Mild acute pancreatitis with vildagliptin use
A 42-year-old man presented with a 7-day history of severe abdominal pain radiating to back, nausea, and fever. Type 2 diabetes mellitus had been diagnosed 5 years earlier and was initially treated with metformin. Six months before presentation, he commenced therapy with vildagliptin 50 mg in combination with metformin 500 mg daily before dinner. His post-prandial sugar was below 160 mg/dl. His glycemic control was good (HBA1c, 7%). He was also taking rosuvastatin 5 mg, s-omeprazole, and domperidone.\nMild acute pancreatitis was diagnosed on the basis of findings on abdominal ultrasound done 3 days after the episode, which showed swollen and echogenic pancreas, loss of peripancreatic fat plane and pancreatic duct was not dilated; and elevated levels of serum pancreatic enzymes (amylase, 202 U/l [reference range, <110 U/l]; lipase, 669 U/l [reference range, <60 U/l]). Other tests: FPG-97 mg/dl, Triglyceride-143 mg/dl, LDL-65 mg/dl, LFT-normal. He stopped taking vildagliptin and metformin on doctor's advice 3 days after the episode on the day of the test. Next day, there was a decrease in serum amylase to 118 U/l and lipase to 184 U/l. He was managed conservatively with liquid diet, pancreatic enzyme supplement, and antispasmodics as he refused admission in his local place and came to Kolkata for further evaluation and management. Blood tests were repeated on 6th day which showed the following results: TC-7800/cu mm, Hb%-15.9g%, ESR-3 mm/hr, CRP-4 mg/l, FPG-99 mg/dl, Calcium-9.4 mg/dl, urea-20 mg/dl, creatinine-1 mg/dl, amylase-75 U/l, lipase-130 U/l. His lipase was still elevated. CT scan upper abdomen (both oral and IV contrast) done on 6th day show mild diffuse swelling of pancreas with normal contour without any necrosis or collection [].\nA notable feature of this patient's condition was the distinct absence of an identifiable cause for his pancreatitis. There was no radiographic evidence of cholelithiasis or biliary dilatation. He abstained from alcohol use and was not receiving any medication other than metformin and vildagliptin for control of diabetes. He was not obese (body mass index, 27 kg/m2). His triglyceride was not raised. In the absence of an obvious secondary cause for pancreatitis and considering the temporal sequence of events, this case suggests a causal link between the initiation of vildagliptin and the late development of pancreatitis. The patient's condition and biochemical parameters improved with the timely cessation of vildagliptin.