Abstract
Morbid obesity is a lifelong disease, and all patients require complementary follow-up including nutritional surveillance by a multidisciplinary team after bariatric procedures. Pancreatic exocrine insufficiency (PEI) refers to an insufficient secretion of pancreatic enzymes and/or sodium bicarbonate. PEI is a known multifactorial complication after upper gastrointestinal surgery, and might constitute an important clinical problem due to the large number of bariatric surgical procedures in the world. Symptoms of PEI often overlap with sequelae of gastric bypass, making the diagnosis difficult. Steatorrhea, weight loss, maldigestion and malabsorption are pathognomonic for both clinical conditions. Altered anatomy after bypass surgery can make the diagnostic process even more difficult. Fecal elastase-1 (FE1) is a useful diagnostic test. PEI should be considered in all patients after bariatric surgery with prolonged gastrointestinal complaints that are suggestive of maldigestion and/or malabsorption. Appropriate pancreatic enzyme replacement therapy should be part of the treatment algorithm in patients with confirmed PEI or symptoms suggestive of this complication.
Highlights
Obesity is the most prevalent metabolic disease worldwide, and represents a global epidemic in both developed and developing countries [1,2]
In a recently published study, 188 consecutive patients were followed for 52 months after bariatric surgery, and exocrine pancreatic function was evaluated by clinical symptoms, Fecal elastase-1 (FE1) and positive dechallenge-rechallenge test with pancreatic enzyme replacement therapy [45]. 31% of these patients were diagnosed with Pancreatic exocrine insufficiency (PEI)
Symptoms of PEI often overlap with sequelae of gastric bypass, making the diagnosis difficult
Summary
Obesity is the most prevalent metabolic disease worldwide, and represents a global epidemic in both developed and developing countries [1,2]. Pancreatic secretions play an essential role in digestion, and are controlled by a host of neuronal and hormonal signaling pathways which modulate secretion, and the cellular integrity of the gland [3] Neural regulation of this secretion involves the enteric nervous system in the gut and the central nervous system. Cholecystokinin (CCK) is known to induce pancreatic exocrine secretion by the activation of CCK1 receptor-mediated signaling pathways, but other hormones play an important role in pancreatic function, including ghrelin, leptin, melanocortin, obestatin, apelin, orexin-A and B and glucagon-like peptide-1 (GLP-1)—Table 1 [3,4,6,7]. Central administration in rats could activate vagal afferents to initiate enteropancreatic reflex and to stimulate pancreatic exocrine secretion.
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