**11. Treatment of exocrine pancreatic insufficiency**

The assessment of functional deficiencies should be part of the initial evaluation and monitoring of patients with CP. Exocrine pancreatic insufficiency (EPI) is indicated by symptoms of steatorrhea (foul-smelling, oily stool), diarrhea, and weight loss. The gold standard for the diagnosis of EPI is a decreased coefficient of fat absorption (CFA) [1]. CFA of less than 93% (or >7 g of fat per 24 hours from a 72-hour fecal fat collection in a patient who is consuming 100 g of dietary fat each day during stool collection) defines steatorrhea or fat malabsorption [112]. Although this is a highly accurate test for fat malabsorption, it is rarely used in clinical practice because it is difficult for patients to perform properly. Several other indirect measures (e.g. fecal elastase (FE-1), serum trypsin) and clear tests (endoscopic secretin) are used to diagnose exocrine insufficiency [126]. The accuracy of these tests is highest in the presence of severe exocrine insufficiency (defined as steatorrhea). FE −1 is an indirect measure of exocrine function that is performed on a random stool sample. Since false positive test results are common due to diarrhea, the fecal elastase-1 test should not be used to evaluate patients with unexplained diarrhea [127]. Furthermore, the sensitivity and specificity of this test is open to discuss [126]. Shortly, there are no established criterion standard for mild to moderate exocrine insufficiency. The lack of a reliable and easy test to diagnose and monitor the treatment of EPI remains one of the biggest challenges for the management of EPI. All patients with chronic pancreatitis and pancreatic exocrine insufficiency, or signs of malnutrition should be treated with 40,000–50,000 lipase units of pancreatic enzymes per meal, and dose should be increased until symptoms are relieved [2]. In patients with EPI with persistent symptoms despite pancreatic enzyme replacement therapy (PERT) initiation, additional treatment strategies to consider are increase in the dosage of PERT, addition of a proton pump inhibitor (if not currently used), consideration of alternative etiologies of symptoms in CP, such as small intestinal bacterial overgrowth or lactose intolerance, and consideration of other causes of fat malabsorption [128]. According to a large randomized controlled trial in unselected noncritically ill inpatients, nutritional evaluation and treatment can reduce morbidity and mortality [129].
