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Recurrent Acute Pancreatitis following Colonoscopic Fecal Microbiota Transplantation for Ulcerative Colitis
Address for correspondence Avnish Kumar Seth, MBBS, MD, DM, Gastroenterology and Hepatobiliary Sciences, Fortis Memorial Research Institute, Sector 44, Gurugram, Haryana 122002, India. (e-mail: akseth2003@yahoo.com)
This article was originally published by Thieme Medical and Scientific Publishers Pvt. Ltd. and was migrated to Scientific Scholar after the change of Publisher.
Abstract
A 37-year-old man with corticosteroid-dependent ulcerative pancolitis was taken up for colonoscopic fecal microbiota transplant (FMT). Preparation for colonoscopy was done with 118 g polyethylene glycol (PEG) in 2 L water ingested over 2 hours, followed by clear fluids. 200 g of screened donor stool, blended with water was instilled into terminal ileum; cecum; and ascending, transverse, and descending colon. Eighteen hours following ingestion of PEG and 2 hours following FMT, he complained of severe epigastric pain with radiation to back. Serum lipase was 6,756 U/L. He was managed with intravenous (IV) fluids and symptomatic treatment with discontinuation of corticosteroids and 6-MP. Ultrasound did not reveal gall bladder stones or sludge. There was no history of alcohol intake. Contrast-enhanced computed tomography scan at 48 hours showed bulky pancreas with peripancreatic stranding. He recovered over a week with normalization of lipase. Three weeks later he again reported severe epigastric pain 14 hours following ingestion of PEG, this time prior to colonoscopic FMT. Serum lipase was 1,140 U/L; the procedure was deferred and he recovered with symptomatic treatment over 3 days. Maintenance colonoscopic FMT was performed 4 times over the following 2 years with sodium phosphate preparation with no recurrence of pain. MRCP showed no evidence of chronic pancreatitis. He remains in clinical and endoscopic steroid-free, thiopurine-free remission. PEG is a rare cause of acute pancreatitis and merits consideration in appropriate clinical setting.
Keywords
fecal microbiota transplantation
acute pancreatitis
polyethylene glycol
Introduction
Several randomized control trials and meta-analysis suggest that patients with ulcerative colitis (UC) may benefit from fecal microbiota transplantation (FMT).1 We describe a patient who developed recurrent acute pancreatitis (AP) following colonoscopic FMT.
Case Report
A 37-year-old man with corticosteroid-dependent UC for 1 year was taken up for colonoscopic FMT. He was receiving prednisolone 20 mg, 6-mercaptopurine 50 mg, and 5-aminosalicylates 3.6 g daily and his Mayo score was five. Preparation for colonoscopy was done with 118 g polyethylene glycol (PEG) in 2 L water over 2 hours, followed by clear fluids. Eighteen hours following ingestion of PEG and 2 hours following FMT, he complained of severe epigastric pain with radiation to back. There was marked epigastric tenderness. Serum lipase was 6,756 U/L and ultrasound showed normal gallbladder and common bile duct. There was no history of alcohol intake. He was managed with intravenous (IV) fluids, pantoprazole, and tramadol. Corticosteroids and 6-MP were discontinued. Contrast-enhanced CT scan at 48 hours showed bulky pancreas with peripancreatic stranding (Fig. 1). He recovered over 1 week with normalization of lipase. Three weeks later, he again reported severe epigastric pain, 14 hours following ingestion of PEG, this time prior to colonoscopic FMT. Serum lipase was 1,140 U/L. FMT was deferred and he recovered over 3 days with symptomatic treatment. Maintenance colonoscopic FMT was performed four times over the following 2 years with oral sodium phosphate preparation, with no recurrence of pain. MRCP showed no evidence of chronic pancreatitis. He remains in clinical and endoscopic steroid-free, thiopurine-free remission on maintenance FMT protocol.
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Fig. 1 Contrast-enhanced computed tomography scan showing diffuse pancreatic edema and peripancreatic fat stranding, suggestive of acute pancreatitis. Incidental large left renal cyst is also noted.
Discussion
Causes of AP in a setting of UC include gallstones and drugs like corticosteroids and thiopurines.2 A Danish cohort study of 15,526 patients, showed four times increased risk of AP in Crohn’s disease and two times higher risk in UC as compared with general population.3 There was no history of alcohol intake or metabolic cause of pancreatitis in our patient. Pancreatitis has also reported due to PEG.4 Postulated mechanisms include stimulation of pancreatic secretions due to gastric distension and reflux of high-pressure duodenal contents into pancreatic duct. Pancreatitis has also been described following colonoscopy, possibly due to trauma to the pancreas while negotiating splenic flexure.5 There are no reports linking AP to FMT. The temporal relation between use of PEG and onset of AP, symptom cessation with discontinuation, recurrence after re-exposure to PEG, no recurrence of AP during subsequent FMT without use of PEG, and no evidence of chronic pancreatitis at MRCP suggest PEG-induced recurrent AP. We did not test for genetic mutations like cationic trypsinogen (PRSS1), CFTR, SPINK1, and CTRC that have been linked with AP.
Conflict of Interest
None declared.
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