Oral pH-modified release budesonide versus 6-methylprednisolone in active Crohn's disease. German/Austrian Budesonide Study Group.

OBJECTIVE: Corticosteroids are effective in acute Crohn's disease (CD). The present study assessed the effectiveness and safety of oral pH-modified release budesonide (BUD) in patients with active CD in comparison with 6-methylprednisolone (MPred). DESIGN: This was a prospective multicentre, randomized, double-blind, double-dummy study. METHODS: A total of 67 patients with active CD (CDAI > 150) were included. Patients were treated with 3 x 3 mg BUD (n = 34) or MPred (n = 33) according to a weekly tapering schedule (48-32-24-20-16-12-8 mg). The primary aim was remission of CD (CDAI < 150 and decrease by at least 60 points from baseline) after eight weeks. RESULTS: Baseline demographics, disease activity and localization of CD in the small bowel and the colon were similar in both treatment groups. On an intention-to-treat basis 19/34 patients in the BUD group (55.9%) and 24/33 patients in the MPred group (72.7%) were in remission after eight weeks (P = 0.237). Therapy failed in 15/34 patients (44.1%) of the BUD group and in 9/33 patients (27.3%) of the MPred group. The mean CDAI decreased from 262 +/- 50 to 118 +/- 69 in the BUD-group and from 262 +/- 81 to 95 +/- 61 in the Mored group (P = 0.183, final CDAI BUD vs. MPred). Steroid-related side effects appeared in 28.6% of the patients in the BUD group and in 69.7% of the patients in the Mored group (P = 0.0015). CONCLUSIONS: Oral pH-modified release budesonide (3 x 3 mg/day) is almost as effective as a conventional corticosteroid in patients with active CD but causes significantly less corticosteroid-related side effects.

[Reactive hemophagocytosis syndrome as a rare cause of fatal pancytopenia]. / Reaktives Hämophagozytosesyndrom als seltene Ursache einer fatalen Panzytopenie.

CASE REPORT: We present the case of a feverish 36-year-old female patient with unspecific pain and weight loss. After initial diagnosis of an unclear infection with Candida esophagitis, unspecific duodenitis, proctitis and liver damage there was a further clinical deterioration during antibiotic and symptomatic therapy. A newly developed pancytopenia could be identified as caused by reactive hemophagocytosis using bone marrow analysis. The patient died despite maximal supportive and specific therapy. Cause of death was a retroperitoneal hematoma and an invasive aspergillosis, the latter not identified premortem. CONCLUSION: The reactive infect-associated hemophagocytosis is a rare differential diagnosis in feverish pancytopenia. The prognosis is poor. In absence of a proven causal therapy supportive therapy and maximal diagnostics for detection of curable underlying diseases are essential. Antimycotic therapy should be considered generally.