
Pancreatic exocrine insufficiency is failure of the pancreas to produce enough enzymes to achieve normal digestion. This is caused by a disease in the pancreas or an issue with digestion that prevents the pancreas from being stimulated properly. This causes deficiencies in both macro and micro nutrients.
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Multiple micronutrient feficiencis can occur, as well as the more general nutritional debilitation which may impact physical activity levels, poor wound healing and increase rehabilitation times.
Untreated or undertreated pancreatic exocrine insufficency is associated with osteoporosis, significantly increased fracture rates and sarcopenia, which is independelty associated with poor survival.
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Pancreatic exocrine insufficiency is treated by the prescription of pancreatic enzyme replacement
therapy. These capsules or tablets contain a mixture of enzymes, proteases to digest proteins, liapases
to digest lipids and amylases to digest carbohydrate.
It is important that patients understand how their pancreatic enzymes work in order to dose properly
and to help optimise compliance and timing of administration.
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When you start a patient on pancreatic enzyme replacement therapy, the recommended starting dose is fifty thousand units of lipase with meals and twenty five thousand units with snacks. Some patients snacks will be bigger than their meals and some patients will graze throughout the day or take oral nutritional supplements. So it’s important that their dose is adjusted to allow for that.
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If patients symptoms have improved but not completely resolved, it’s necessary to increase the dose. Once you’ve done this, the symptoms should continue to get better. Patients with pancreatic exocrine insufficiency are predisposed to other GI conditions, so if their symptoms aren’t improving with dose escalation, it’s important that you look for other causes.
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Some patients who are prescribed pancreatic enzyme replacement therapy are unable to swallow the capsules. In this instance, it is acceptable to open the capsule. But there are a couple of important factors that patients need to be aware of. Because these are proteolytic enzymes. If they are exposed and activated within the mouth, they can cause damage to the oral mucosa, particularly around the gums or under dentures. So it’s important that the enzymes are not chewed. We don’t recommend that they’re sprinkled on food, but instead mixed in with a small acidic puree such as apple or pear puree, swallowed immediately and then the mouth rinsed with water and that water swallowed.
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It’s important to remember that patients who have pancreatic disease, a sudden change in pancreatic function such as severe insufficiency occurring very rapidly or a new onset of diabetes may be considered a red flag symptom for deterioration in their disease and patients with even benign disease of the pancreas are more susceptible to developing pancreatic cancer. So it’s important to look out for red flag symptoms.
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Capsules containing 10000 units of lipase are small and easy to take so are useful for those patients who struggle to swallow capsules. However, the pill burden can be overwhelming. To reduce the pill burden and patients can be transitioned onto the highest strength capsules containing 25000 units of lipase. It is Important when you transition patients from one strength capsule to another, that you make sure the dose is equivalent.
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Every patient needs a different dose of enzymes to digest their meal. Having started enzymes, it’s often the case that the dose isn’t adequate and the patient may suffer on-going symptoms. If the patient is experiencing on-going bowel symptoms and consider doubling the dose of enzymes and potentially adding in a proton pump inhibitor (PPI).
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References
- Smith RC, Smith SF, Wilson J, Pearce C, Wray N, Vo R, et al. Australasian Pancreatic Club, October 2015.pp 1-122.
- Dumsay V, Delhaye M, Cotton F. et al. Am J Gastroenterol. 2004; 99:1350-4.
- Domínguez-Muñoz JE. J Gastroenterol Hepatol. 2011;26(Suppl 2):12-16.
- Walkowiak J, Lisowska A, Przyslawski J. et al. Acta Paediatr. 2004; 93:1042-5.
- Domínguez-Muñoz JE. HPB (Oxford). 2009; 11(Suppl 3):3-6.
- lcks A, Haastert B, Giani G, et al. Gastroenterol. 2001; 39:823-30.
- Rathmann W, et al. Scand J Gastroenterol. 2001; 36:1056-61.
- Maconi G, et al. Dig Dis Sci. 2008; 53:262-70.
- Leeds JS, Hopper AD, Huristone DP, et al. Aliment Pharmacol Ther. 2007; 25:265-71.
- Leeds JS, Hopper AD, Sidhu R, et al. Clin Gastroenterol Hepatol. 2010; 8:433-8.
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