Abstract
Objective: To assess the prevalence of pancreatic exocrine insufficiency (PEI) inpatients with diabetes mellitus (DM). Design: Meta-analysis of prospective, observational studies that used fecal elastase-1 estimation to determine PEI in patients with DM. Data extraction: A total of 11 studies out of 1156 retrieved references, published between 2000 and 2013, fulfilled the inclusion criteria. The primary outcome measure was proportions of patients with DM and PEI. Results: Of the 2891 patients enrolled, 921 (31.8%) showed abnormal (i.e, 100 but <200 μg/g) in elastase-1 excretion. In 921 patients with type-1 DM, the weighted rate of PEI was 37.7% (CI 27.2-49.5), and 26.2% (CI 19.4-34.3) in 1970 type-2 diabetic patients, a difference of 11.5% (p=0.09). Of patients with abnormal (<200 μg/g) fecal elastase-1 concentrations, severe PEI was present in 53.4% (CI 45.2-61.4) of type-1, and in 50.3% (CI 40.7-59.9) of type-2 diabetic patients. Limitation: Some variables, which may influence fecal elastase-1 excretion, could not be controlled due to missing data. Conclusions: When explored by fecal elastase-1 testing, one in three patients with DM showed signs of impaired exocrine function. The results suggest that testing for PEI should be part of the diagnostic work-up of patients with DM.
Highlights
90% of the pancreas is made up of exocrine tissue comprising acinar cells which secrete pancreatic enzymes, and ductal cells which secrete bicarbonate rich fluid
The results suggest that testing for Pancreatic Exocrine Insufficiency (PEI) should be part of the diagnostic work-up of patients with diabetes mellitus (DM)
This study is the first meta-analysis of the prevalence of PEI, ascertained by means of fecal elastase-1 excretion, in patients with DM, an issue that has been mentioned for a long time
Summary
90% of the pancreas is made up of exocrine tissue comprising acinar cells which secrete pancreatic enzymes, and ductal cells which secrete bicarbonate rich fluid. As long as 20-40% of the ß-cell mass is preserved, fasting plasma glucose and insulin levels are often normal. When around 80% of the ß-cells have been destroyed does fasting hyperglycemia develop [1]. In patients with diabetes mellitus (DM), several reports have documented gross and microscopic alterations of the morphology of acinar cells, some showing pancreatic duct changes recalling a chronic pancreatitis [2,3,4,5]. Pancreatic Exocrine Insufficiency (PEI) is present in a considerable percentage of diabetics [6,7,8,9]. As more than 90% of exocrine function is usually lost before fat malabsorption manifests [10], it is intriguing to speculate how the damage of the 1% endocrineportion of the parenchyma, which will manifest itself as DM, may impact on the function of the remaining 90% exocrine-secreting portion
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