Original Article
A Comparison of Budesonide and Mesalamine for Active Crohn's Disease
N Engl J Med 1998; 339:370-374August 6, 1998
- Abstract
Background
Crohn's disease is often treated with glucocorticoids or mesalamine. We compared the efficacy and safety of controlled-ileal-release budesonide capsules and slow-release mesalamine tablets in patients with active Crohn's disease affecting the ileum, the ascending colon, or both.
Methods
In a double-blind, multicenter trial, we enrolled 182 patients with scores of 200 to 400 on the Crohn's Disease Activity Index (with higher scores indicating greater disease activity) and randomly assigned 93 to receive 9 mg of budesonide once daily and 89 to receive 2 g of mesalamine twice daily for 16 weeks. The primary efficacy variable was clinical remission, defined as a score of 150 or less on the Crohn's Disease Activity Index.
Results
In the analysis of all patients who received at least one dose of study drug, the rates of remission after 8 weeks of treatment were 69 percent in the budesonide group and 45 percent in the mesalamine group (P=0.001); the respective rates after 16 weeks of treatment were 62 percent and 36 percent (P<0.001). Seventy-seven patients in the budesonide group completed the 16 weeks of treatment, as compared with 50 patients in the mesalamine group (P<0.001). The numbers of patients with adverse events were similar in the two groups, but those assigned to budesonide had fewer severe adverse events. Among patients who completed 16 weeks of treatment, the morning plasma cortisol value was normal in 67 percent of budesonide-treated patients and 83 percent of mesalamine-treated patients (P=0.06); 90 percent and 100 percent, respectively, had normal increases in cortisol in response to cosyntropin (P=0.02).
Conclusions
In patients with active Crohn's disease affecting the ileum, the ascending colon, or both, a controlled-ileal-release formulation of budesonide was more effective in inducing remission than a slow-release formulation of mesalamine.
Media in This Article
Figure 2
Mean (±SE) Rates of Remission among 91 Patients in the Budesonide Group and 83 Patients in the Mesalamine Group.Figure 1
Proportions of Patients with Crohn's Disease Who Completed the Study.Article Activity
- Article
Crohn's disease is a chronic inflammatory disorder of the bowel whose cause is unknown. During the acute phase of the disease, glucocorticoids such as prednisolone and prednisone are commonly used.1,2 However, this treatment is often associated with clinically important side effects, such as moon face, hirsutism, and acne.
Budesonide is a glucocorticoid that is a highly potent topical antiinflammatory agent with lower systemic activity than conventional glucocorticoids,3 because it is nearly 90 percent metabolized during its first pass through the liver to forms with minimal or no steroidal activity.3 Budesonide capsules contain granules that allow the slow release of the drug, mainly in the ileum and the ascending colon. Thus, this topical treatment for Crohn's disease has a reduced risk of glucocorticoid-associated side effects.
In a placebo-controlled, dose-finding study, this form of budesonide was significantly more effective than placebo in inducing remission of active Crohn's disease affecting the ileum and the ascending colon, with an optimal daily dose of 9 mg.4 This dose of budesonide has also been found, in two studies, to be as effective as oral prednisolone,5,6 but with fewer glucocorticoid-associated side effects.
Slow-release formulations of mesalamine that facilitate delivery of the drug to the small intestine are often used as first-line treatment in patients with Crohn's disease that is mild to moderately active, although results of controlled studies are conflicting.7-10 We compared the efficacy and safety of budesonide and mesalamine for active Crohn's disease.
Methods
Selection of Patients
The study was performed between November 1994 and August 1996. Eligible patients were at least 18 years of age and had a confirmed diagnosis of active Crohn's disease, as defined by a score of 200 to 400 on the Crohn's Disease Activity Index. The index assesses eight variables: the number of liquid stools, the extent of abdominal pain, general well-being, the occurrence of extraintestinal symptoms, the need for antidiarrheal drugs, the presence of abdominal masses, hematocrit, and body weight.11 Scores can range from 0 (no active disease) to 700 (severe disease). Scores of 151 to 400 are associated with disease that is mild to moderatively active. Scores of 150 or less are considered to indicate remission.
To be eligible, patients had to have disease that was confined to the distal ileum, the ileocecal region, and the ascending colon, except for scattered aphthous ulcers, and was verified by colonoscopy, small-bowel follow-through, or barium enema within 24 months before randomization. Patients with active Crohn's disease in the rectum were not eligible, nor were those with septic complications, abscess, perforation or active fistulas, ileostomy, or colostomy; those who had undergone resection of more than 100 cm of the ileum; or those who required immediate surgery. No patient received immunosuppressive drugs within three months before the study or glucocorticoids or more than 2 g of mesalamine per day within two weeks before the study. Patients with diabetes mellitus, active peptic ulcer disease, systemic infection, or clinically significant renal, hepatic, or cardiovascular disease or asthma were ineligible, as were pregnant or breast-feeding women and patients who were allergic to glucocorticoids or mesalamine.
The study was approved by the institutional review board at each center and was conducted according to the principles of the Second Declaration of Helsinki. All participants provided written informed consent.
Study Medication
The budesonide formulation used is a gelatin capsule containing acid-stable microgranules (Entocort, 3-mg capsules, Astra Draco, Lund, Sweden). The microgranules (each measuring approximately 1 mm) are composed of an inner sugar core surrounded by a layer of budesonide in ethylcellulose and an outer acrylic-based resin coating (Eudragit L100-55) that dissolves at a pH of 5.5 or higher. The mesalamine formulation (Pentasa, 500-mg tablets, Ferring, Vanløse, Denmark) disintegrates in the stomach into several hundred microgranules (each measuring approximately 1 mm) that are coated with ethylcellulose, so that mesalamine is released slowly throughout the gastrointestinal tract. Placebo medications were identical in appearance and taste to the investigational drugs.
Design of the Study
The trial was a randomized, double-blind, double-dummy study performed at 25 centers in Denmark, France, the United Kingdom, Norway, Italy, Spain, Portugal, Greece, South Africa, Austria, Australia, and Ireland. Randomization of patients in permuted blocks of four was performed separately at each center with sealed, opaque treatment-code envelopes. Treatment was scheduled to last 16 weeks. Patients received 9 mg of budesonide once daily (and a placebo once daily) or 2 g of mesalamine twice daily. Compliance was assessed by pill counts.
At entry, each patient's demographic characteristics, medical history, current and past diagnoses, and current medications were recorded. Sigmoidoscopy of the distal part of the colon was performed to rule out rectal inflammation. Disease activity was assessed with the Crohn's Disease Activity Index before treatment; after 2, 4, 8, 12, and 16 weeks of treatment; and in the event that treatment was discontinued. Efficacy was not evaluated after the discontinuation of treatment in patients who withdrew from the study before week 16. At each visit, a physical examination, quality-of-life assessment, laboratory tests, and a global evaluation were conducted and patients were asked whether any adverse events had occurred. At week 16, within 24 hours after the last dose of medication, adrenal function was assessed between 8 and 10 a.m. by the administration of cosyntropin. No medication for Crohn's disease other than the study drugs was allowed. Loperamide or opiates to control diarrhea were allowed.
Quality of life was assessed with the self-administered Psychological General Well-Being index,12 which includes 22 questions covering six categories (anxiety, depressed mood, positive well-being, self-control, general health, and vitality). The worst possible score is 22, and the best possible is 132.
The patients were asked to record on diary cards their intake of study medication, the frequency of loose stools, the extent of abdominal pain, and general well-being during the seven days before each visit. Blood samples were taken for hematologic and biochemical assessments, liver-function tests, and measurements of indicators of inflammatory activity (the erythrocyte sedimentation rate and C-reactive protein levels). Blood was drawn for measurements of plasma cortisol at the time intravenous cosyntropin (Synacthen, Ciba–Geigy, Summit, N.J.) was administered and 30 and 60 minutes later. A normal response was defined as an increase in the plasma cortisol concentration of 7.2 μg per deciliter (200 nmol per liter) from base line or an absolute value above 18.1 μg per deciliter (500 nmol per liter) at 30 or 60 minutes.
All adverse events were recorded, whether or not they were considered to be related to the study medication. A serious adverse event was defined as one that was life threatening or led to permanent disability, hospitalization, or death. The intensity of adverse events was graded as mild, moderate, or severe, with a severe event considered to be one that was incapacitating, leading to an inability to work or take part in normal activities. Patients could be withdrawn from the study at any time if their physicians believed their condition had substantially deteriorated.
Statistical Analysis
We estimated that 85 patients were needed in each group in order to detect a difference of 22 percent between groups in the proportion of patients in remission, assuming a remission rate of 50 percent with budesonide treatment. The primary outcome was the remission rate. The primary analysis (as stated in the study protocol) included all patients who received at least one dose of study medication. Patients who were found to be ineligible after randomization and patients who were less than 85 percent compliant with treatment were excluded from the per-protocol analysis (but were included in the analysis according to the intention to treat). The study protocol called for an investigation of the influence of prognostic factors on remission rates by two-way analysis of variance, with treatment, subgroup (e.g., sex), and the interaction of treatment and subgroup as factors. Secondary end points were a decrease in the Crohn's Disease Activity Index of at least 100 points or a score of 150 or less (or both), other changes in this score, the length of time to remission, changes in the Psychological General Well-Being index, changes in adrenal function, and adverse events.
The chi-square test was used to compare proportions. The time to the discontinuation of treatment and the time to remission were analyzed by Kaplan–Meier estimates and a generalized Wilcoxon test.13 Student's t-test, Wilcoxon's test, and analysis of variance were used to assess quantitative variables. All tests were two-sided. P values of less than 0.05 were considered to indicate statistical significance.
For analysis of remission rates at 2, 4, 8, 12, and 16 weeks, we divided the number of patients in the group who were evaluated and in remission at that time or who had already been withdrawn from the study while in remission by the number of patients who were evaluated at that time or who had withdrawn before that time and who had been evaluated at least once during treatment. The secondary end point of a decrease in the Crohn's Disease Activity Index of at least 100 points or a score of 150 or less (or both) was analyzed similarly. In the analysis of the time to remission, data on patients who were lost to follow-up were censored at the time of the last study visit and data on patients who were withdrawn from the study because of a deterioration in their condition were censored at 16 weeks.
Results
A total of 182 patients were enrolled; 93 were randomly assigned to receive budesonide, and 89 were assigned to receive mesalamine. All patients took at least one dose of medication. The base-line characteristics of the two groups of patients were similar (Table 1Table 1
Base-Line Characteristics of the Patients.). Seventy-seven patients (83 percent) in the budesonide group and 50 patients (56 percent) in the mesalamine group (P<0.001) completed the scheduled 16 weeks of treatment and follow-up (Figure 1Figure 1Proportions of Patients with Crohn's Disease Who Completed the Study.). Worsening Crohn's disease led to the withdrawal of 10 patients in the budesonide group and 27 in the mesalamine group. Adverse events led to the withdrawal of three patients in the budesonide group and eight patients in the mesalamine group. Three patients in the budesonide group declined to continue the study. In the mesalamine group, two patients were found to be ineligible after randomization, one patient was lost to follow-up, and one was noncompliant. The mean length of treatment was 104 days in the budesonide group and 80 days in the mesalamine group (P<0.001). The results were very similar whether the data were analyzed according to the intention to treat or per protocol.Clinical Efficacy
The rates of remission were higher in the budesonide group than in the mesalamine group throughout the study. The respective rates were 69 percent and 45 percent (P=0.001) after 8 weeks, 64 percent and 42 percent (P=0.004) after 12 weeks, and 62 percent and 36 percent (P<0.001) after 16 weeks (Figure 2Figure 2
Mean (±SE) Rates of Remission among 91 Patients in the Budesonide Group and 83 Patients in the Mesalamine Group.). Disease activity was not assessed during treatment in two patients in the budesonide group and six patients in the mesalamine group, and thus, these patients could not be included in the analysis of remission. The median time to remission was also shorter in the budesonide group than in the mesalamine group (28 vs. 84 days, P=0.04).Sex, previous intestinal resection, and previous use of mesalamine had no influence on the remission rates. In both groups, the rates of remission were lower among patients with more severe disease at entry (Crohn's Disease Activity Index, 301 to 400), but budesonide was still more effective. After 16 weeks, the remission rate was 41 percent among the 27 patients in the budesonide group with more severe disease and 11 percent among the 28 patients in the mesalamine group with more severe disease (P=0.001). The rates of remission were also lower among patients who also had colonic involvement. After 16 weeks the rate was 56 percent among the 37 patients in the budesonide group who also had colonic involvement and 23 percent among the 39 patients in the mesalamine group with such involvement (P<0.001).
Seventy-one percent of patients in the budesonide group had a decrease in the Crohn's Disease Activity Index of at least 100 points or a score of 150 or less after 16 weeks, or both, as compared with 51 percent of patients in the mesalamine group (P=0.005). These data are based on all patients, regardless of the disease site.
Scores on the Psychological General Well-Being index after 16 weeks had improved significantly more in the budesonide group than in the mesalamine group (mean increase in total score, 23 vs. 14; P= 0.05). Scores on all six subscales of the index (anxiety, depressed mood, positive well-being, self-control, general health, and vitality) showed the same pattern of improvement, with larger increases in the budesonide group, in particular after 12 and 16 weeks of treatment. There were no clinically significant changes in hematologic and biochemical variables in either group.
Adverse Events
The numbers of patients with adverse events were similar in the two groups; the most frequent events are shown in Table 2Table 2
Adverse Events in the Two Treatment Groups.. Serious adverse events (P=0.16) and severe adverse events (P=0.04) were more frequent in the mesalamine group. All serious adverse events resulted in hospitalization. Only one serious adverse event in each group was considered to be possibly related to treatment: aggressive behavior in the budesonide group and fever in the mesalamine group.Adrenal Function
Among the 76 patients who completed 16 weeks of treatment with budesonide and in whom adrenal function was assessed, the mean (±SD) morning plasma cortisol concentration was 11.3±7.3 μg per deciliter (312±201 nmol per liter); the corresponding value for the 46 patients who completed 16 weeks of mesalamine therapy was 15.3±7.9 μg per deciliter (422±218 nmol per liter). The peak value after stimulation with cosyntropin was 23.3±9.8 μg per deciliter (643±270 nmol per liter) in the budesonide group and 35.9±15.2 μg per deciliter (991±420 nmol per liter) in the mesalamine group. Sixty-seven percent of budesonide-treated patients and 83 percent of mesalamine-treated patients had normal plasma cortisol values before the cosyntropin challenge (P=0.06). Ninety percent of the budesonide-treated patients and 100 percent of the mesalamine-treated patients had normal increases in cortisol in response to cosyntropin (P=0.02).
Discussion
We found that slow-release budesonide capsules were more effective than slow-release mesalamine tablets in inducing remission in patients with mildly to moderately active Crohn's disease of the ileum or the ascending colon (or both). Sex, previous intestinal resection, and previous use of mesalamine did not influence the remission rates.
The condition of patients in both groups improved after two weeks of treatment and reached a plateau after eight weeks. The degree of improvement was greater in the budesonide group. In a study comparing methylprednisolone with mesalamine,14 the results for methylprednisolone were similar to ours for budesonide. Budesonide has fewer side effects than systemic glucocorticoids such as prednisolone.5,6
Some patients who received budesonide had impaired adrenal function, as assessed by a cosyntropin stimulation test, but the clinical significance of this finding is not known. Typical glucocorticoid-related side effects (such as moon face, hirsutism, and acne) were not among the most frequently reported adverse events in either treatment group. Both compounds were well tolerated, and the higher rate of severe adverse events and serious adverse events in the mesalamine group may relate in part to the lower efficacy of this medication.
The 9-mg dose of budesonide was safe and effective, as has been found in previous studies.4,5 The results with the use of the 4-g dose of mesalamine were in accordance with data from a previous study,7 in which the remission rate was 43 percent and the mean score on the Crohn's Disease Activity Index decreased by 72 points 16 weeks after the start of treatment (the corresponding figures in our study were 36 percent and 76 points).7 However, neither a 4-g dose10 nor a 1.5-g dose8 of mesalamine was shown to be superior to placebo in other studies, nor was a 2-g dose effective against active Crohn's disease.14 We did not include a placebo group in our study, but remission rates of 18 to 35 percent have been reported with placebo in patients with active Crohn's disease.4,7-9
Ethical principles of biomedical research require that patients be withdrawn from a controlled trial if their condition deteriorates substantially. Seventeen percent of the patients in the budesonide group and 44 percent of those in the mesalamine group did not complete the study. Approximately two thirds of the patients were withdrawn because of an insufficient therapeutic effect. These findings are similar to those in other studies.4,5,7 We did not collect data on the treatment the patients received after withdrawal.
The long-term effects of budesonide and mesalamine should be studied further, as well as the effect of higher doses of mesalamine. We studied a select group of patients with Crohn's disease of the ileum or ascending colon that was mild to moderately active, and the effect of these treatments in other groups of patients is not known. However, the therapeutic benefit of both drugs was less in patients with more active Crohn's disease and patients who also had colonic involvement.
Supported by Astra Draco, Lund, Sweden.
Source Information
From the Department of Medical Gastroenterology C, Herlev Hospital, University of Copenhagen, Herlev, Denmark (O.Ø.T.); the Gastroenterology Service, Hôpital Claude Huriez, Lille, France (A.C.); the Gastroenterology Unit, John Radcliffe Hospital, Oxford, United Kingdom (D.J.); the Gastrointestinal Clinic, Kingsbury Hospital (J.P.W.), and the Department of Gastroenterology, Groote Schuur Hospital (T.W.), Cape Town, South Africa; the Gastroenterology Department, Hospital de S. João, Porto, Portugal (F.T.V.); the Department of Medicine, Rikshospitalet, Oslo, Norway (M.V.); and Clinical Research and Development, Astra Draco, Lund, Sweden (T.P., E.P.).
Address reprint requests to Dr. Thomsen at the Department of Medical Gastroenterology C, Herlev Hospital, University of Copenhagen, DK-2730 Herlev, Denmark.
Members of the International Budesonide–Mesalamine Study Group are listed in the Appendix.
Appendix
In addition to the authors, the following persons and institutions participated in the International Budesonide–Mesalamine Study Group: Odense University Hospital, Odense, Denmark — K. Lauritsen; Hôpital Cochin, Paris — S. Chaussade; Rotherham District General Hospital, Rotherham, United Kingdom — K. Bardhan; Leigh Infirmary, Manchester, United Kingdom — V. Mani; Aker Sykehus, Oslo, Norway — E. Aadland; Università degli Studi di Bologna, Bologna, Italy — C. Brignola; Ospedale Nuovo Regina Margherita, Rome — C. Prantera; Hospital General Vall d'Hebron, Barcelona, Spain — J.-R. Malagelada; Hospital Germans Trias i Pujol, Badalona, Spain — M. Gassull; Instituto Portugues de Oncologia Francisco Gentil, Lisbon, Portugal — F. Mira; University Hospital of Heraklion, Heraklion, Greece — O. Manousos; District General Hospital of Athens, Athens, Greece — N. Skandalis; Tygerberg Hospital, Cape Town, South Africa — C. van Rensburg; Johannesburg Hospital, Johannesburg, South Africa — A. Mohamed; Sozial Medizinisches Zentrum Ost, Vienna, Austria — C. Sebesta; St. Vincent's Hospital, Fitzroy, Australia — W. Connell; Royal Prince Alfred Hospital, Camperdown, Australia — W. Selby; Meath Hospital, Dublin, Ireland — C. O'Morain; and Astra Draco, Lund, Sweden — I. Nylander.
- References
References
1
Meyers S ,Sachar DB . Medical management of Crohn's disease. Hepatogastroenterology 1990;37:42-55
Web of Science | Medline2
Summers RV ,Switz DM ,Sessions JT Jr , et al. National Cooperative Crohn's Disease Study: results of drug treatment. Gastroenterology 1979;77:847-869
Web of Science | Medline3
Brattsand R . Overview of newer glucocorticosteroid preparations for inflammatory bowel disease. Can J Gastroenterol 1990;4:407-4144
Greenberg GR ,Feagan BG ,Martin F , et al. Oral budesonide for active Crohn's disease. N Engl J Med 1994;331:836-841
Full Text | Web of Science | Medline5
Rutgeerts P ,Lofberg R ,Malchow H , et al. A comparison of budesonide with prednisolone for active Crohn's disease. N Engl J Med 1994;331:842-845
Full Text | Web of Science | Medline6
Campieri M ,Ferguson A ,Doe W ,Persson T ,Nilsson LG . Oral budesonide is as effective as oral prednisolone in active Crohn's disease. Gut 1997;41:209-214
CrossRef | Web of Science | Medline7
Singleton JW ,Hanauer SB ,Gitnick GL , et al. Mesalamine capsules for the treatment of active Crohn's disease: results of a 16-week trial. Gastroenterology 1993;104:1293-1301
Web of Science | Medline8
Rasmussen SN ,Lauritsen K ,Tage-Jensen U , et al. 5-Aminosalicylic acid in the treatment of Crohn's disease: a 16-week double-blind, placebo-controlled, multicentre study with Pentasa. Scand J Gastroenterol 1987;22:877-883
CrossRef | Web of Science | Medline9
Mahida YR ,Jewell DP . Slow-release 5-amino-salicylic acid (Pentasa) for the treatment of active Crohn's disease. Digestion 1990;45:88-92
CrossRef | Web of Science | Medline10
Singleton J . Second trial of mesalamine therapy in the treatment of active Crohn's disease. Gastroenterology 1994;107:632-633
Web of Science | Medline11
Best WR ,Becktel JM ,Singleton JW ,Kern F Jr . Development of a Crohn's disease activity index: National Cooperative Crohn's Disease Study. Gastroenterology 1976;70:439-444
Web of Science | Medline12
Dupuy HJ. The Psychological General Well-Being (PGWB) index. In: Wenger NK, Mattson ME, Furberg CD, Elinson J, eds. Assessment of quality of life in clinical trials of cardiovascular therapies. New York: Le Jacq Publishing, 1984:170-83.
13
Kalbfleisch JD, Prentice RL. The statistical analysis of failure time data. New York: John Wiley, 1980:144-9.
14
Scholmerich J ,Jenss H ,Hartmann F , et al. Oral 5-aminosalicylic acid versus 6-methylprednisolone in active Crohn's disease. Can J Gastroenterol 1990;4:446-451
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Citing Articles
1
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CrossRef4
Barrett G. Levesque, William J. Sandborn. (2011) Setting a high threshold for noninferiority: Mesalamine and budesonide in crohn's disease. Inflammatory Bowel Diseasesn/a-n/a
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CrossRef6
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CrossRef7
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CrossRef8
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CrossRef9
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A. Dignass, G. Van Assche, J.O. Lindsay, M. Lémann, J. Söderholm, J.F. Colombel, S. Danese, A. D'Hoore, M. Gassull, F. Gomollón, D.W. Hommes, P. Michetti, C. O'Morain, T. Öresland, A. Windsor, E.F. Stange, S.P.L. Travis. (2010) The second European evidence-based Consensus on the diagnosis and management of Crohn's disease: Current management. Journal of Crohn's and Colitis 4:1, 28-62
CrossRef15
Shane M. Devlin, Remo Panaccione. (2010) Evolving Inflammatory Bowel Disease Treatment Paradigms: Top-Down Versus Step-Up. Medical Clinics of North America 94:1, 1-18
CrossRef16
C Ciacci, L Maiuri, I Russo, R Tortora, C Bucci, C Cappello, A Santonicola, A Luciani, V Passananti, P Iovino. (2009) Efficacy of budesonide therapy in the early phase of treatment of adult coeliac disease patients with malabsorption: An in vivo / in vitro pilot study. Clinical and Experimental Pharmacology and Physiology 36:12, 1170-1176
CrossRef17
Shane M. Devlin, Remo Panaccione. (2009) Evolving Inflammatory Bowel Disease Treatment Paradigms: Top-Down Versus Step-Up. Gastroenterology Clinics of North America 38:4, 577-594
CrossRef18
Arie Levine, Michal Kori, Gabriel Dinari, Efrat Broide, Ron Shaoul, Baruch Yerushalmi, Avi On, Yoram Bujanover, Markus Pröls, Roland Greinwald, . (2009) Comparison of two dosing methods for induction of response and remission with oral budesonide in active pediatric Crohn's disease: A randomized placebo-controlled trial. Inflammatory Bowel Diseases 15:7, 1055-1061
CrossRef19
David H. Bruining, Edward V. Loftus. (2009) Crohn’s disease clinical issues and treatment: what the radiologist needs to know and what the gastroenterologist wants to know. Abdominal Imaging 34:3, 297-302
CrossRef20
Mary E Sherlock, Cynthia H Seow, A Hillary Steinhart, Anne Marie Griffiths, Mary E Sherlock. 2009. Oral budesonide for induction of remission in ulcerative colitis. .
CrossRef21
G. R. LICHTENSTEIN, B. BENGTSSON, L. HAPTEN-WHITE, P. RUTGEERTS. (2009) Oral budesonide for maintenance of remission of Crohn’s disease: a pooled safety analysis. Alimentary Pharmacology & Therapeutics 29:6, 643-653
CrossRef22
Debra J. Helper. (2009) Medical management of Crohn's disease: A guide for radiologists. European Journal of Radiology 69:3, 371-374
CrossRef23
Gary R Lichtenstein, Stephen B Hanauer, William J Sandborn. (2009) Management of Crohn's Disease in Adults. The American Journal of Gastroenterology 104:2, 465-483
CrossRef24
Dawn B. Beaulieu, Ashwin N. Ananthakrishnan, Mazen Issa, Lydia Rosenbaum, Sue Skaros, Julianne R. Newcomer, Randall S. Kuhlmann, Mary F. Otterson, Jeanne Emmons, Josh Knox, David G. Binion. (2009) Budesonide induction and maintenance therapy for Crohn's disease during pregnancy. Inflammatory Bowel Diseases 15:1, 25-28
CrossRef25
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CrossRef26
Christopher Teshima, Richard N. Fedorak. (2008) Are there differences in type, dosage, and method of administration for the systemic steroids in IBD treatment?. Inflammatory Bowel Diseases 14:S2, S216-S218
CrossRef27
Cynthia H Seow, Eric I Benchimol, Anne Marie Griffiths, Anthony R Otley, A Hillary Steinhart, Cynthia H Seow. 2008. Budesonide for induction of remission in Crohn's disease. .
CrossRef28
Volker Gross. (2008) Oral pH-modified release budesonide for treatment of inflammatory bowel disease, collagenous and lymphocytic colitis. Expert Opinion on Pharmacotherapy 9:7, 1257-1265
CrossRef29
E. Ricart Gómez, E. Domènech Morral. (2008) Tratamiento médico de la enfermedad de Crohn. Medicine - Programa de Formación Médica Continuada Acreditado 10:5, 298-306
CrossRef30
Sang-Ji Choi, Eun-Kyung Choe, Sung-Chan Park, Kyu-Joo Park. (2008) Long-term Result of Surgical Treatment for Crohn's Enteritis. Journal of the Korean Society of Coloproctology 24:6, 409
CrossRef31
Karen Wong, Brian Bressler. (2008) Mild to Moderate Crohn’s Disease. Drugs 68:17, 2419-2425
CrossRef32
Cynthia H Seow, Eric I Benchimol, Anne Marie Griffiths, A Hillary Steinhart, Cynthia H Seow. 2008. .
CrossRef33
David Schwartz, John R. Ferguson. (2007) Current pharmacologic treatment paradigms for inflammatory bowel disease and the potential role of granulocyte/monocyte apheresis. Current Medical Research and Opinion 23:11, 2715-2728
CrossRef34
Timothy L Zisman, Sunanda V Kane. (2007) Current and future therapies for inflammatory bowel disease. Expert Review of Gastroenterology & Hepatology 1:1, 89-100
CrossRef35
W. J. SANDBORN, B. G. FEAGAN, G. R. LICHTENSTEIN. (2007) Medical management of mild to moderate Crohn’s disease: evidence-based treatment algorithms for induction and maintenance of remission. Alimentary Pharmacology & Therapeutics 26:7, 987-1003
CrossRef36
Seymour Katz. (2007) “Mind the Gap”. Journal of Clinical Gastroenterology 41:9, 799-809
CrossRef37
Trevor A Winter, William J Sandborn, Willem JS de Villiers, Stefan Schreiber. (2007) Treatment of Crohn’s disease with certolizumab pegol. Expert Review of Clinical Immunology 3:5, 683-694
CrossRef38
Antonio Tursi, Gian Marco Giorgetti, Giovanni Brandimarte, Walter Elisei. (2007) Safety and effectiveness of long-term budesonide treatment in maintaining remission in patients with mild-to-moderate Crohn's disease. Inflammatory Bowel Diseases 13:9, 1184-1186
CrossRef39
P. M. IRVING, R. B. GEARRY, M. P. SPARROW, P. R. GIBSON. (2007) Review article: appropriate use of corticosteroids in Crohn’s disease. Alimentary Pharmacology & Therapeutics 26:3, 313-329
CrossRef40
Ryan Carvalho, Jeffrey S. Hyams. (2007) Diagnosis and management of inflammatory bowel disease in children. Seminars in Pediatric Surgery 16:3, 164-171
CrossRef41
Jianan Ren, Qingsong Tao, Xinbo Wang, Zhiming Wang, Jieshou Li. (2007) Efficacy of T2 in Active Crohn’s Disease: A Prospective Study Report. Digestive Diseases and Sciences 52:8, 1790-1797
CrossRef42
Cyrus P. Tamboli. (2007) Current Medical Therapy for Chronic Inflammatory Bowel Diseases. Surgical Clinics of North America 87:3, 697-725
CrossRef43
Daniel C Baumgart, William J Sandborn. (2007) Inflammatory bowel disease: clinical aspects and established and evolving therapies. The Lancet 369:9573, 1641-1657
CrossRef44
Paul E Evans, Darrell S Pardi. (2007) Inflammatory bowel disease in the elderly. Aging Health 3:1, 77-84
CrossRef45
Michael Siassi, Alexander Weiger, Werner Hohenberger, Hermann Kessler. (2007) Changes in surgical therapy for Crohn’s disease over 33 years: a prospective longitudinal study. International Journal of Colorectal Disease 22:3, 319-324
CrossRef46
Brian Feagan. (2006) Infliximab, Adalimumab and Certolizumab. Inflammatory Bowel Diseases 12:Supplement 3, S6
CrossRef47
C. SCHMIDT, B. M. WITTIG, C. MOSER, M. ZEITZ, A. STALLMACH. (2006) Cyclophosphamide pulse therapy followed by azathioprine or methotrexate induces long-term remission in patients with steroid-refractory Crohn's disease. Alimentary Pharmacology and Therapeutics 24:2, 343-350
CrossRef48
Gary R. Lichtenstein, Maria T. Abreu, Russell Cohen, William Tremaine. (2006) American Gastroenterological Association Institute Technical Review on Corticosteroids, Immunomodulators, and Infliximab in Inflammatory Bowel Disease. Gastroenterology 130:3, 940-987
CrossRef49
Brian W Behm, Stephen J Bickston. (2006) Medical management of Crohn's disease: current therapy and recent advances. Expert Review of Clinical Immunology 2:1, 109-120
CrossRef50
Ashish Chopra, Darrell S Pardi, Edward V Loftus, William J Tremaine, Laurence J Egan, William A Faubion, Karen A Hanson, Therese A Johnson, William J Sandborn. (2006) Budesonide in the treatment of inflammatory bowel disease: The first year of experience in clinical practice. Inflammatory Bowel Diseases 12:1, 29-32
CrossRef51
2006. Aminosalicylates. , 138-148.
CrossRef52
Kim L Isaacs, James D Lewis, William J Sandborn, Bruce E Sands, Stephan R Targan. (2005) State of the art: IBD therapy and clinical trials in IBD. Inflammatory Bowel Diseases 11:S1, S3-S12
CrossRef53
Britta Siegmund, Martin Zeitz. (2005) Standards of medical treatment and nutrition in Crohn’s disease. Langenbeck's Archives of Surgery 390:6, 503-509
CrossRef54
A Otley, AH Steinhart, Anthony Otley. 2005. Budesonide for induction of remission in Crohn's disease. .
CrossRef55
William J. Sandborn, Robert Lofberg, Brian G. Feagan, Stephen B. Hanauer, Massimo Campieri, Gordon R. Greenberg. (2005) Budesonide for Maintenance of Remission in Patients with Crohn's Disease in Medically Induced Remission: A Predetermined Pooled Analysis of Four Randomized, Double-Blind, Placebo-Controlled Trials. The American Journal of Gastroenterology 100:8, 1780-1787
CrossRef56
Stephen B Hanauer. (2005) The case for using 5-aminosalicyclates in Crohn's disease. Pro. Inflammatory Bowel Diseases 11:6, 609-612
CrossRef57
Eduard F Stange. (2005) The case against using 5-aminosalicyclates in Crohn's disease con. Inflammatory Bowel Diseases 11:6, 613-615
CrossRef58
John W SINGLETON. (2005) Progress in inflammatory bowel disease. Chinese Journal of Digestive Diseases 6:2, 59-61
CrossRef59
S. Hanauer, W. J. Sandborn, A. Persson, T. Persson. (2005) Budesonide as maintenance treatment in Crohn's disease: a placebo-controlled trial. Alimentary Pharmacology and Therapeutics 21:4, 363-371
CrossRef60
Shamina Dhillon, Edward V. Loftus. (2005) Medical therapy of Crohn’s disease. Current Treatment Options in Gastroenterology 8:1, 19-30
CrossRef61
Richard N. Fedorak, Lana Bistritz. (2005) Targeted delivery, safety, and efficacy of oral enteric-coated formulations of budesonide. Advanced Drug Delivery Reviews 57:2, 303-316
CrossRef62
William J. Sandborn, Laurence J. Egan. (2005) Reply. Gastroenterology 128:1, 246
CrossRef63
Axel Dignass, P. Marteau. (2005) Mesalamine in the treatment of active Crohn’s disease. Gastroenterology 128:1, 245-246
CrossRef64
J. Scholmerich. (2004) Systemic and topical steroids in inflammatory bowel disease. Alimentary Pharmacology and Therapeutics 20:s4, 66-74
CrossRef65
Gary R. Lichtenstein, Carmen Cuffari, Sunanda V. Kane, Stephen Hanauer, Daniel H. Present. (2004) Maintaining remissions across the lifespan. A roundtable discussion with Crohn's disease experts. Inflammatory Bowel Diseases 10:8, S11-S21
CrossRef66
Jeffry A Katz. (2004) Treatment of inflammatory bowel disease with corticosteroids. Gastroenterology Clinics of North America 33:2, 171-189
CrossRef67
Laura E Harrell, Stephen B Hanauer. (2004) Mesalamine derivatives in the treatment of Crohn's disease. Gastroenterology Clinics of North America 33:2, 303-317
CrossRef68
Laurence J Egan, William J Sandborn. (2004) Advances in the treatment of Crohn’s disease. Gastroenterology 126:6, 1574-1581
CrossRef69
Johanna C Escher. (2004) Budesonide versus prednisolone for the treatment of active Crohn's disease in children. European Journal of Gastroenterology & Hepatology 16:1, 47-54
CrossRef70
Staffan Edsb??cker, Tommy Andersson. (2004) Pharmacokinetics of Budesonide (Entocort??? EC) Capsules for Crohn???s Disease. Clinical Pharmacokinetics 43:12, 803-821
CrossRef71
Faruque D Ghanchi, Bjorn J Rembacken. (2003) Inflammatory bowel disease and the eye. Survey of Ophthalmology 48:6, 663-676
CrossRef72
W. J. Sandborn, B. G. Feagan. (2003) Mild to moderate Crohn's disease - defining the basis for a new treatment algorithm. Alimentary Pharmacology and Therapeutics 18:3, 263-277
CrossRef73
R. Lofberg. (2003) Medical treatment of mild to moderately active Crohn's disease. Alimentary Pharmacology and Therapeutics 17:s2, 18-22
CrossRef74
Marla C. Dubinsky, Phillip P. Fleshner. (2003) Treatment of Crohn’s disease of inflammatory, stenotic, and fistulizing phenotypes. Current Treatment Options in Gastroenterology 6:3, 183-200
CrossRef75
Arie Levine, Tamir Milo, Hans Buller, James Markowitz. (2003) Consensus and Controversy in the Management of Pediatric Crohn Disease: An International Survey. Journal of Pediatric Gastroenterology and Nutrition 36:4, 464-469
CrossRef76
Gerassimos J. Mantzaris, Kalliopi Petraki, Michael Sfakianakis, Emmanuel Archavlis, Angeliki Christidou, Helen Chadio-Iordanides, George Triadaphyllou. (2003) Budesonide versus mesalamine for maintaining remission in patients refusing other immunomodulators for steroid-dependent Crohn's disease. Clinical Gastroenterology and Hepatology 1:2, 122-128
CrossRef77
Arie Levine, Zvi Weizman, Efrat Broide, Raanan Shamir, Ron Shaoul, Avi Pacht, Gabriel Dinari, Avi On, Batya Weiss, Yoram Bujanover. (2003) A Comparison of Budesonide and Prednisone for the Treatment of Active Pediatric Crohn Disease. Journal of Pediatric Gastroenterology and Nutrition 36:2, 248-252
CrossRef78
S. Edsbacker, P. Larsson, M. Bergstrand. (2003) Pharmacokinetics of budesonide controlled-release capsules when taken with omeprazole. Alimentary Pharmacology and Therapeutics 17:3, 403-408
CrossRef79
Stephen B. Hanauer. (2003) Crohn's disease: step up or top down therapy. Best Practice & Research Clinical Gastroenterology 17:1, 131-137
CrossRef80
S. Edsbacker, B. Bengtsson, P. Larsson, P. Lundin, A. Nilsson, J. Ulmius, P. Wollmer. (2003) A pharmacoscintigraphic evaluation of oral budesonide given as controlled-release (Entocort) capsules. Alimentary Pharmacology and Therapeutics 17:4, 525-536
CrossRef81
P. D. P. Lundin, S. Edsbacker, M. Bergstrand, J. Ejderhamn, H. Linander, L. Hogberg, T. Persson, J. C. Escher, B. Lindquist. (2003) Pharmacokinetics of budesonide controlled ileal release capsules in children and adults with active Crohn's disease. Alimentary Pharmacology and Therapeutics 17:1, 85-92
CrossRef82
Staffan Edsbäcker, Per Larsson, Per Wollmer. (2002) Gut delivery of budesonide, a locally active corticosteroid, from plain and controlled-release capsules. European Journal of Gastroenterology & Hepatology 14:12, 1357-1362
CrossRef83
Chinyu Su, Gary R Lichtenstein. (2002) Recent developments in inflammatory bowel disease. Medical Clinics of North America 86:6, 1497-1523
CrossRef84
Geert D’Haens, Marco Daperno. (2002) Advances in medical therapy for Crohn’s disease. Current Gastroenterology Reports 4:6, 506-512
CrossRef85
R. D. Cohen. (2002) The quality of life in patients with Crohn's disease. Alimentary Pharmacology and Therapeutics 16:9, 1603-1609
CrossRef86
Podolsky, Daniel K., . (2002) Inflammatory Bowel Disease. New England Journal of Medicine 347:6, 417-429
Full Text87
S. V. Kane, P. Schoenfeld, W. J. Sandborn, W. Tremaine, T. Hofer, B. G. Feagan. (2002) Systematic review: the effectiveness of budesonide therapy for Crohn's disease. Alimentary Pharmacology and Therapeutics 16:8, 1509-1517
CrossRef88
Hans Buller, Simon Chin, Barbara Kirschner, Joanchin Kohn, James Markowitz, David Moore, Simon Murch, Jan Taminiau. (2002) Inflammatory Bowel Disease in Children and Adolescents: Working Group Report of the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition. Journal of Pediatric Gastroenterology and Nutrition 35, S151-S158
CrossRef89
M. L. Scribano, C. Prantera. (2002) Medical treatment of active Crohn's disease. Alimentary Pharmacology and Therapeutics 16:s4, 35-39
CrossRef90
R Mark Beattie, A Ronald F Bremner. (2002) Therapy of Crohn’s disease in childhood. Expert Opinion on Pharmacotherapy 3:7, 809-825
CrossRef91
Subhas Banerjee, Mark A Peppercorn. (2002) Inflammatory bowel disease. Gastroenterology Clinics of North America 31:1, 185-202
CrossRef92
Janet Harrison, Stephen B Hanauer. (2002) Medical treatment of Crohn's disease. Gastroenterology Clinics of North America 31:1, 167-184
CrossRef93
Ali Keshavarzian, Ashkan Farhadi, Ece A Mutlu. (2002) New developments in the treatment of inflammatory bowel disease. Expert Opinion on Investigational Drugs 11:3, 365-385
CrossRef94
Cornelia M. Gelbmann, Gerhard Rogler, Michael Gierend, Volker Gross, Jürgen Schölmerich, Tilo Andus. (2001) Association of HLA-DR genotypes and IL-1ra gene polymorphism with treatment failure of budesonide and disease patterns in Crohn's disease. European Journal of Gastroenterology & Hepatology 13:12, 1431-1437
CrossRef95
Fernando Tavarela Veloso, Jos?? Tom?? Ferreira, Lu??sa Barros, Susana Almeida. (2001) Clinical Outcome of Crohn's Disease: Analysis According to the Vienna Classification and Clinical Activity. Inflammatory Bowel Diseases 7:4, 306-313
CrossRef96
P. Kundhal, M. Zachos, J. L. Holmes, Anne M. Griffiths. (2001) Controlled Ileal Release Budesonide in Pediatric Crohn Disease: Efficacy and Effect on Growth. Journal of Pediatric Gastroenterology and Nutrition 33:1, 75-80
CrossRef97
Douglas J. Robertson, Ian S. Grimm. (2001) INFLAMMATORY BOWEL DISEASE IN THE ELDERLY. Gastroenterology Clinics of North America 30:2, 409-426
CrossRef98
Paul J. Rutgeerts. (2001) Conventional treatment of Crohn's disease: Objectives and outcomes. Inflammatory Bowel Diseases 7:S1, S2-S8
CrossRef99
Adriaan C. I. T. L. Tan, Johanna W. Kruimel, Ton H. J. Naber. (2001) Eosinophilic gastroenteritis treated with non-enteric-coated budesonide tablets. European Journal of Gastroenterology & Hepatology 13:4, 425-427
CrossRef100
Stephen B. Hanauer, Themistocles Dassopoulos. (2001) E
VOLVING TREATMENT STRATEGIES FOR INFLAMMATORY BOWEL DISEASE . Annual Review of Medicine 52:1, 299-318
CrossRef101
Paul Rutgeerts. (2001) The Use of Budesonide in the Treatment of Active Crohn's Disease Is Good Clinical Practice. Inflammatory Bowel Disease60-61
CrossRef102
Robert B. Stein, Gary R. Lichtenstein. (2001) Medical Therapy for Crohn's Disease. Surgical Clinics of North America 81:1, 71-101
CrossRef103
Sauid Ishaq, Jonathan R. Green. (2001) Tolerability of Aminosalicylates in Inflammatory Bowel Disease. BioDrugs 15:5, 339-349
CrossRef104
C. Papi, R. Luchetti, L. Gili, S. Montanti, M. Koch, L. Capurso. (2000) Budesonide in the treatment of Crohn's disease: a meta-analysis. Alimentary Pharmacology and Therapeutics 14:11, 1419-1428
CrossRef105
Brian R. Stotland, Robert B. Stein, Gary R. Lichtenstein. (2000) ADVANCES IN INFLAMMATORY BOWEL DISEASE. Medical Clinics of North America 84:5, 1107-1124
CrossRef106
Martine de Vos. (2000) Clinical Pharmacokinetics of Slow Release Mesalazine. Clinical Pharmacokinetics 39:2, 85-97
CrossRef107
E. Jan Irvine, Gordon R. Greenberg, Brian G. Feagan, Francois Martin, Lloyd R. Sutherland, Alan B. R. Thomson, Lars-Goran Nilsson, Tore Persson. (2000) Quality of life rapidly improves with budesonide therapy for active Crohn's disease. Inflammatory Bowel Diseases 6:3, 181-187
CrossRef108
William J. Sandborn. (2000) Therapy for Crohn disease. Current Opinion in Gastroenterology 16:4, 318-323
CrossRef109
Delyth Clemett, Anthony Markham. (2000) Prolonged-Release Mesalazine*. Drugs 59:4, 929-956
CrossRef110
Brian C McKaig, William A Stack. (1999) Current pharmacotherapy for inflammatory bowel disease. Expert Opinion on Pharmacotherapy 1:1, 3-14
CrossRef111
Geoffrey C. Wall, Catherine Heyneman, Timothy P. Pfanner. (1999) Medical Options for Treating Crohn’s Disease in Adults: Focus on Antitumor Necrosis Factor-α Chimeric Monoclonal Antibody. Pharmacotherapy 19:10, 1138-1152
CrossRef112
William J. Sandborn, William J. Tremaine, Douglas C. Wolf, Stephan R. Targan, Charles A. Sninsky, Lloyd R. Sutherland, Stephen B. Hanauer, John W.D. McDonald, Brian G. Feagan, Richard N. Fedorak, Kim L. Isaacs, M.Gennette Pike, Dennis C. Mays, James J. Lipsky, Susan Gordon, Christi S. Kleoudis, Robert H. Murdock. (1999) Lack of effect of intravenous administration on time to respond to azathioprine for steroid-treated Crohn's disease. Gastroenterology 117:3, 527-535
CrossRef113
Stephen B. Hanauer. (1999) Medical therapy for Crohn’s disease. Current Opinion in Gastroenterology 15:4, 308
CrossRef114
Robert B. Stein, Stephen B. Hanauer. (1999) MEDICAL THERAPY FOR INFLAMMATORY BOWEL DISEASE. Gastroenterology Clinics of North America 28:2, 297-321
CrossRef115
Cosimo Prantera, Mario Cottone, Francesco Pallone, Vito Annese, Angelo Franzè, Renata Cerutti, Gabriele Bianchi Porro. (1999) Mesalamine in the treatment of mild to moderate active Crohn's ileitis: Results of a randomized, multicenter trial. Gastroenterology 116:3, 521-526
CrossRef116
Eduard F. Stange. (1999) Konsequenzen der galenischen Unterschiede und klinischen Studienergebnisse mit Budesonid und 5-Aminosalicylaten für die Therapie des Morbus Crohn. Medizinische Klinik 94:S1, 39-41
CrossRef117
. (1999) Ziekte van Crohn. Medisch Farmaceutische Mededelingen 37:2, 51-51
CrossRef118
Jürgen Schölmerich. (1999) Klinische Wirkung der verschiedenen Budesonid-Präparationen bei Morbus Crohn. Medizinische Klinik 94:S1, 30-38
CrossRef119
Stephen B. Hanauer, Russell D. Cohen, Russell V. Becker, Leanne R. Larson, Mary Glenn Vreeland. (1998) Advances in the management of Crohn's disease: economic and clinical potential of infliximab. Clinical Therapeutics 20:5, 1009-1028
CrossRef120
Bickston, Stephen J., Cominelli, Fabio, . (1998) Treatment of Crohn's Disease at the Turn of the Century. New England Journal of Medicine 339:6, 401-402
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