Pancreatic atrophy and exocrine insufficiency associate with the presence of diabetes in chronic pancreatitis patients, but additional mediators are operative.

OBJECTIVES

Diabetes mellitus is a frequent complication of chronic pancreatitis (CP) and has traditionally been considered to develop as a consequence of pancreatic islet cell loss. However, additional mechanisms may be operative including accumulation of pancreatic fat and fibrosis. We used advanced magnetic resonance imaging (MRI) to study pancreatic morphology and exocrine function in a reference population and in CP patients with and without diabetes.

METHODS

This was a cross-sectional mono centre study. All subjects underwent advanced MRI including assessment of pancreatic ductal parameters (Cambridge classification and main pancreatic duct diameter), parenchymal parameters (DIXON technique and diffusion weighted imaging as proxies for pancreatic fat content and fibrosis, as well as pancreatic volume segmentation). Pancreatic exocrine function was determined as duodenal secretion following secretin stimulation and by the faecal elastase test.

RESULTS

The study included 76 patients with definite CP of whom 23 (30.1%) had diabetes and 23 sex- and age matched healthy volunteers. Compared to their non-diabetic counterparts, diabetic patients were characterised by a low pancreatic volume (20 vs. 36 ml; p = .02) and impaired pancreatic exocrine function (faecal elastase 19 vs. 48 µg/g; p = .008), while no difference between patients with and without diabetes were seen in relation to MRI derived proxies for fibrosis and pancreatic fat accumulation and pancreatic duct parameters. A large proportion of non-diabetic patients (49%) had similar morphological and functional characteristics as patients with diabetes.

CONCLUSION

Pancreatic atrophy and exocrine insufficiency are present in most CP patients with diabetes, but additional mediators seem to be operative in post pancreatitis diabetes mellitus.