A 61-year-old woman underwent orthotopic liver transplantation 7 years previously for end stage liver disease secondary to hepatitis C virus (HCV) related cirrhosis. She was initially maintained on cyclosporine A. Two years after liver transplantation, because of recurrent hepatitis C and a liver biopsy already showing a staging score of 4 (according to the Ishak classification), she was administered pegylated interferon α2a, 180 μg weekly. Serum HCV RNA became undetectable after 3 months and remained negative for 9 months. At this time, however, treatment was withdrawn because of a pronounced flare up of liver enzymes (up to 700 IU/l). Liver biopsy showed a histological picture suggesting features of both acute and chronic rejection, with eosinophilic and lymphomononuclear infiltrates, granulomatous cholangiolitis and initial ductopenia. The patient was treated with multiple doses of prednisone, which was followed by improvement of serum biochemistry and sudden reappearance of serum HCV RNA. The patient was then started on ribavirin monotherapy, 400 mg/day, which was continued until 6 months ago, and maintenance immunosuppression was changed from cyclosporine A to tacrolimus.
In July 2004 the patient suffered of an episode of upper gastrointestinal (GI) bleeding of unknown origin at endoscopy, despite the presence of medium sized (F2) oesophageal varices. In the following 18 months she developed frequent diarrhoea, weight loss and severe anaemia, with faecal occult blood test repeatedly positive, reaching haemoglobin concentrations as low as 6.9 g/dl (normal range 13.6–17 g/dl), requiring multiple blood transfusions. Serology for cytomegalovirus (CMV) and Epstein–Barr virus (EBV) infections as well as focal culture and parasitological focal examinations were negative. At this stage maintenance immunosuppression was changed from tacrolimus to mycophenolate mofetil. An upper GI endoscopy confirmed the presence of oesophageal varices F2 and of a single sessile polyp in the stomach, 5 mm in diameter, which was removed. A colonoscopy and terminal ileoscopy were negative. Abdominal ultrasonography revealed slightly enlarged ileal walls (3.5 mm). The patient underwent multiple blood transfusions and intravenous infusion of iron and folates, resulting in only a transient improvement of the anaemia. Because of this clinical picture and a further episode of melena, a capsule endoscopy examination was performed in July 2006, which suggested the bleeding source to be in the jejunum; the recording showed, 17 minutes after starting (presumably in the proximal jejunum), a polypoid lesion, not bleeding at the moment of the exploration and, from the 25th to the 88th minute of recording, fresh blood in the absence of an identifiable mucosal lesion. The patient was therefore referred to undergo an SBE (Olympus, Tokyo, Japan), to confirm the diagnosis.
At admission to our hospital, the physical examination was negative and the haemoglobin concentration was 8.5 g/dl. Based on the results of the capsule endoscopy, the patient underwent push-and-pull enteroscopy (PPE) via the oral approach. The instrument consists of a high resolution videoendoscope 2 m long and a soft flexible overtube with one inflatable balloon attached to its distal end. Due to its extreme flexibility, the tip of the endoscope has a broad bending capability, which allows it to anchor to the small bowel wall without a balloon. Gripping the intestinal wall this way, the endoscope can be inserted further without forming redundant loops in the small bowel. In our patient, enteroscopic examination reached about 200 cm from the pylorus. On enteroscopy, gastric and duodenal mucosa appeared normal, while the small bowel had three polypoid lesions located in the jejunum, 5–15 mm in diameter. However, active bleeding was not observed from any of the polyps during the procedure. Only one polyp had ulcerations, which could account for the recent previous GI bleeding, thus requiring endoscopic treatment (). Treatment was achieved with an epinephrine injection and thermal coagulation with argon plasma coagulation (APC 2, Erbe, 40 W). No other lesions were detected in the length of small bowel that was explored. A biopsy sample taken from the hyperaemic mucosa of the polyps disclosed a pronounced eosinophilic infiltration (). Other specimens from the gastric antrum and duodenal bulb had no evidence of eosinophilic infiltration.
Endoscopic view of two different jejunal polyps (SBE-Olympus, Tokyo, Japan).
Jejunal mucosa showing intense eosinophilic infiltration (haematoxylin and eosin, (a) 200×; (b) 400×).