Two cases of conventional fulminant type 1 diabetes: following the depletion process of endogenous insulin secretion and literature review.

Abstract

Fulminant type 1 diabetes (FT1D) is a rapidly progressive form of diabetes in which the endogenous capacity to secrete insulin is depleted. The onset is unpredictable with conventional FT1D, and a few reports have tracked C-peptide in patients with conventional FT1D pre-onset. In this report, we present two typical cases of conventional FT1D where C-peptide was monitored from the onset of precursor symptoms to the development of diabetic ketoacidosis (DKA). Furthermore, we conducted a literature review and provide a detailed description of the process of C-peptide depletion in conventional FT1D. Case 1 involved a 72-year-old woman who initially presented with fever and fatigue. Case 2 involved a 45-year-old woman with fever, abdominal pain, and acute pancreatitis. In both cases, DKA developed five days after initial symptoms. A noteworthy observation in both cases was the drastic drop in C-peptide, which was detectable at initial presentation but depleted by the time of DKA diagnosis. These cases emphasize the importance of close follow-up of plasma glucose and serum C-peptide in cases presenting with infection and pancreatitis. Our literature review revealed that in conventional FT1D, endogenous insulin secretion becomes deficient in an average of 5.3 days. Regardless of any concomitant acute pancreatitis and/or pancreas enlargement, the period until endogenous insulin secretion became deficient showed no substantial variation. This result supports the concept that progression of conventional FT1D is more rapid than that of immune checkpoint inhibitor-related FT1D, which deplete insulin secretion in approximately 2 weeks.

Supplementary information: The online version contains supplementary material available at 10.1007/s13340-024-00755-0.