History of a penetrating duodenal ulcer as a cause of acute necrotizing pancreatitis.

438 Figure S1A–C). After 3 months, control contrastenhanced computed tomography (CECT) demonstrated complete regression of the WOPN; therefore, the transmural stent was removed. After 1 year of follow-up, no recurrence of collection was detected on CECT. Control gastroduodenoscopy demonstrated a diverticulum of the duodenal bulb (diameter, 3 cm) where the penetrating ulcer had previously been positioned (FIGURE 1B; Supplementary material online, Figure S1D–F). The patient is now in a good general condition and has regained full physical fitness and the ability to perform everyday activities. Cholelithiasis and excessive alcohol consumption are the most common causes of AP, accounting for about 80% of cases.2 Idiopathic AP is diagnosed in approximately 10% of patients.2 Other rarer causes of AP include iatrogenic factors, use of some medicines, abdominal injuries, malformations of the pancreas, hereditary gene mutations, hypercalcemia, and hypertriglyceridemia.2,3 A penetrating peptic ulcer is a very rare cause of AP.2-5 AP can lead to local consequences, in the form of pancreatic and peripancreatic fluid collection. According to the revised Atlanta classification, there are 4 types of fluid collection, which are distinguished by the duration and morphology To the Editor In the 9/2015 issue of the Polish Archives of Internal Medicine (Pol Arch Med Wewn), we published a clinical image titled “Penetrating duodenal ulcer as a cause of necrotizing pancreatitis”, where we described a case of a female patient with a penetrating duodenal ulcer as a rare cause of acute pancreatitis (AP).1 The consequence of acute necrotizing pancreatitis in this case was primary sterile walled-off pancreatic necrosis (WOPN), which became infected after transgastric passive drainage at another medical center. The patient was admitted to our department for continued endoscopic treatment owing to infection at the WOPN. During gastroduodenoscopy, a perforation of the penetrating duodenal ulcer (diameter, 3 cm) was detected, which was determined to be the cause of AP. Communication between the lumen of the gastrointestinal tract and that of the necrotic cavity through the duodenal ulcer was confirmed. A nasocystic drain was guided through this perforation into the necrotic cavity. After 7 days of active transduodenal drainage, the WOPN gradually improved. The nasocystic drain was removed; however, the transmural endoprosthesis that was inserted into the necrotic area through the peptic ulcer perforation was retained to prevent recurrence of necrotic collection (FIGURE 1A; Supplementary material online, LETTER TO THE EDITOR