Abstract
A 28-year-old male with an 8-year history of type 2 diabetes mellitus was admitted for consciousness disturbance. He had been receiving treatment with metformin and pioglitazone. His blood glucose control was worsening due to binge drinking of soft drinks. On admission, the laboratory data showed a blood glucose level of 1,620 mg/dl, an HbA1c level of 15.0 %, a Cr level of 2.89 mg/dl and an amylase level of 548 IU/l in addition to elevation of the serum level of ketone bodies and metabolic acidosis. A CT scan of the abdomen revealed swelling of the pancreas and inflammatory changes over the left prerenal cleft. A diagnosis of diabetic ketoacidosis (DKA) and acute pancreatitis was made. Because the patient did not have gallstones or dyslipidemia and did not report excessive alcohol consumption, we considered the etiology of the acute pancreatitis to be DKA. After admission, the patient went into respiratory failure. Continuous hemodiafiltration (CHDF) was performed to treat the severe acute pancreatitis, and the patient fully recovered. Dysfunction of autophagy, a protein degradation system, has been implicated in the pathogenesis of acute pancreatitis. In this case, hyperglycemia may have caused autophagy dysfunction via ER stress. The fructose contained in soft drinks promotes lipogenesis, hyperuricemia and chronic inflammation in fat tissue. These characteristics are suspected to have caused the onset and exacerbation of acute pancreatitis in this patient via endothelial dysfunction and lipotoxicity, respectively.
