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[Advertorial] Does your patient with diabetes have gastrointestinal symptoms? A PERT-inent question to ask

Mike Cummings
A piece looking at the importance of being alert to pancreatic exocrine insufficiency in people with diabetes and exploring management considerations.

Production of this advertorial has been funded by Mylan. Mylan have had no input into the content but have reviewed for factual accuracy only.

How often as a health care professional do you hear a person with type 2 diabetes mention in passing about gastrointestinal (GI) symptoms? When this happens, how often do you attribute the symptoms to their medications, such as metformin? How often do you ask that person spontaneously as part of their diabetes review about GI symptoms? If this is not something you typically do, it is worth considering that GI symptomatology such as loose motions, flatulence and vague abdominal pain are very common in diabetes, and over 80% of people with this condition may report them.1 It is also worth considering that where these symptoms are present, they are frequently not mentioned to the diabetes health care professional since they are deemed irrelevant to the management of the condition. 
All of this means that we may be missing a vital piece in the puzzle of diabetes care. Pancreatic exocrine insufficiency (PEI) may be the underlying cause of patients’ GI symptoms in around 25% of cases.2 Damage to the exocrine pancreas is associated with symptoms due to reduced availability of pancreatic enzymes such as lipase that are crucial for nutrient absorption. Whilst steatorrhoea (described as fatty, smelly motions that are difficult to flush away) and weight loss are the hallmark symptoms of PEI, they only occur in severe cases. More commonly observed are the often relatively mild GI symptoms referred to above. To help describe motion types, the Bristol Stool Chart is a useful guide (types 5, 6 and 7 would raise suspicion about the condition).3 Previously, complex tests were typically used by GI specialists to diagnose the condition; these included 3-day faecal fat collections and the pancreolauryl test. These days it is much easier to test for PEI and assessment can be done within primary care. A faecal elastase measurement of less than 200 μg/g in the presence of symptoms is consistent with a diagnosis of PEI and severe cases are associated with a level less than 100 μg/g.4
Once the diagnosis is made, some individuals may need referral to a specialist because of concerns about alternative diagnoses such as pancreatic cancer or recurrent pancreatitis, which may be evident from the medical history. The majority of the cases, however, are related to diabetes. There are a number of proposed mechanisms to account for this including reduced pancreatic blood supply, a specific neuropathy affecting the pancreas or hormonal and peptide changes.5 Alternatively, the individual may have another pathology such as chronic pancreatitis that is responsible for causing both diabetes and PEI (so-called type 3c diabetes).6
Having established a diagnosis of diabetes-related PEI, it is possible to manage the condition within primary care through the use of pancreatic enzyme replacement therapy (PERT).7 A typical regimen would be 50000 units of PERT with meals and 25000 units of PERT with snacks. This resolves GI symptoms in the majority of cases but sometimes it may be necessary to double the dose of PERT or add in a proton pump inhibitor, which reduces the gastric acid release that may be responsible for attenuating the benefits of pancreatic enzyme supplementation. Another potential benefit of PERT may lie in an impact upon metabolic control. Some studies have suggested an improvement of glycaemic control in individuals with diabetes and PEI, such as reduced HbA1c and hypoglycaemic episodes,8,9 alongside resolving GI symptoms.
In summary, it behoves us to enquire about the presence of GI symptoms in our patients with diabetes. PEI is common and we have the tools to diagnose and treat the majority of individuals with this condition within primary care. The trick is to remember to ask them as part of our holistic approach to diabetes management.



1  Gustafsson RJ (2011) Esophageal dysmotility is more common than gastroparesis in diabetes mellitus and is associated with retinopathy. Rev Diab Stud 8: 268–75.
Cummings MH et al (2015) Gastrointestinal symptoms and pancreatic exocrine insufficiency in type 1 and type 2 diabetes. Pract Diabetes 32: 54–8.
3  Lewis SJ et al (1997) Stool form scale as a useful guide to intestinal transit time. Scand J Gastroenterol 32: 920–4.
4  Loser C et al (1996) Faecal elastase 1: a novel highly specific and sensitive tubeless pancreatic function test. Gut 39: 580–6.
5  Hardt PD and Ewald N (2011) Exocrine pancreatic deficiency in diabetes mellitus. Exp Diabetes Res 2011: 761950.
6  Hardt PD et al (2008) Is pancreatic diabetes (type 3c diabetes) underdiagnosed and misdiagnosed? Diabetes Care 31(Suppl 2): S165–S169.
7  Domínguez-Muñoz JE (2011) Pancreatic exocrine insufficiency: Diagnosis and treatment. J Gastro-enterol Hepatol 26: 12–16.
8  Ebert R and Creutzfeldt W (1980) Reversal of impaired GIP and insulin secretion in patients with pancreatic steatorrhea following enzyme substitution. Diabetologia 19: 198–204.
9  Ewald N et al (2007) Pancreatin therapy in patients with insulin-treated diabetes mellitus and exocrine pancreatic deficiency according to low fecal elastase 1 concentrations. Diabetes Metab Res Rev 23: 386–91.

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