# Normal glycosylated hemoglobin masking glucose dysregulation in a patient with pancreatic and hematologic disease

**Authors:** Jean Carlos Ramos Cardona, Jacqueline Rodriguez Gilmore, Tathana Rivera Hernandez, Suzanne Quinn Martinez

PMC · DOI: 10.1210/jcemcr/luag037 · 2026-03-13

## TL;DR

A patient's normal HbA1c masked severe glucose issues due to pancreatic and blood conditions, highlighting the need for alternative tests like CGM and OGTT.

## Contribution

Demonstrates HbA1c limitations in patients with pancreatic and hematologic conditions, advocating for alternative glucose monitoring methods.

## Key findings

- Normal HbA1c failed to detect significant hyperglycemia in a patient with pancreatic and hematologic disease.
- CGM and OGTT revealed marked glucose dysregulation despite normal HbA1c levels.
- Pancreatic pathology and CHIP likely contributed to the glycemic discordance.

## Abstract

Although hemoglobin A1c (HbA1c) is widely used to assess long-term glycemia, its reliability declines in conditions that alter red blood cell turnover or hemoglobin glycation. Pancreatic structural diseases, including pancreatic neuroendocrine tumors (pNETs) and intraductal papillary mucinous neoplasms (IPMNs), may further affect glucose regulation through impaired endocrine function. Systemic inflammation and specific hematologic conditions can also create discordant glycemic markers, complicating diagnosis, and management. We report a 59-year-old woman with autoimmune disease who presented with fatigue and fluctuating glucose levels. Her HbA1c remained within normal limits; however, continuous glucose monitoring (CGM) and an oral glucose tolerance test (OGTT) demonstrated marked hyperglycemia. Imaging revealed pancreatic lesions concerning for a pNET in the setting of known IPMNs. Laboratory evaluation was notable for elevated ferritin and clonal hematopoiesis of indeterminate potential (CHIP). Additional studies, including hemoglobin, albumin, renal and hepatic function, and hemoglobin electrophoresis, were normal, ruling out anemia and hemoglobinopathies. Her glycemic discordance likely reflects impaired insulin secretion due to pancreatic pathology combined with inflammation driven alterations in erythrocyte lifespan associated with CHIP. This case underscores the limitations of HbA1c in complex metabolic or inflammatory states and highlights the value of CGM and OGTT when A1c does not align with clinical findings.

## Linked entities

- **Diseases:** autoimmune disease (MONDO:0007179), hyperglycemia (MONDO:0002909), clonal hematopoiesis of indeterminate potential (MONDO:0100543)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** pNETs (MESH:D018358), autoimmune disease (MESH:D001327), impaired insulin secretion (MESH:D007333), Pancreatic structural diseases (MESH:D010182), clonal hematopoiesis of indeterminate (MESH:C536227), anemia (MESH:D000740), fatigue (MESH:D005221), hyperglycemia (MESH:D006943), IPMNs (MESH:D000077779), hemoglobinopathies (MESH:D006453), glucose dysregulation (MESH:D018149), pNET (MESH:D018242), inflammation (MESH:D007249), pancreatic and hematologic disease (MESH:D006402)
- **Chemicals:** glycemia (MESH:D001786), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12983454/full.md

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Source: https://tomesphere.com/paper/PMC12983454