Thank you for sending us the letter written by Bolaman and colleagues commenting on our article “Plasmapheresis in asparaginase-induced pancreatitis.” We read carefully the comments and we hereby reply to them:

First, we would like to draw your attention to add the citation of our article in the reference section; our article is mentioned in the text but the reference is missing.

Second, we never expected the comments to be regarding the diagnosis issue or suspecting an alternative diagnosis to acute pancreatitis. Bolaman and coworkers wanted to rule out typhlitis and mucositis first before making the diagnosis of pancreatitis. We would like to draw the author's attention to the fact that the differential diagnosis of typhlitis, mucositis, and even gastroenteritis was ruled out clinically, by laboratory testing, and radiologically.

We start with typhlitis: This diagnosis was ruled out by the computed tomography (CT) findings. The most common CT finding in typhlitis is cecal wall thickening, which is either isodense to surrounding normal gut or of lower density, reflecting edema. Additionally, pericolonic inflammation may be demonstrated by increased attenuation of the adjacent fat and thickening of fascial planes. Our patient had normal CT findings. We would also like to add that the work-up done, including stool studies that were normal, was not mentioned in the article because we wanted to focus on the relevant tests done.

As for mucositis, the patient came to the emergency department with the mentioned complaint and he never complained of any pain involving the whole gastrointestinal (GI) tract except for the localized left abdominal pain. He could also eat without any GI pain, although he was vomiting; he did not have oral mucositis, which is usually the first finding in patients with neutropenia complaining of mucositis symptoms.

The clinical findings and physical examination support the diagnosis of pancreatitis: abdominal pain localized to the left quadrant, nausea, and vomiting (even bloody diarrhea can accompany acute pancreatitis). In addition, the elevated serum lipase level supports our diagnosis, although the amylase was normal. We have discussed this point extensively in the article and we referred to the article by Ridola and colleagues for that purpose. More importantly, the diagnosis of acute pancreatitis is made in the setting of abdominal pain, elevated lipase, and hypertriglyceridemia. We add to this that the patient improved clinically after the plasmapheresis procedure and after the triglyceride level dropped, which further supports the diagnosis of acute pancreatitis.

We thank you again and we are ready to reply to any further questions.