Crohn’s disease (CD) is a chronic and relapsing gastrointestinal disease. New therapies to maintain patients in remission are needed. An 18-year-old white women developed abdominal pain, vomiting, and diarrhea in June 2000. Her hemoglobin was 11 g/dL, white blood cell count 9.3 x 109/L, platelet count 505 (normal 150Y450) x 109/L, and the sedimentation rate (SR) 73 (normal 1Y18) mm/1st hour. Radiologic examination showed ulcers in the terminal ileum and narrowing of the lumen. At colonoscopy, ulceration of the ileocecal valve and ileum was seen. A biopsy specimen of the mucosa of terminal ileum and ileocecal valve showed mucosal ulceration with extensive inflammatory infiltrate. On the basis of clinical, radiologic, and histologic findings, a diagnosis of CD was made. Since 2001 she had been treated with prednisolone 40 mg/day and mesalamine 3 g/day. However, she was frequently symptomatic with abdominal pain and diarrhea, and the levels of SR were frequently high (Fig. 1A). For the treatment of chronic active disease, azathioprine was proposed; however, she refused. In September 2002, she developed fever and abdominal pain. The hemoglobin was 9.6 g/dL, white blood cell count 21.57 (normal, 4.0 Y10. 0) x 109/L, platelets 906 x 109/L, C-reactive protein 138.9 (normal G 5.0) mg/L, and SR was 47 mm/1st hour. After a single infusion of infliximab (5 mg/kg intravenous), she became asymptomatic, without abdominal pain or diarrhea. At that moment, she was taking prednisolone 40 mg/day and mesalamine 3 g/day orally. After improvement with infliximab, prednisolone tapering was started. However, although there was clinical induction of remission, platelet counts were persistently high (Fig. 1B), and a hematologic evaluation was performed. Laboratory findings were as follows: white blood cell count 19 x 109/L (neutrophils 79%, eosinophils 2%, basophils 1%, lymphocytes 10%, monocytes 1%, myelocytes 3%, metamyelocytes 3%, myeloblasts 1%), leukocyte alkaline phosphatase 120 (normal G 90) U/L, iron 10 (normal, 49Y151) mg/dL. Genetic analysis disclosed 46, XX, BCR-ABL positive tested by reverse-transcriptase polymerase chain reaction (RT-PCR). Since the diagnosis of chronic myeloid leukemia BCRABL (+) with thrombocythemia was made, she started hydroxyurea at a dose of 1,000 mg/day over 2 to 3 weeks without any improvement (white blood cells count 25.3 x 109/L, platelet count 1300 x 109/L). Thus, treatment with imatinib 600 mg/day was started (February 2003). A remarkable clinical, hematologic, and cytogenetic response was observed. Hematologic remission was kept under maintenance therapy with imatinib 400 mg/day until present. Bone marrow (aspirate and trephine) was normocellular. Genetic analysis showed complete molecular remission in qualitative (tested RT-PCR) and quantitative (real time-quantitative PCR) analysis.

Because of the unexpected hematologic problem, the normal sequence of infliximab therapy was not performed. The therapy with imatinib was started in February 2003, when she was taking 15 mg/day of prednisolone. It is interesting to note that after imatinib, the patient experienced a sensation of general well being and stopped prednisolone and mesalamine at her own initiative. Surprisingly, the patient persisted asymptomatically despite the very long period without any medication known to be active against CD. Clinically, she never again complained of abdominal pain, vomiting, diarrhea, or other symptoms. The inflammatory parameters changed to normal