrocortisone acetate" @default.
• W2255357183 created "2016-06-24" @default.
• W2255357183 creator A5023182644 @default.
• W2255357183 creator A5044524314 @default.
• W2255357183 creator A5060840103 @default.
• W2255357183 creator A5081463259 @default.
• W2255357183 date "2006-03-01" @default.
• W2255357183 modified "2023-10-14" @default.
• W2255357183 title "American Gastroenterological Association Institute Technical Review on Corticosteroids, Immunomodulators, and Infliximab in Inflammatory Bowel Disease" @default.
• W2255357183 cites W126860265 @default.
• W2255357183 cites W1553613620 @default.
• W2255357183 cites W1574138851 @default.
• W2255357183 cites W1593679868 @default.
• W2255357183 cites W1613868394 @default.
• W2255357183 cites W1717444875 @default.
• W2255357183 cites W1748466511 @default.
• W2255357183 cites W1752248076 @default.
• W2255357183 cites W1761355724 @default.
• W2255357183 cites W18063648 @default.
• W2255357183 cites W1851622679 @default.
• W2255357183 cites W1876519312 @default.
• W2255357183 cites W1948846488 @default.
• W2255357183 cites W1961133398 @default.
• W2255357183 cites W1965566622 @default.
• W2255357183 cites W1966445767 @default.
• W2255357183 cites W1967356756 @default.
• W2255357183 cites W1967435782 @default.
• W2255357183 cites W1967490229 @default.
• W2255357183 cites W1967587114 @default.
• W2255357183 cites W1967745415 @default.
• W2255357183 cites W1968115398 @default.
• W2255357183 cites W1969971113 @default.
• W2255357183 cites W1970895990 @default.
• W2255357183 cites W1971012473 @default.
• W2255357183 cites W1971685694 @default.
• W2255357183 cites W1972837466 @default.
• W2255357183 cites W1974104914 @default.
• W2255357183 cites W1974631406 @default.
• W2255357183 cites W1974868609 @default.
• W2255357183 cites W1975192137 @default.
• W2255357183 cites W1976546496 @default.
• W2255357183 cites W1976676963 @default.
• W2255357183 cites W1976789706 @default.
• W2255357183 cites W1977757507 @default.
• W2255357183 cites W1978145728 @default.
• W2255357183 cites W1978270674 @default.
• W2255357183 cites W1978489871 @default.
• W2255357183 cites W1978993934 @default.
• W2255357183 cites W1979236956 @default.
• W2255357183 cites W1980212383 @default.
• W2255357183 cites W1980752381 @default.
• W2255357183 cites W1982828640 @default.
• W2255357183 cites W1983176706 @default.
• W2255357183 cites W1983306049 @default.
• W2255357183 cites W1984754431 @default.
• W2255357183 cites W1985502244 @default.
• W2255357183 cites W1987651998 @default.
• W2255357183 cites W1987925515 @default.
• W2255357183 cites W1989304148 @default.
• W2255357183 cites W1990322954 @default.
• W2255357183 cites W1992650609 @default.
• W2255357183 cites W1995044162 @default.
• W2255357183 cites W1995055794 @default.
• W2255357183 cites W1996166904 @default.
• W2255357183 cites W1997291566 @default.
• W2255357183 cites W1997800388 @default.
• W2255357183 cites W1997999969 @default.
• W2255357183 cites W2000138652 @default.
• W2255357183 cites W2000658018 @default.
• W2255357183 cites W2000707836 @default.
• W2255357183 cites W2001525276 @default.
• W2255357183 cites W2003157339 @default.
• W2255357183 cites W2003608585 @default.
• W2255357183 cites W2003681655 @default.
• W2255357183 cites W2003984333 @default.
• W2255357183 cites W2005049926 @default.
• W2255357183 cites W2005855555 @default.
• W2255357183 cites W2006196505 @default.
• W2255357183 cites W2007232045 @default.
• W2255357183 cites W2007498173 @default.
• W2255357183 cites W2008212776 @default.
• W2255357183 cites W2008629972 @default.
• W2255357183 cites W2009643606 @default.
• W2255357183 cites W2011866056 @default.
• W2255357183 cites W2012274022 @default.
• W2255357183 cites W2013064714 @default.
• W2255357183 cites W2015201947 @default.
• W2255357183 cites W2016696505 @default.
• W2255357183 cites W2017060960 @default.
• W2255357183 cites W2017606775 @default.
• W2255357183 cites W2018072530 @default.
• W2255357183 cites W2018758406 @default.
• W2255357183 cites W2019873785 @default.
• W2255357183 cites W2020536678 @default.
• W2255357183 cites W2021015942 @default.
• W2255357183 cites W2021886057 @default.
• W2255357183 cites W2023931001 @default.
• W2255357183 cites W2024162533 @default.

• next