• Crohn’s disease
• bile acids
• gene regulation
• intestinal transport
• steroid receptors

Steroids are among the mainstays of medical therapy for Crohn’s disease but may lead to unfavourable long term complications. Recently, budesonide has been shown to be effective in inducing remission in mild to moderate disease while undergoing less systemic absorption compared with other corticosteroids.¹ It is hypothesised that steroids exert their salutary effect through an immunomodulatory action on the small bowel mucosa.² In this issue of Gut, Jung and colleagues³ shed light on the possibility of another potentially beneficial effect of steroid therapy—namely, the partial restoration of impaired bile salt absorption in Crohn’s patients with distal ileal involvement [see page 78].

The integrity of the enterohepatic circulation of bile salts is dependent on active uptake from the ileum, which is mediated by SLC10A2, known previously as the apical sodium dependent bile acid transporter (ASBT).⁴ Given the malady’s proclivity for the distal ileum, one of the classic hallmarks of intestinal Crohn’s disease is bile salt malabsorption.^5–7 Bile salt malabsorption occurs when intestinal transport is appreciably disrupted, and the degree to which this occurs depends on the length of ileal involvement and/or resection.⁸ Therefore, the activity and functioning of the remaining ASBT, as well as colonic compensation by passive absorption of bacterially modified (secondary) bile acids are essential for keeping the enterohepatic circulation of bile salts partially intact.^9,10 Mild bile salt malabsorption may result in cholerrhoeic enteropathy that is easily controlled with low dose bile …