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Exocrine pancreatic insufficiency

The exocrine pancreas contains clusters of acini producing bicarbonate anion, a mild alkali, as well as an array of digestive enzymes that together empty by way of the interlobular and main pancreatic ducts into the duodenum.

Exocrine pancreatic insufficiency (EPI) is the inability to properly digest food due to a lack of digestive enzymes made by the pancreas. 

EPI is prevalent in many condition: as cystic fibrosis,[Shwachman–Diamond syndrome, different types of pancreatitis, multiple types of diabetes mellitus (Type 1 and Type 2 diabetes), advanced renal disease, older adults, celiac disease, IBS-D, IBD, HIV, alcohol-related liver disease, Sjogren syndrome, tobacco use, and use of somatostatin analogues.

It is caused by a progressive loss of the pancreatic cells that make digestive enzymes.

The loss of digestive enzymes leads to maldigestion and malabsorption of nutrients from normal digestive processes.

The most common causes of EPI are likely related to diabetes (10.5% global prevalence of diabetes, with EPI rates of ranging from 30-50% in Type 1 and 20-30% of Type 2 and IBS-D (7.6-10.8% global prevalence of IBS-D, with EPI rates around 5-6%.

Other causes of EPI include acute or chronic pancreatitis and cystic fibrosis, Crohn’s disease, ulcerative colitis, celiac, advanced renal disease, older age, IBD, HIV, alcohol-related liver disease, Sjogren’s syndrome, tobacco use, and use of somatostatin analogues.

EPI can also occur in 10-20% of the general population.

The hormones cholecystokinin and secretin secreted by the stomach and duodenum in response to distension and the presence of food in turn stimulate the production of digestive enzymes by the exocrine pancreas.

The alkalization of the duodenum neutralizes the acidic chyme produced by the stomach that is passing into it.

Digestive enzymes catalyze the breakdown of complex foodstuffs into smaller molecules for absorption and integration into metabolic pathways.

The pancreatic enzymes include: proteases (trypsinogen and chymotrypsinogen), hydrolytic enzymes that cleave lipids (the lipases phospholipase A2 and lysophospholipase, and cholesterol esterase), and amylase to digest starches. 

EPI results from progressive failure in the exocrine function of the pancreas to provide its digestive enzymes.

 genetic condition or other disease state, results in the inability to properly digest food.

Loss of pancreatic enzymes leads to maldigestion and malabsorption.

Symptoms of exocrine pancreatic insufficiency include:

Abdominal discomfort or pain

Bloating

Diarrhea

anemia (Vitamin B12, iron, folate deficiency)

bleeding disorders (Vitamin K malabsorption)

edema (hypoalbuminemia)

fatigue

flatulence and abdominal distention (bacterial fermentation of unabsorbed food)

hypocalcemia

metabolic bone disease (Vitamin D deficiency)

neurologic manifestation

steatorrhea

weight loss

Chronic pancreatitis is the most common cause of EPI.

EPI causes symptoms even before reaching the stages of malnutrition.

The exocrine pancreas is stimulated to produce digestive enzymes by the hormones cholecystokinin and secretin secreted by the stomach and duodenum in response to distention in the presence of food.

Duodenal alkanization neutralizes the acidic chyme produced by the stomach that is passing into it.

Pancreatic digestive enzymes catalyze the breakdown of complex foodstuffs into smaller molecules for absorption and integration into metabolic pathways.

Such enzymes include proteases (trypsinogen and chymotrypsinogen), hydrolytic enzymes that cleave lipids (the lipases phospholipase A2 and lysophospholipase, and cholesterol esterase), and amylase to digest starches. 

EPI results from progressive failure to provide its digestive enzymes, often in response to a genetic condition or other disease state, resulting in the inability to properly digest food.

The loss of pancreatic enzymes leads to maldigestion and malabsorption, which may in turn lead to:

anemia (Vitamin B12, iron, folate deficiency)

bleeding disorders (Vitamin K malabsorption)

edema (hypoalbuminemia)

fatigue

flatulence and abdominal distention by bacterial fermentation of unabsorbed food

hypocalcemia

metabolic bone disease due to Vitamin D deficiency

neurologic manifestations

steatorrhea

weight loss

The most common causes of EPI are chronic pancreatitis and cystic fibrosis.

DIAGNOSIS:

The three main tests used in considering a diagnosis of EPI are: fecal elastase test, fecal fat test, and a direct pancreatic function test.

Exocrine pancreatic function can be assessed by fecal elastase-1 measured in a single stool sample and quantitative fecal fat measured in stool collected over a period of 48 to 72 hours following a diet of 100 g of fat daily.

Elastase levels of less than 50 µg per gram or reasonably predictive of steatorrhea.

Mild or moderate EPI is present when fecal elastase levels are <200 ug/g, whereas ‘severe’ EPI is considered to be when fecal elastase levels is <100 ug/g.

Pancreatic function test assesses exocrine function in the pancreas by inserting a tube into the small intestine to collect pancreatic secretions.

TREATMENT: 

Pancreatic enzyme replacement products (PERPs) such as pancrelipase, that are used to break down fats, proteins, and carbohydrates into units that can be digested.

Treatment with pancreatic enzyme replacement mitigates steatorrhea and are indicated if there is elevated fecal elastase levels, low micronutrient levels, and fecal fat levels.

Approve enzymes are of porcine in  origin, and most the coated to delay degradation by gastric acid.

Pancrelipase is typically porcine derived.

 Over-the-counter options also exist, including those made with plants and other non-porcine materials. 

Pancrelipase is considered to be safe, effective, and tolerable for people with EPI.

Nutrient deficiencies can be caused by EPI.

Because of malabsorption, serum levels of cyanocobalamin (vitamin B12) and tocopherol (vitamin E) may be low. 

 

 

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