Diabetes
Patients with different types of diabetes mellitus frequently show alterations in pancreatic morphology and exocrine function. PEI can therefore occur as a result of long-standing type 1 and type 2 diabetes or can be related to the development of diabetes in chronic pancreatitis.1,2
- In a recent audit, 24% of patients with diabetes had abnormal stools (score 5 on the Bristol Stool Chart), steatorrhoea or unexplained weight loss3
- 42% of symptomatic patients who provided a stool sample had FE-1 levels indicative of PEI3
One study examined the efficacy of Creon® in patients with tropical calculous pancreatitis, a form of chronic pancreatitis largely attributed to malnutrition that’s prevalent in India and other Afro-Asian countries in which patients present with abdominal pain, pancreatic calculi and insulin-resistant diabetes.4
After 6 months of Creon® treatment patients achieved better control of diabetes, improvement in nutrition, and overall improvement in quality of life.4 This included a significant reduction in post-prandial plasma glucose and glycosylated haemoglobin at six months vs. baseline.5
Significant reduction in post-prandial plasma glucose and glycosylated haemoglobin at baseline vs. 6 months treatment with Creon® (total dose 8,000 lipase units)4
Adapted from Mohan V et al. Int J Pancreatol. 1998.
Furthermore, these patients showed significant improvements in PEI symptoms, including the following:4
Coeliac disease
Pancreatic exocrine insufficiency can be observed in up to 40% of patients with coeliac disease. In a prospective, longitudinal follow-up study of adult coeliac patients with PEI, 90% of patients who received pancreatin were found to have significant long-term improvements in their chronic diarrhoea. This was demonstrated by a reduction in stool frequency (p ≤ 0.0001). These patients also reported subjective improvements in both consistency and urgency, and a significant symptomatic benefit.6,7
References
- Hardt PD, Ewald N. Exp Diabetes Res. 2011; doi: 10.1155/2011/761950. Epub 2011 Aug 1.
- Ewald N et al. World J Gastroenterol. 2013; 19(42):7276-7281
- Cummings MH et al. Practical Diabetes 2015; 32(2): 54-58.
- Mohan V et al. Int J Pancreatol. 1998; 24(1): 19-22.
- Ewald N et al. Diabetes Metab Res Rev. 2007; 23: 386-91.
- Evans KE et al. Dig Dis Sci. 2010; 55: 2999-3004.
- Keller J et al. Gut 2005; 54(Suppl 6): 1–28
- Lohr JM. United Eur Gastroenterol J. 2013; 1(2): 79-83.
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