7456 Artifactual Hypoglycemia Leading To the Diagnosis of Monoclonal Gammopathy

7456 人为低血糖导致单克隆丙种球蛋白病诊断

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Abstract

Disclosure: L.T. Ha: None. M. Maximous: None. C.K. LaValley: None. J. Lado: None. Background: Low glucose readings in the absence of classic hypoglycemic symptoms are not unusual, especially among diabetic patients with unaware hypoglycemia. Discrepant measurements between capillary and venous blood are well-described, mostly due to poor reagent quality or circulatory deficits causing interference with the former. Less commonly, monoclonal gammopathies have been observed to cause true or artifactual hypoglycemia in venous blood sampling related to the presence of insulin antibodies or interference with chemistry assays, respectively. Because this interference is rare and occurs unpredictably with different testing modalities, detection is challenging and often preceded by extensive workup for underlying causes of true hypoglycemia. Clinical Case: A 69-year-old man with Parkinson’s disease, hypertension, dyslipidemia, chronic kidney disease stage 3, and obesity was referred to us for evaluation of hypoglycemia. His fasting venous glucose was consistently measured as undetectable (<10 mg/dl) on serial routine bloodwork (using the hexokinase method on Beckman-Coulter AU 5800 analyzer). He remained asymptomatic, with normal home and in-office fasting fingerstick levels. A thorough medication review did not reveal a clear etiology for this recurrent hypoglycemia. Initial workup by his primary care physician was notable for elevated total protein of 9.0 g/dl (n 6.1-8.1 g/dl), elevated globulin of 4.5 g/dl (n 1.9-3.7 g/dl), and elevated erythrocyte sedimentation rate of 111 mm/h (n<20 mm/h). Hemoglobin A1c, proinsulin, beta-hydroxybutyrate, insulin, and C-peptide were within normal range. On repeat evaluation at our institution (using the hexokinase method on Roche cobas 8000 c702 analyzer), his sample was flagged for a high lipemic index but displayed no evidence of lipemia upon visual inspection, suspicious for paraprotein presence. Protein electrophoresis was performed on the same plasma sample, revealing hypergammaglobulinemia (1.5 g/dl) subsequently characterized by serum immunofixation as a monoclonal IgM kappa. Conclusion: Recurrent “hypoglycemia” in an asymptomatic patient without other metabolic abnormalities should prompt clinicians to consider etiologies of falsely measured low glucose, including hyperleukocytosis, prolonged specimen delivery time, and paraproteinemia. In the appropriate clinical context, such as an elevated serum or plasma lipemic index, these cases should be further investigated with protein electrophoresis to rule out an underlying gammopathy. As the hexokinase method relies on optical parameters susceptible to interference by paraprotein-induced turbidity, an alternative sampling device utilizing amperometry (point-of-care glucometer or blood gas analyzers) may be employed to differentiate between true hypoglycemia as a rare complication of monoclonal gammopathy versus laboratory artifact. Presentation: 6/1/2024

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