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To the Editor:

Crohn's disease (CD) is a chronic granulomatous transmural inflammatory bowel disease (IBD). It is well known that clinical behavior varies over time with a trend from nonstricturing–nonpenetrating disease to a penetrating behavior. Over half of CD patients will develop penetrating disease at 10 years after diagnosis,1,2 with a significant increase in terms of disability and direct and indirect costs and a decrease in perceived quality of life. For this reason, in the last 2 years the use of biological agents early after CD diagnosis as been proposed, starting from the assumption that these agents could be able to modify the natural history of CD by mucosal healing.3,4 Furthermore, biological agents have been demonstrated to be able to reduce the number of surgical procedures and hospitalizations for CD patients.5 Here we present the case of a 33-year-old female patient with a diagnosis of colonic nonstricturing–nonpenetrating CD since 1997. In the patient's history 2 disease flare-ups have been reported, in 1997 and 2002, both successfully treated with prednisone as induction treatment and mesalazine as maintenance treatment. On March 2006, after a third flare-up of the disease with diarrhoea, abdominal pain, and weight loss (6 kg in 2 months), a colonoscopy was performed showing aphtoid ulcers in the rectum and sigmoid colon. Histological examination of the specimens was compatible with active CD. Systemic and topical treatment with steroids (prednisone and beclomethasone dipropionate, respectively) was started, with poor success. On November 2006, due to chronically active CD, the patient was referred to our IBD center. Laboratory tests showed increased C-reactive protein (3.1 mg/dL), erythrocyte sedimentation rate (56 mm/h), and platelet count (420,000). A colonoscopy showed a canal anal substenosis and cobblestone aspect with serpiginous ulcers in the rectosigmoid region. Magnetic resonance imaging (MRI) showed slight wall thickening of the rectum-sigmoid region for an extension of 15 cm and flogosis in the perianal region. For the chronically active disease together with the appearance of axial arthralgia, immunosuppressive treatment (azathioprine, 2.5 mg/kg/day) was started. At the same time systemic steroids were tapered. Four months after azathioprine was started without clinical benefit, a perianal abscess appeared and an MRI was repeated, showing an extrasphincteric fistula (Fig. 1a).

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