C-Peptide-Positive, Autoantibody-Negative Type 1 Diabetes Mellitus

A 30-year-old female previously diagnosed with C-peptide (CP)-positive, autoantibody-negative type 1 diabetes mellitus (T1DM) at 19 years old presented to the clinic at age 28 for management of diabetes mellitus (DM) that had previously been controlled by insulin since diagnosis. Laboratory results from May 2011 showed low-normal C-peptide of 1 ng/mL (normal range: 0.8-4 ng/mL) with no corresponding glucose, glutamic acid decarboxylase (GAD)-65 antibody (GADA) of <1 U/mL (N<1.1 U/mL at the time of laboratory draw), and HbA1c of 6.4%. Almost 10 years later, in December 2020, laboratory results showed normal Cpeptide of 2.1 ng/mL with a glucose of 198 mg/dL, GAD-65 antibody of 38.2 U/mL (current reference range: 0-5 U/mL), negative pancreatic islet antibody (IA), and undetectable zinc transporter 8 (ZnT8) antibody, consistent with a diagnosis of T1DM. This increase in CP indicates the possibility of pancreatic beta cell regeneration and/or increased function. The commonly accepted belief that individuals with T1DM quickly lose all function of pancreatic beta cells has led to academic consequences; many immunotherapy clinical trials' inclusion criteria require participants to have a new diagnosis of T1DM based on the assumption that those with a longer duration of diabetes have unrecoverable cessation of insulin secretion. CP could influence inflammation, microvascular circulation, and endothelial function. Further, it could affect the neuronal and glomendar structure and/or function. These potential functions of CP are seen by the correlation between measurable CP levels and decreased diabetic complication rates.

Automated summary

This article describes a case of a female patient who was previously diagnosed with C-peptide positive type 1 diabetes mellitus and had been controlling the disease with insulin. Ten years later, her C-peptide levels increased along with other markers associated with type 1 diabetes, suggesting the possibility of pancreatic beta cell regeneration or increased function. This finding challenges the commonly accepted belief that individuals with type 1 diabetes lose all function of pancreatic beta cells.