Type 1 diabetes is a chronic disease characterized by abnormal metabolism and hyperglycemia due to insulin deficiency. There is a rapid decline in insulin production due to autoimmune destruction of the pancreatic beta cells. Partial remission (honeymoon phase) of type 1 diabetes is common in children and young adults with newly diagnosed type 1 diabetes. There is temporary restoration of beta cell function such that little or no exogenous insulin is required. Stopping insulin therapy soon after an emergency admission requiring intravenous insulin and subsequent subcutaneous insulin therapy can be frightening for both patient and healthcare provider. Affected patients require education and support during this period. This report describes a case of a 28-year-old man who presented to the emergency department with features of type 1 diabetes and diabetic ketoacidosis. He was treated with intravenous fluids and intravenous insulin and discharged on a subcutaneous insulin regimen. Despite testing positive for several types of islet cell autoantibodies, the patient was able to stop insulin therapy within three months of diagnosis. The patient maintained a self-initiated low-carbohydrate diet, regular weight-reducing exercise, and normal glucose levels without the need for insulin therapy. The honeymoon phase of type 1 diabetes, latent autoimmune diabetes, and ketosis-prone type 2 diabetes are discussed as important differential diagnoses.

Latent autoimmune diabetes of adults (LADA) is a type of autoimmune diabetes that begins in adulthood (usually after the age of 35 years); its main feature is the presence of diabetes-associated autoantibodies (most often autoantibody against glutamic acid decarboxylase), which leads to progressive destruction of the islets of Langerhans. This is a heterogeneous condition that presents with clinical and laboratory manifestations common to type 1 diabetes and type 2 diabetes. We report a case of a 71-year-old man diagnosed with type 2 diabetes two years ago, poorly controlled with oral antidiabetic therapy, and worsening in the third year. He had a positive family history of type 2 diabetes in two second-degree relatives (nephews). No pathologic findings at the physical examination were found. His body mass index was 23 kg/m2 and glycated hemoglobin was 10.6%. Laboratory workup revealed low basal C-peptide (<0.1 ng/mL) and positive glutamic acid decarboxylase antibodies, and the LADA diagnosis was confirmed. This case highlights the importance of being aware of this disease, especially in patients previously diagnosed with type 2 diabetes who remain uncontrolled with diet and oral hypoglycemic agents. LADA is often confused with type 2 diabetes, and therefore, the management is frequently inadequate. An early diagnosis and treatment are crucial to delaying disease progression.