SAT-665 A Case of Hyperglycemia in Post Pancreas Transplant Patient-Is It Insulin Deficiency or Insulin Resistance

Introduction Pancreatic transplant (PTx) is a less commonly utilized option for patients with Type 1 Diabetes (DM1), usually with co-morbid end stage renal disease. Hyperglycemia in the post-PTx population can be multifactorial. We report a case of hyperglycemia with ketosis in a post-PTx patient due to insulin resistance and relative insulin deficiency. Case Presentation 55-year-old male patient with DM1 who underwent simultaneous kidney-PTx. His immunosuppressant (IS) medications were tacrolimus, mycophenolate and prednisone. Tacrolimus levels were therapeutic and his transplant course was benign. He did not require insulin or other glucose-lowering medications post-PTx for 29 years. However, during evaluation for subacute illness with his PCP, he was found to have HbA1c of 12.6%, plasma glucose (PG) 776 mg/dl, and positive urine ketones. He was started on insulin degludec 24 units daily, which was quickly tapered to 8 units daily due to hypoglycemia. OGTT showed fasting PG of 93 mg/dl, 2-hour PG of 115 mg/dl, and stimulated C-peptide of 7.5 ng/ml. HbA1c improved to 7.4% after being on insulin for 1 month. Insulin degludec was tapered and discontinued within 2 months due to hypoglycemia despite low doses and robust PTx function. Home blood glucoses (BG) were controlled and HbA1c stable at 6% off insulin therapy. Eighteen months later, he was hospitalized for hyperglycemia with ketosis, without acidosis, during an upper respiratory infection. He was restarted on insulin (glargine, aspart). Once the acute stress resolved, his insulin dose needs reduced significantly, tapering down to insulin glargine 5 units daily. Along with daily home BG monitoring, HbA1c and C-peptide are performed every 3 months, with recent HbA1c 5.2% and C-peptide 3.0 ng/ml (simultaneous PG of 103 mg/dl). Discussion Causes of post-PTx hyperglycemia include graft failure due to acute or chronic rejection, insulin resistance, beta cell dysfunction due to IS medications, pancreatitis, or, rarely, recurrence of autoimmunity. Factors predicting hyperglycemia are pre-PTx insulin dose, BMI and acute rejection. New onset type 2 diabetes can occur due to insulin resistance from IS medications and genetic predisposition. Measurement of C-peptide after OGTT can help determine the cause. Insulin is the standard treatment even with detectable C-peptide, though oral glucose-lowering medications have been used in the setting of insulin resistance. In this patient, severe hyperglycemia occurred during stress. He had very low insulin dose requirements when the stress and hyperglycemia resolved and reasonable C-peptide values. This scenario was most consistent with hyperglycemia due to insulin resistance and subsequent relative insulin deficiency during stress, with continued PTx function. This illustrates the importance of detailed assessment and personalized treatment in patients with post-PTx hyperglycemia.