Low-dose budesonide for maintenance of clinical remission in collagenous colitis: a randomised, placebo-controlled, 12-month trial.

OBJECTIVE: This 1-year study aimed to assess low-dose budesonide therapy for maintenance of clinical remission in patients with collagenous colitis. DESIGN: A prospective, randomised, placebo-controlled study beginning with an 8-week open-label induction phase in which patients with histologically confirmed active collagenous colitis received budesonide (Budenofalk, 9 mg/day initially, tapered to 4.5 mg/day), after which 92 patients in clinical remission were randomised to budesonide (mean dose 4.5 mg/day; Budenofalk 3 mg capsules, two or one capsule on alternate days) or placebo in a 12-month double-blind phase with 6 months treatment-free follow-up. Primary endpoint was clinical remission throughout the double-blind phase. RESULTS: Clinical remission during open-label treatment was achieved by 84.5% (93/110 patients). The median time to remission was 10.5 days (95% CI (9.0 to 14.0 days)). The maintenance of clinical remission at 1 year was achieved by 61.4% (27/44 patients) in the budesonide group versus 16.7% (8/48 patients) receiving placebo (treatment difference 44.5% in favour of budesonide; 95% CI (26.9% to 62.7%), p<0.001). Health-related quality of life was maintained during the 12-month double-blind phase in budesonide-treated patients. During treatment-free follow-up, 82.1% (23/28 patients) formerly receiving budesonide relapsed after study drug discontinuation. Low-dose budesonide over 1 year resulted in few suspected adverse drug reactions (7/44 patients), all non-serious. CONCLUSIONS: Budesonide at a mean dose of 4.5 mg/day maintained clinical remission for at least 1 year in the majority of patients with collagenous colitis and preserved health-related quality of life without safety concerns. Treatment extension with low-dose budesonide beyond 1 year may be beneficial given the high relapse rate after budesonide discontinuation. TRIAL REGISTRATION NUMBERS: http://www.clinicaltrials.gov (NCT01278082) and http://www.clinicaltrialsregister.eu (EudraCT: 2007-001315-31).

Prognostic value of plasma interleukin-6 concentrations and the -174 G > C and -572 G > C promoter polymorphisms of the interleukin-6 gene in patients with acute myocardial infarction treated with thrombolysis.

The present study was performed to investigate the prognostic value of plasma interleukin-6 (IL-6) concentrations and promoter polymorphisms of the IL-6 gene in patients with acute myocardial infarction treated with thrombolysis. Two hundred and eight patients with myocardial infarction treated with thrombolysis were included and followed for 2-5 years. Plasma concentrations of IL-6 were measured at admission and 48 h after admission. Genotyping for the -174 G > C and -572 G > C IL-6 polymorphisms was performed. Patients who died of cardiovascular causes or suffered a new myocardial infarction during follow-up had increased plasma concentrations of IL-6 at admission (P < 0.002) and at 48 h after admission (P < 0.05) compared with patients who had an uneventful course. IL-6 levels above the median at admission were independently associated with a worse prognosis. No associations were found between IL-6 levels and the promoter polymorphisms. The -174 G > C polymorphism was not associated with cardiovascular death or a new myocardial infarction, whereas the -572 G > C polymorphism showed a borderline significant increase in risk (P = 0.05) in univariate analysis. In conclusion, the early IL-6 response during myocardial infarction is associated with prognosis in patients with Q-wave myocardial infarction, whereas no associations were found between IL-6 genotype and phenotype.

Plasma C-reactive protein and lipoprotein levels, and progression of coronary artery disease after myocardial infarction treated with thrombolysis.

BACKGROUND: There is a paucity of studies using quantitative coronary angiography (QCA) to determine progression of coronary artery disease (CAD) after an acute coronary event. Furthermore, despite a great interest in effects of inflammation and 'early' lipid lowering therapy, no data have been published on the role of plasma C-reactive protein (CRP) and lipoprotein levels in CAD progression after myocardial infarction. METHODS: Seventy-two patients with myocardial infarction treated with thrombolysis, but not with statins, were investigated with QCA during admission and after 6 months. Plasma CRP concentrations were measured by a high sensitive method 2 days after the acute event, and plasma high-sensitive CRP and lipoprotein levels were determined 3 months after myocardial infarction. RESULTS: Overall, there was no significant progression of CAD, but when stenoses were grouped into those reducing the lumen diameter greater or less than 50%, progression was seen in stenoses originally <50%, whereas regression was seen in stenoses >50%. No consistent associations were seen between plasma CRP, lipoprotein lipid or lipoprotein(a) levels and CAD. CONCLUSIONS: Progression of stenoses <50% might be of clinical importance since these stenoses are more prone to rupture. Furthermore, the lack of associations between change in minimum lumen diameter and plasma CRP and lipoprotein concentrations suggests that positive effects on CAD progression of early treatment with anti-inflammatory or lipid-lowering drug therapy may not be expected in this subset of patients.