Discussion

T3cDM is an underrecognized form of secondary diabetes resulting from structural or functional pancreatic disease. Chronic pancreatitis is the leading cause of T3cDM, although pancreatic surgery, including partial pancreatectomy, also substantially increases the risk of endocrine insufficiency and diabetes development [3-6]. The prevalence of diabetes among patients with chronic pancreatitis increases with disease duration because of progressive destruction of pancreatic parenchyma [5,8]. Our patient had multiple features strongly suggestive of pancreatogenic diabetes, including chronic alcoholic pancreatitis, prior partial pancreatectomy, and severe hyperglycemia accompanied by a low C-peptide level, indicating markedly impaired endogenous insulin secretion rather than the insulin resistance that typically predominates in type 2 diabetes mellitus [2,6]. Although she had previously been diagnosed with type 2 diabetes mellitus, these clinical findings prompted reconsideration of the underlying etiology.

The diagnosis of T3cDM remains challenging because no universally accepted diagnostic criteria exist, and many patients are initially misclassified as having type 2 diabetes mellitus [6]. Ewald and Hardt proposed diagnostic criteria that include pancreatic exocrine insufficiency, pathological pancreatic imaging, and the absence of type 1 diabetes associated autoantibodies [4]. In our patient, pancreatic exocrine insufficiency was not formally assessed, available pancreatic imaging demonstrated postoperative changes consistent with prior partial pancreatectomy, and autoimmune diabetes associated antibodies, including glutamic acid decarboxylase 65 (GAD65), islet antigen-2 (IA-2), and zinc transporter 8 (ZnT8), were not obtained. These limitations precluded definitive confirmation using the proposed diagnostic criteria. Nevertheless, the combination of chronic alcoholic pancreatitis, prior pancreatic resection, low C-peptide level despite profound hyperglycemia, and the absence of clinical features strongly suggestive of autoimmune diabetes made pancreatogenic diabetes the most likely diagnosis.

Management of T3cDM differs substantially from that of type 2 diabetes mellitus because impaired insulin secretion is the predominant pathophysiologic mechanism. Insulin therapy is often required early in the disease course, particularly in patients with severe pancreatic damage or post-pancreatectomy diabetes [1,2]. Our patient's markedly elevated hemoglobin A1c and serum glucose reflected longstanding poor glycemic control and progressive β-cell dysfunction. Patients with T3cDM are generally considered less likely to develop diabetic ketoacidosis because pancreatic destruction results in the loss of both insulin-producing β-cells and glucagon-producing α-cells, thereby limiting ketogenesis despite severe insulin deficiency. However, diabetic ketoacidosis may still occur in the setting of profound insulin depletion or significant physiologic stress [9]. This pathophysiologic mechanism may explain why our patient did not develop diabetic ketoacidosis despite persistent severe hyperglycemia with serum glucose levels exceeding 400 mg/dL and a hemoglobin A1c of 19%.

Although the association between chronic pancreatitis, pancreatic resection, and T3cDM is well established [3-6], this case highlights the diagnostic challenges of distinguishing pancreatogenic diabetes from type 2 diabetes mellitus in patients with structural pancreatic disease. It underscores the importance of integrating pancreatic history, biochemical findings such as low C-peptide levels, and the overall clinical context to avoid diagnostic misclassification and guide appropriate management [2,4,6]. The case also illustrates the additional challenges posed by psychosocial instability and persistent insulin refusal despite repeated counseling, emphasizing that successful management of T3cDM requires not only appropriate insulin therapy but also individualized multidisciplinary strategies to address barriers to treatment adherence.