{
  "abstract": "A man in his 70s was admitted to a regional hospital with a 1-day history of upper abdominal pain and no other contributory history. Physical examination was unremarkable. Laboratory data revealed high near normal serum level of carcinoembryonic antigen (5.6 ng/mL, reference 0–5.0), but normal levels of carbohydrate antigen 19–9 (24.7 ng/mL, reference 0–37.0) and immunoglobulin G4 (12 mg/dL, reference 4–108). CT revealed peripancreatic effusion and a 30 mm low-density mass with weak enhancement in the pancreatic tail ( figure 1a, baseline CT), which had shrunk over time (figure 1b: 2 weeks later CT, figure 1c: 3 months later CT). There was no dilation of the main pancreatic duct. The weakly enhanced wall of the lesion had disappeared on 3 months CT. 3 months later, MRI revealed a mass lesion in the pancreatic tail that was low signal on T1 weighted imaging (figure 2a), isosignal on T2 weighted imaging (figure 2b), partially high signal on diffusion-weighted imaging (figure 2c) and magnetic resonance cholangiopancreatography revealed pancreas divisum (figure 2d). 4 months later, he was referred to our hospital for further examination of the lesion. Endoscopic ultrasonography revealed a hypoechoic lesion at the pancreatic tail, and fine needle aspiration was performed because imaging findings could not rule out a malignant pancreatic tumour. Histological findings revealed aggregation of foamy histiocytes and multinucleated cells (figure 3a, H&E staining), and immunohistochemistry revealed positive staining for CD68 (figure 3b, CD68 staining), leading to a diagnosis of xanthogranulomatous pancreatitis (XGP). He has been monitored annually with CT (figure 1d: 1 year later CT), and no recurrence has been observed. Xanthogranulomatous inflammation is a chronic inflammatory reaction microscopically characterised by aggregation of foamy histiocytes, fibrous tissue and infiltration of various inflammatory cells including multinucleated giant cells, neutrophils, lymphocytes and plasma cells.1 XGP is extremely rare, and its pathogenesis remains unclear2 3; however, it is likely caused due to a combination of ductal obstruction, infection, repeated haemorrhage or leakage of pancreatic juice resulting in a macrophage response. The imaging appearance of XGP is often non-specific and it is often difficult to differentiate XGP from other solid or cystic pancreatic masses. The weak enhanced wall of the lesion observed in our case may be a characteristic radiological finding of XGP as reported previously.4 The differential diagnosis for XGP includes mucinous cystic neoplasm, cystic neuroendocrine tumour, intraductal papillary mucinous neoplasm and solid pseudopapillary neoplasm. Most cases were treated surgically, and previous reports have shown no postoperative recurrence and a good prognosis.3 Consideration of benign diagnosis and guided biopsy can avoid unnecessary surgery.",
  "authors": [
    {
      "affiliations": [
        "Gastroenterology, Iwate Prefectural Central Hospital, Morioka, Japan"
      ],
      "name": "Atsushi Ikehata"
    },
    {
      "affiliations": [
        "Division of Gastroenterology and Hepatology, Department of Internal Medicine, Iwate Medical University School of Medicine, Morioka, Japan"
      ],
      "name": "Shunsuke Honta"
    },
    {
      "affiliations": [
        "Pathology, Iwate Prefectural Central Hospital, Morioka, Japan"
      ],
      "name": "Sadahide Ono"
    }
  ],
  "title": "Xanthogranulomatous pancreatitis mimicking a pancreatic tail tumour",
  "uid": "58e39e82-bab1-5d92-9a9b-68e77275c34f"
}