MON-559 - A Diagnosis Not to Forget: Latent Autoimmune Diabetes in Adults Presenting in the Elderly

Latent Autoimmune Diabetes in Adults (LADA) is an autoimmune disease with slow islet-beta cell destruction that shares characteristics of Type I and Type II diabetes mellitus. Due to shared characteristics, the diagnosis can be challenging in the elderly but should remain in the differential. This case presents an 86-year-old patient who was initially diagnosed with Type II DM but found to have LADA.

An 86-year-old female with a BMI of 20 and past medical history of atrial fibrillation, hypothyroidism, and dyslipidemia presented to the hospital after a fall. She was diagnosed with a urinary tract infection, and other notable labs included a glucose of 393 mg/dL and A1C of 14.4%. Her A1C recorded six years earlier was 5.7%. Treatment was initiated with IV antibiotics and subcutaneous insulin. With a family history of diabetes, unknown to the patient if Type I or II, GAD-65 and IA-2 antibodies were ordered. Antibodies were pending at the time of discharge, but due to the patient’s age, a higher suspicion for Type II diabetes, and patient refusal to use insulin, she was discharged on metformin and pioglitazone. The patient was readmitted weeks later due to encephalopathy and hyperglycemia. Workup revealed elevated LFTs, and hyperglycemia of 421 mg/dL. The patient was given fluids, insulin, and admitted for evaluation with a differential of drug-induced liver injury vs cholelithiasis based on imaging. Endocrinology was consulted for hyperglycemia, positive GAD-65 antibodies (102 nmol/L), and decreased free and total insulin. The c-peptide result was 1.2 ng/mL. The patient was diagnosed with LADA and discharged with a continuous glucose monitor, 70/30 insulin, and follow-up with hepatology. Pioglitazone and metformin were stopped.

LADA shares a slower but similar pathogenesis of immune-related destruction of pancreatic islet cells with autoantibodies, typically GADA, but can also be IA-2 or ZnT8. Characteristics similar to Type II DM include initial response to oral diabetic agents, older age of diagnosis, and insulin resistance. Diagnostic criteria are age >30 years old, positive for at least one diabetes associated antibody, and no insulin requirement for six months. LADA onset typically occurs around the ages of 30-40 and encompasses 2-12% of all patients with adult-onset diabetes. Research shows that around 10% of adults initially diagnosed with type II diabetes have LADA, but data is limited on the prevalence of people diagnosed with LADA outside the typical age ranges of 30-40. This case demonstrates that LADA can be a challenging diagnosis in the elderly due to its similarities with Type II DM and can lead to misdiagnosis and ineffective management. It should remain in the differential on someone who does not respond to oral agents or rapidly progresses to insulin dependence, no matter the age.

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