Pancreatic Cancer Heralded By Worsening Glycemic Control: A Case Series
Presentation Number: SAT 634
Date of Presentation: April 1st, 2017
Dimpi Desai*1, Vineeth Sukrithan1, Devika Rao1, Akankasha Goyal2, Eleanor Weinstein1 and Ulrich K Schubart3
1Jacobi Medical Center & Albert Einstein College of Medicine, Bronx, NY, 2Albert Einstein College of Medicine, Bronx, NY, 3Jacobi Medical Center, Albert Einstein College of Medicine, Bronx, NY
Long-term type 2 diabetes mellitus (T2DM) is known to be a modest risk factor for pancreatic ductal adenocarcinoma (PDAC). However, three meta-analyses concluded that the risk of PDAC was inversely proportional to the duration of diabetes and was highest among patients who were diagnosed with diabetes less than a year prior to the diagnosis of PDAC1. We report two cases in whom worsening glycemic control led to the diagnosis of PDAC.
A 96 year old woman with a history of hypertension, diet-controlled T2DM and hyperlipidemia was admitted for sudden onset of confusion and was found to be in hyperglycemic hyperosmolar non-ketotic state (HHS) with serum glucose 1037 mg/dl, osmolality 363 mOsm/kg, normal bicarbonate level 26.5mEq/L. No obvious precipitating factor of HHS was found. After being treated for HHS, she was discharged home, with initiation of glargine insulin. Two weeks after discharge, prandial insulin regimen was begun at out-patient follow up due to persistent post-prandial hyperglycemia. One month after initial admission, the patient was noted to have anorexia, weight loss, jaundice, dark urine and clay colored stools. Laboratory investigations revealed obstructive jaundice (AST 397 U/L, ALT 354 U/L, ALP 1481 U/L and a total bilirubin of 17 mg/dl). A Computed Tomography (CT) scan showed a lesion concerning for a pancreatic neoplasm which was confirmed by biopsy to be PDAC.
A 59 year old man with a history of left eye blindness due to glaucoma and a one year history of T2DM presented for routine outpatient follow up with a two month history of 20 pounds of unintentional weight loss, poor appetite and lethargy. Routine blood tests revealed a glucose level of 495mg/dl and Hemoglobin A1c (A1c) of 13.0%. Complete blood count, chemistry and liver function tests were within normal limits. A prior A1c measured 6 months earlier was 7.5% for which he was prescribed metformin 500mg twice daily. Given the history of unexplained weight loss, the patient underwent CT scan of the abdomen which revealed a lesion within the body of pancreas compatible with pancreatic cancer along with multiple metastatic lesions to the liver. Interventional Radiology guided liver biopsy confirmed the diagnosis of PDAC.
These cases suggest that sudden decompensation in well controlled T2DM or newly diagnosed T2DM could be an early presentation of PDAC. In vitro, intracellular defects in insulin action, decreased glycogen synthase activity and thereby impaired glucose disposal have been the suggested mechanisms for PDAC induced insulin resistance2. It may be prudent to consider an underlying pancreatic malignancy in the differential diagnosis when evaluating patients with hyperglycemic non-ketotic state or an acute worsening of glycemic control in the appropriate clinical setting.
Nothing to Disclose: DD, VS, DR, AG, EW, UKS