Background: type II and eosinophilic pancreatitis are two rare etiologies of pancreatitis, with an uncertain pathophysiology. The diagnosis may be challenging, especially because no clear cut-off of eosinophilic infiltration has been identify for the differential diagnosis, and it is still debated if they can be considered two separate diseases.
Case report: This is a case of a 19-year-old male who was admitted to our hospital for acute pancreatitis in July 2025 (acute abdominal pain, serum lipase up to 6857 mg/dl, and an enlarged edematous pancreatic gland at transabdominal ultrasound). The patient had a history of pollen allergy, recurrent episodes of diarrhea, a perforated duodenal ulcer with a need for a surgical raffia two months earlier, and a recent diagnosis of eosinophilic esophagitis with an ongoing treatment of proton pump inhibitors (PPI) twice a day.
The patient underwent a CT-scan 72 hours later, which showed a diffuse edema of the pancreatic gland without signs of necrosis. Therefore an MRI and CP-MRI were performed, confirming an enlargement of the body-tail of the pancreas, with an inhomogeneous contrast captain and an area of hypo-perfusion at the tail. The was no dilation of the biliary tree, no gallbladder stones. Serum eosinophils, triglycerides, Ig-G4, and anti-nucleus antibody (ANA) were negative, while elevated values of fecal calprotectin (790 g/g) were found.
Therefore, we decided to perform an endoscopic ultrasound (EUS) showing a diffuse enlargement of the pancreatic parenchyma, with a diffusely hypoechoic echostructure, with hyperechoic strands and dilation of secondary ducts, without evidence of cystic or solid lesions. A heterogeneous enhancement was observed at contrast agent evaluation. A fine needle biopsy (FNB) was performed by using a 19 G needle. The histological examination was suggestive of type 2 autoimmune pancreatitis (perilobular fibrosis and parenchymal and periductal and perivascular lymphomonocytic and plasmacell inflammation, rare granulocytic epithelial lesion), although a significant eosinophilic infiltration was also observed.
The diagnostic work-up was completed with an esophagogastroduodenoscopy (EGDS), which showed signs of esophagitis and a diffuse gastritis, and a colonoscopy that demonstrated the presence of right-sided colitis. At histological examinations an eosinophilic infiltration extending to the esophagus, duodenum, and colon was found, providing a diagnosis of eosinophilic enteritis.
A multidisciplinary evaluation, including Immunologists, in a referral Center was done, concluding that this may represent a case of association of type II autoimmune pancreatitis and eosinophilic gastroenteritis, rather than a eosinophilic pancreatitis. A systemic therapy with steroids was started with a rapid clinical and biochemical amelioration.
Conclusions: this is a rare case of association of type II pancreatitis and eosinophilic gastro-enteritis. However, more defined criteria are needed for a better establishment of eosinophilic pancreatitis and type II pancreatitis.