Case: A 61-year-old man with Type II Diabetes Mellitus, hypertension, hyperlipidemia, and morbid obesity presented with lightheadedness, nausea, polyuria, and blurry vision. He was diagnosed with severe hyperglycemia with serum glucoses in the 600’s. Although admission HbA1C was 3.6%, the patient denied hypoglycemic symptoms. He did not monitor blood sugars at home since discontinuation of his insulin several months earlier following his last clinic HbA1C 5.2% and glucose 111 mg/dL. At the time of admission, he was admittedly non- adherent with his Metformin and diabetic diet. CBC was normal except a MCV of 73 raising a concern for possible hemoglobinopathy especially with the discordance of measured serum glucoses levels and HbA1c. A fructosamine level was 664 mmol/L indicating poorly controlled DM for the preceding
2 or 3 weeks consistent with the elevated glucose values during hospitalization (uncontrolled DM: fructosamine 268-870mmol/L). The hemoglobin electrophoresis revealed 36.8% Hb F and 61% HbS consistent with previously undiagnosed HbS/HPFH (Hereditary Persistence of Fetal Hemoglobin). Discussion: This case demonstrates the utility of checking a fructosamine level in patients in whom the HbA1C does not correlate with fasting glucose levels. In this case, the patient’s hemoglobinopathy was responsible for the falsely lowered HbA1C which was ultimately diagnosed when the very low HbA1C was incongruent with elevated fasting glucose levels. His “normal” HbA1Cs may have led to premature cessation of the patient’s insulin and Metformin and ultimately to this hospitalization.
AN UNUSUAL PRESENTATION OF DIABETES MELLITUS Ashley Misky, Laura Hutchins, Kasha Bornstein, Lee Engel; Department of Medicine, LSU Health Sciences Center, New Orleans, LA.
Introduction: Latent autoimmune diabetes in adulthood (LADA) is an uncommon but not rare form of diabetes accounting for 2-12% of all cases of new onset diabetes in adulthood. As many as 14% of adult patients diagnosed with T2DM are seropositive for T1DM-associated autoantibodies, which are diagnostic for LADA. Case: A 74-year-old woman with type II diabetes mellitus (T2DM) and hypothyroidism presented with confusion. She was diagnosed with T2DM six months prior following an admission for diabetic ketoacidosis (DKA) and sent home on insulin. To simplify her regimen, due to labile blood sugars, she was switched to metformin only therapy three weeks prior to presentation. The week prior to presenting, her blood glucose was persistently elevated. On presentation, she was minimally responsive with marked acidosis and profoundly elevated beta-hydroxybutyrate. Despite requiring a high insulin infusion initially, she developed frequent episodes of hypoglycemia after transitioning to subcutaneous long-acting insulin. Insulin, GAD, and IA-2 antibodies were positive consistent with
LADA. She was discharged with glucose control on five units of insulin glargine. The patient returned four days later with a repeat episode of DKA and again had repeated episodes of labile blood sugars without a consistent pattern. Normoglycemia was achieved, and she was discharged on insulin glargine and insulin lispro. Endocrinology appointment was arranged to expedite continuous glucose monitoring. Prior to her follow up, she experienced a third episode of DKA with cardiac arrest, was effectively resuscitated, and discharged to skilled nursing facility for closer glucose monitoring. Discussion: This patient’s glycemic lability may have resulted from her brief prior insulin use with antibody formation or insulin antibody syndrome (IAS). These antibodies have been found to produce labile blood glucose levels in patients due to formation of insulin antibody complexes that cause unpredictable release and action of both exogenous and endogenous insulin. Treatment of IAS consists of controlling diabetes via oral glycemic agents and/or immunosuppressants in T1DM.
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