Nutrition
This case highlights the importance of an understanding of pancreatic cellular function and pharmacology in the context of pancrelipase replacement, and the need to consider a possible new entity of fatty pancreas disease as a consequence of the metabolic syndrome.
Abstract
A 53-year-old obese male with a past medical history of idiopathic acute pancreatitis was referred to our centre with 3 years of pale watery diarrhea up to 20 times per day and an undetectable faecal elastase level. The severity of his symptoms had resulted in him leaving work and was significantly affecting his quality of life. He had been trialled on pancrelipase without effect. An extensive nutritional work-up was unremarkable with the exception of vitamin B12 deficiency, likely due to R-factor deficiency. Gastrin and VIP levels were normal. Endocrine function was preserved with a normal plasma insulin and C-peptide level. Panendoscopy andbiopsies did not reveal pathology.MRCPand endoscopic ultrasound imaging demonstrated complete fatty replacement of the pancreatic parenchyma and onlymild fatty liver disease. Fatty pancreas is widespread, clinically under-recognized and poorly understood. It can occur following pancreatic injury (such as pancreatitis or bile duct obstruction), disease processes such as diabetes, Cushing Syndrome, as a drug reaction or rarely associated with the metabolic syndrome. There is a high correlation between fatty liver and fatty pancreas. It can result in both exocrine and endocrine deficiency which is often clinically underdiagnosed and/or underappreciated. Pancreatic lipase functions optimally at pH 8, and it was hypothesised that acinar cell insufficiency from fatty pancreas was resulting in insufficient bicarbonate production. To offset this, pancrelipase was reinstituted with high dose pantoprazole to increase stomach and small bowel pH. This resulted in a rapid reduction in symptoms and improvement in the patient's quality of life. This case highlights the importance of an understanding of pancreatic cellular function and pharmacology in the context of pancrelipase replacement. Simple intervention can have marked impact on quality of life. It also highlights the need to consider a possible new entity of fatty pancreas disease as a consequence of the metabolic syndrome.