Cephalic Duodenopancreatectomy for Hyperalgic Duodenal Crohn's Disease Fistulized in the Pancreatic Gland
We report herein the case of a 23-year-old man with a past history of gastric pain in 1999 in relation with an ulcer of the bulb successfully treated by proton pomp inhibitors. Between 1999 and 2008, the patient had no symptoms. In October 2008, the abdominal pain reappeared with anorexia and weight loss (from 67 to 54 kg). Upper digestive endoscopy showed a giant ulcer covering the whole surface of the bulb (fig. ). Histological analysis reported antral gastritis, presence of Helicobacter pylori and non-caseating granulomas composed of epithelioid cells and multinucleated giant cells. Ziehl staining and quantiferon test were negative. Chest X-ray did not show any abnormality. C-reactive protein was 10 mg/l, hemoglobin level 12.2 g/dl with a mean corpuscular volume at 81 fl, and the gastrin blood rate was normal.\nThe diagnosis of duodenal CD was strongly suspected. However, we first decided to treat H. pylori infection with a 7-day regimen of proton pomp inhibitor b.i.d., amoxicillin 1 g b.i.d. and a 500 mg metronidazole b.i.d., without evidence of clinical improvement. A second upper digestive endoscopy confirmed the persistence of a large ulcer with suspicion of a plugged perforation and a stenosis of the bulboduodenal junction. Non-caseating granulomas without H. pylori were still found on biopsies.\nTo assess the extent of CD, ileocolonoscopy with multiple biopsy sampling, abdominal computed tomography and capsule endoscopy were performed. On ileocolonoscopy, the ileum and colon were macroscopically and microscopically healthy. The abdominal computed tomography scan only reported thickening of the pylorus wall and bulb. The capsule endoscopy showed mild bulb stricture with a large inflammatory ulcer with a sclerosus bottom.\nIn January 2009, oral corticosteroid treatment was introduced with a dose of 60 mg/day. The abdominal pain partially improved, but promptly reappeared with identical macroscopic lesions at upper endoscopy. Azathioprine 125 mg/day and infliximab 5 mg/kg (300 mg) scheduled at weeks 0, 2, 6 and every 8 weeks were then introduced. After 8 infliximab infusions, the gastric pain did not disappear, with a significant social impact on the patient's life (work absenteeism a week per month). We decided to optimize the treatment by increasing the azathioprine dose to 150 mg/day and infliximab to 10 mg/kg (600 mg) every 8 weeks. The patient received three new injections of infliximab, but without clinical improvement. Surgery was considered at that point, but gastrojejunostomy was excluded because of evidence of proximal jejunal wall thickening on magnetic resonance enterography. We then switched to another combo therapy with subcutaneous methotrexate injection 25 mg/week and adalimumab 160 mg followed by 80 mg at 2 weeks and by 40 mg every other week. No improvement was noticed after 3 months of this new treatment strategy. The isolated gastric pain became stronger, leading to complete socio-professional inability and requiring daily use of opioid medications. The failure of two lines of combined treatment led us to a salvage surgical option.\nA median laparotomy was performed. Abdominal exploration showed two short inflammatory small bowel stenoses 50 and 70 cm from the angle of Treitz. The stomach was plate with a retracted aspect of the bulb. The bulboduodenal block was inflammatory and thickened. Cephalic duodenopancreatectomy and cholecystectomy were performed. The pancreas was hard at section. The jejunal stenoses were left in place in the absence of tight stricture. Histological analysis reported a large fissuring pylorus ulceration with micro abscesses reaching the pancreas (fig. ).\nRegarding the severity of the disease, adalimumab 40 mg every other week was maintained after surgery to prevent CD recurrence. Six months after the surgery, the patient had stopped antalgic treatment and did not have residual abdominal pain. He had gained 11 kg weight and had no diarrhea with pancreatic enzymes.