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Is Pancreatic Exocrine Insufficiency in Celiac Disease Tied to Changes in Pancreatic Parenchyma?
Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.View all articles by Jefferson Adams
What's the connection between pancreatic exocrine insufficiency in celiac disease and changes in pancreatic parenchyma?
Photo: CC--Véronique Debord-Lazaro
Celiac.com 11/09/2016 - Although exocrine pancreatic insufficiency (EPI) has been reported in a number of patients with celiac disease (CD), it is not clear if this is primarily a functional or a structural defect. We studied pancreatic structural abnormalities by endoscopic ultrasound (EUS) in adult CD patients with EPI.
A team of researchers recently set out to prospectively assess pancreatic exocrine function in recently diagnosed celiac patients. The research team included Surinder S. Rana, Arvind Dambalkar, Puneet Chhabra, Ravi Sharma, Vishal Sharma, Satyavati Rana, Deepak K. Bhasin and Ritambhra Nada. They are variously affiliated with the Department of Gastroenterology, and the Department of Histopathology at the Post Graduate Institute of Medical Education and Research (PGIMER) in Chandigarh, India.
For their study, the team measured fecal elastase to prospectively assess pancreatic exocrine function in 36 recently diagnosed celiac patients. They relied on EPI by EUS and elastography to assess pancreatic structural changes in celiac patients. The team then reassessed exocrine functions in these patients after 3 months of gluten-free diet.
Of the 36 celiac patients the team studied, 30 patients had anemia, 21 had diarrhea, and 7 had hypothyroidism. Ten patients had EPI with mean elastase levels of 141.6 μg/g of stool, only one of whom had a history of recurrent acute pancreatitis, while the other 9 patients had no history of either acute or chronic pancreatitis. Of these 10 patients, 8 (80%) had diarrhea, 8 (80%) anemia, and 2 (20%) had hypothyroidism.
The team performed EUS in 8 patients. Five showed normal pancreas, 3 showed hyperechoic strands, and 2 patients showed hyperechoic foci without shadowing. None showed lobularity or parenchymal calcification. All patients, except the patient with recurrent pancreatitis, showed normal strain ratio. In 6 of the remaining 7 patients, follow-up fecal elastase fell within normal range.
EPI, as measured by fecal elastase levels in adult celiac patients, possibly does not relate to structural alterations in the pancreatic parenchyma, and may be reversible by following a gluten-free diet.
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