Endocrine Abstracts

Introduction: Type 1 diabetes (T1D) is a progressive autoimmune disease, the diagnosis is obvious in classic forms. However, misleading forms are possible, sometimes leading to inappropriate treatment. We report the case of two type 1 diabetic patients who were treated for years with oral hypoglycemic drugs.

Case report: Patient 1: Mr. M, aged 34, with a family medical history of type 2 diabetes (T2D), was diagnosed with diabetes revealed by a polyurea-polydipsic syndrome (PPS), 8 years ago, without acute decompensation. He was treated with oral dual therapy: glimiperide 2 mg and metformin. He recently consulted for unintentional weight loss of 3 Kg in 3 months with non-controlled diabetes: fasting plasma glucose (FPG) = 10 mmol/l, glycated hemoglobin (HbA1C) = 10.7%. Biology showed peptide C = 1.06 ng/ml, anti-GAD65 antibodies were negative but anti-AI2 antibodies were positive at 28 IU/ml (ⁿ<8), confirming autoimmune T1D. Patient 2: Mr. N, aged 34, with no previous medical history, was diagnosed with diabetes revealed by PPS with no weight loss or acute decompensation. His BMI was 25.05 kg/m²; and biology showed an HbA1C = 12%. The patient received oral dual therapy: glimepiride 2 mg/d and metformin. At 6-month follow-up, PPS disappeared and HbA1C fell to 6.7%. The patient described occasional hypoglycemia, leading us to decrease the dose of glimiperide to 1 mg/day. HbA1C has remained stable at around 7.5-8.5% for 5 years, then rose sharply to 12%, associated with weight loss. Increasing the dose of glimepiride was ineffective. We asked for anti-GAD65 antibodies, which were markedly positive at 1625 IU/ml (ⁿ<10), thus indicating T1D.

Discussion and conclusion: T1D is easy to diagnose in the presence of abrupt onset, inaugural ketosis, and young age, especially in the presence of autoimmune stigmata. The absence of these elements makes T1D unlikely. The diagnosis was more diverted by the clinical-biological improvement with oral hypoglycemic drugs for years, classically incompatible with T1D. This equilibrium would be explained by the autoimmune destruction, slowly progressive and incomplete, of the beta cells of the islets of Langerhans. This persistent insulin secretory capacity, enabled good glycemic balance to be achieved for a while. Reascension of glycemic parameters reflected an utter decline in pancreatic beta cells. Although T2D is increasingly seen at a younger age, the diagnosis of diabetes at an age <35 should raise the possibility of T1D.