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.
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.
