Progressive Asymptomatic Hyperglycemia and Glucosuria Identified Through Protocol-Driven Monitoring in a Clinical Trial: A Case Report.
Source: PubMed, NCBI / U.S. National Library of Medicine
Severe hyperglycemia may remain clinically silent despite significant metabolic derangement, particularly in patients with inconsistent engagement in care. We report the case of a 50-year-old patient with type 2 diabetes mellitus enrolled in a gout clinical trial, in which protocol-driven laboratory monitoring revealed progressive, asymptomatic hyperglycemia and worsening glucosuria across multiple study visits. Fasting blood glucose increased from 250 mg/dL at baseline to 474 mg/dL at Week 24, while urine glucose exceeded 1000 mg/dL from Week 16 through Week 24. Hemoglobin A1c was 13%, and the patient had class II obesity with a body mass index of 39.7 kg/m². Despite these findings, the patient denied classic symptoms of hyperglycemia and demonstrated no evidence of acute metabolic decompensation. Evaluation of investigational product safety data did not support a drug-related cause. Further assessment identified medication nonadherence, inconsistent primary care follow-up, and socioeconomic barriers as likely contributors. Following coordination with the patient's primary care physician, insulin therapy was initiated, resulting in rapid improvement in fasting blood glucose and complete resolution of glucosuria, although fasting glucose remained elevated at Week 32. This case demonstrates that protocol-driven monitoring can uncover clinically silent metabolic deterioration and highlights the critical role of adherence and social determinants of health in diabetes o
Abstract
Severe hyperglycemia may remain clinically silent despite significant metabolic derangement, particularly in patients with inconsistent engagement in care. We report the case of a 50-year-old patient with type 2 diabetes mellitus enrolled in a gout clinical trial, in which protocol-driven laboratory monitoring revealed progressive, asymptomatic hyperglycemia and worsening glucosuria across multiple study visits. Fasting blood glucose increased from 250 mg/dL at baseline to 474 mg/dL at Week 24, while urine glucose exceeded 1000 mg/dL from Week 16 through Week 24. Hemoglobin A1c was 13%, and the patient had class II obesity with a body mass index of 39.7 kg/m². Despite these findings, the patient denied classic symptoms of hyperglycemia and demonstrated no evidence of acute metabolic decompensation. Evaluation of investigational product safety data did not support a drug-related cause. Further assessment identified medication nonadherence, inconsistent primary care follow-up, and socioeconomic barriers as likely contributors. Following coordination with the patient's primary care physician, insulin therapy was initiated, resulting in rapid improvement in fasting blood glucose and complete resolution of glucosuria, although fasting glucose remained elevated at Week 32. This case demonstrates that protocol-driven monitoring can uncover clinically silent metabolic deterioration and highlights the critical role of adherence and social determinants of health in diabetes outcomes. Early identification and timely intervention remain essential to preventing progression to life-threatening complications.