This insightful paper just published in the journal Clinical Gastroenterology and Hepatology sheds light on why some patients may have persistent diarrhea even when they have no infection, are avoiding allergic foods, and not under unusual stress. The authors begin by observing…

“Patients with irritable bowel syndrome (IBS) might have other underlying pathologies. Pancreatic disease can be elusive—especially in the early stages, and some symptoms overlap with those of IBS. We evaluated the prevalence of exocrine pancreatic insufficiency in diarrhea-predominant IBS (D-IBS) and assessed the effects of pancreatic enzyme supplementation.”

Their study compared patients with chronic diarrhea who met the criteria for D-IBS with a control group without diarrhea for stool frequency, stool consistency and fecal elastase-1 (Fel-1, also called pancreatic elastase 1), a definitive metric for the production of pancreatic digestive enzymes. What did their data show?

“Fel-1 levels were less than 100 μg/g in stool from 19 of 314 patients with D-IBS (6.1%)…and none of 95 controls. After enzyme supplementation, improvements in stool frequency and abdominal pain were observed in patients in group 1 (D-IBS, but not in group 2.”

This result shows that pancreatic enzyme insufficiency may not be the most common cause of chronic diarrhea but it is important to not overlook.

“Pancreatic exocrine insufficiency was detected in 6.1% of patients who fulfilled the Rome II criteria for D-IBS. In these patients, pancreatic enzyme therapy might reduce diarrhea and abdominal pain. Pancreatic exocrine insufficiency should be considered in patients with D-IBS.”

How reliable is fecal pancreatic elastase for diagnosing exocrine (secreting directly or through a duct) pancreatic enzyme deficiency? The authors of this study published in the Journal of Gastroenterology asked the same question. Their conclusion:

“Fecal pancreatic elastase is a reproducible marker for severe exocrine pancreatic insufficiency. This test is valuable for longitudinal follow-up of exocrine pancreatic function.”

This is convenient because fecal pancreatic elastase is part of our regular gastrointestinal function profile. But we still have to ask, “What are the underlying causes of the loss of ability for the pancreas to produce adequate digestive enzymes?” Besides well-known conditions including cystic fibrosis and certain malignancies, idiopathic (cause unknown) chronic pancreatitis (ICP) is a big category. How often may this be an autoimmune condition?

The authors of another paper published earlier in Clinical Gastroenterology and Hepatology looked into this.

“The proportion of patients with idiopathic chronic pancreatitis (ICP) that have an autoimmune origin is unknown. Three forms of ICP have been described: pseudotumoral, duct-destructive, and usual chronic pancreatitis. The aim of this study was to identify autoimmune stigmata in the 3 forms.”

What did their data show?

“Clinical or biochemical autoimmune stigmata are present in 40% of patients with ICP. Autoimmune mechanisms may be frequent in idiopathic pancreatitis.”

Readers here will not be surprised by this fact considering how common autoimmune conditions have become. Is this a concern for the many people who are sensitive to gluten? Is it possible for people with gluten sensitivity to have persistent diarrhea due to pancreatic insufficiency even after they are no longer eating gluten? The authors of this paper published in the journal Alimentary Pharmacology & Therapeutics asked that question having been compelled by this observation:

“Patients with coeliac disease may have diarrhoea despite being on a gluten-free diet.”

They set about their investigation with this aim:

“To assess whether exocrine pancreatic insufficiency causes persisting symptoms compared with controls, we determined whether pancreatic enzyme supplementation provided symptomatic benefit in coeliac patients with chronic diarrhoea.”

What conclusion did their data lead them to?

“Low faecal elastase is common in patients with coeliac disease and chronic diarrhoea, suggesting exocrine pancreatic insufficiency. In this group of patients, pancreatic enzyme supplementation may provide symptomatic benefit.”

Importantly, they also observed that stool frequency reduced from 4 times per day to 1 time per day in 18 of 20 subjects who were given pancreatic enzyme supplementation.

If you’re thinking now that the pancreas is one of the many possible targets for an autoimmune attack with gluten sensitivity, yet another paper published in Clinical Gastroenterology and Hepatology would confirm your suspicion. Elevated pancreatic enzymes in the serum result from destruction of pancreas cells…

“We demonstrated a frequency of about 25% of elevated pancreatic enzymes values in CD (celiac disease) patients, including subjects without gastrointestinal manifestations and apparently asymptomatic subjects. The finding of elevated serum amylase or lipase level, in the absence of signs of pancreatic disease, would appear to suggest a need to screen for celiac disease.”

Another paper published in the World Journal of Gastroenterology reviews the various causes of idiopathic pancreatitis and agrees:

“Intriguingly, recurrent pancreatitis can be caused by celiac disease. The mechanism appears to be duodenal inflammation and associated papillary stenosis causing pancreatitis.”

Important: Consuming gluten for years without knowing (or ignoring) that you have a gluten sensitivity can result in the irretrievable loss of tissues subject to autoimmune attack and their function (such as the cells of the pancreas that produce enzymes). The sooner you find out and adhere to avoidance the better.

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