ECE2021 Eposter Presentations Diabetes, Obesity, Metabolism and Nutrition (82 abstracts)
Centro Hospitalar e Universitário do Porto, Endocrinology, Diabetes and Metabolism, Porto, Portugal
Introduction
Ketosis-Prone Diabetes (KPD) is a heterogeneous condition that shares clinical characteristics of type 1 and type 2 diabetes. It is usually a challenging diagnosis because patients are prone to develop diabetic ketoacidosis (DKA) without having the classic clinical phenotype of autoimmune type 1 diabetes.
Case report
A Caucasian 26-years-old female with known history of renal transplant, morbid obesity (BMI 41.5 kg/m2), hypertension and dyslipidemia was diagnosed with pregestational diabetes during her first pregnancy. During the actual pregnancy, insulin was required to achieve controlled blood glucose levels and maintenance of this therapy was necessary after delivery. Some months after, she was brought to the emergency room due to polydipsia, polyuria, blurred vision, mild asthenia and paresthesias of the upper extremities. The arterial pH was 6.99, glucose 657 mg/dl and bicarbonate and aniogap were unmeasurable. Urinalysis was positive for ketonuria (high unmeasurable value). Laboratory tests revealed no evidence of infection, cardiac ischemia, renal or liver dysfunction. The patient was admitted with severe DKA and promptly received appropriate treatment. Low C-peptide levels (0.19 ng/ml [RR:1.14.4 ng/ml]) and HbA1c 12.3% were document. Beta-cell specific autoantibodies were all negative. She was discharged with a basal-bolus insulin regimen. One month after her C-peptide level was 1.76 ng/ml and HbA1c was 11.8%, her insulin needs were much lower and at that time she initiated GLP-1 receptor agonist.
Discussion
This case report presents us a young obese woman with dysmetabolic traits that clearly suggests a Type 2 DM. The therapeutic non-compliance determined this severe hyperglycemic presentation that usually is a typical expression of insulinopenia and Type 1 diabetes. The autoimmunity against β-cell was negative and after glucotoxicity the presence of pancreatic insulin reserve was proven. The presented case of KPD should alert clinicians to this entity. Although the presentation is similar to Type 1 diabetes the evolution appears to resemble Type 2 DM. This has impact on misclassification and mistreament of patients.