SUN-LB029 A Case of Gestational Diabetes with Diabetic Ketoacidosis, Insulin Injection Site Reaction and Anti Insulin Antibodies in Pregnancy

Background: Gestational diabetes mellitus (GDM) is defined as “impairment of glucose tolerance with first recognition during pregnancy” and is rarely associated with diabetic ketoacidosis (DKA). The incidence of DKA in pregnancy is about 1-3% in those with type 1 or 2 DM. Complications include preterm birth and fetal demise rate of 10-25%. Clinical case: 35-year-old G2P1 Southeast Asian female diagnosed with GDM at 28 weeks of gestation (wGA) via 3hour oral glucose tolerance test. At 35wGA, she presented with asymptomatic hyperglycemia. Blood glucose (BG) was previously well-controlled on once daily detemir (started at 31wGA). Past medical history is significant for Hashimoto’s thyroiditis; pre-pregnancy BMI 22.5kg/m(2). Family history is notable for a sister with GDM and pre-eclampsia and mother with pre-DM. She experienced fasting hypoglycemia (68, 57mg/dL) the 2 preceding mornings, addressed by decreasing detemir dose 20 to 16U QD. The am of her presentation, she awoke asymptomatic with a fasting BG of 200mg/dL and 1 hour post-prandial of 283mg/dL. By lunch, BG rose to 357mg/dL. Physical exam was notable for localized wheal-like reactions on her left thigh and gluteal area, and right arm. Labs demonstrated an anion gap 18, bicarbonate 11mEq/L and beta-hydroxybutyrate (BHB) 7.42mMol/L. The patient was started on intravenous (IV) insulin and was kept NPO per DKA protocol. Urinalysis and culture were negative with no other precipitants identified. C-peptide was undetectable at BG of 260mg/dL and T1DM related antibodies were obtained. After 18 hours on the DKA protocol, BG remained 180-250 mg/dL, bicarbonate 16meq/L, and BHB 1.13mMol/L; the protocol was modified for tighter BG ranges and to allow more frequent feeding for prevention of hypoalimentation ketosis. Allergy team was consulted and diagnosed localized insulin reaction and recommended daily oral H2-blocker, given no true IgE-mediated hypersensitivity or systemic findings. Patient was transitioned to NPH 18u BID and prandial lispro 5u TID (total of 0.88u/kg) on day 2 of admission. Following discharge, only anti-glutamic acid decarboxylase (38IU/ml) and anti-insulin (0.6IU/ml) returned elevated (negative IA-2 and anti-islet cell). At 37wGA, she had prelabor spontaneous rupture of membranes and delivered a 3730g healthy female via repeat cesarean section while receiving IV insulin. Newborn required 2 days of phototherapy for hyperbilirubinemia, no neonatal hypoglycemia. At 6 weeks postpartum, she was breastfeeding, administering 11u NPH BID and 3u of prandial lispro (0.53u/kg). Conclusion: Stress in the third trimester of pregnancy (insulin allergy, starvation ketosis, and physiologic increase in insulin resistance) can result in DKA in a patient with type 1 or 2 DM that initially presents as GDM. Insulin allergy or localized reaction to insulin may contribute to delay in insulin absorption thus precipitating insulinopenia. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.