A double-blind, randomized, placebo-controlled clinical trial on benfotiamine treatment in patients with diabetic nephropathy.

OBJECTIVE: To investigate the effect of benfotiamine on urinary albumin excretion (UAE) and the tubular damage marker kidney injury molecule-1 (KIM-1) in patients with type 2 diabetes and nephropathy. RESEARCH DESIGN AND METHODS: Patients with type 2 diabetes and UAE equivalent to 15-300 mg/24 h, despite ACE inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs), were randomly assigned to 12 weeks of benfotiamine (900 mg/day) (n = 39) or placebo (n = 43). RESULTS: Compared with placebo, benfotiamine treatment resulted in significant improvement of thiamine status (P < 0.001). Benfotiamine treatment did not significantly decrease 24-h UAE or 24-h KIM-1 excretion. CONCLUSIONS: In patients with type 2 diabetes and nephropathy, high-dose benfotiamine treatment for 12 weeks in addition to ACE-Is or ARBs did not reduce UAE or KIM-1 excretion, despite improvement of thiamine status.

Long-term treatment of high intestinal output syndrome with budesonide in patients with Crohn's disease and ileostomy.

PURPOSE: In a previous, controlled study, it was shown that orally administered budesonide increases the absorptive capacity of the intestinal mucosa in patients with ileostomies caused by Crohn's disease. This open, nonrandomized study was designed to analyze this functional, not inflammation-dependent steroid-effect in the long-term course comparing exposure, withdrawal, and reexposure. METHODS: Phase 1: 23 patients without inflammatory activity of the disease received oral budesonide (3 mg t.i.d.) for at least four weeks (36.7 weeks; standard deviation, 45.3 weeks) because of high intestinal output syndrome. Phase 2: Medication was stopped for four weeks. Phase 3: Medication as in Phase 1. In each phase the weight of the ileostomy bags was measured with a spring balance before emptying and documented in a diary. Mean values per day and per week were calculated and the differences statistically evaluated by the Wilcoxon-(Pratt)-test. RESULTS: Comparing the last week of Phase 1 to first week of Phase 2, a significant (P < 0.0001) increase of the intestinal output (295 g; standard deviation, 313 g) was observed after omitting budesonide. In contrast, comparing the last week of Phase 2 to Phase 3, a significant (P < 0.0001) decrease of the intestinal output by 323.7 g (standard deviation, 322.2 g) was noticed reaching the same level as in Phase 1. CONCLUSIONS: These data show that the functional, inflammation-independent effect of budesonide on the intestinal mucosa is strongly correlated to the administration of the drug and may be maintained long-term. These results should be confirmed by a larger number of patients.