AACE endocrinology and diabetes · 2025
Reversible Severe Hyperglycemia Without Ketoacidosis After Initiation of Bictegravir-containing Antiretroviral Therapy.
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Aurora John, Grossman Katlyn, Hudson Sydney, Kogelman Laura, Pittas Anastassios G
Аннотация
BACKGROUND: Bictegravir (BIC), a second-generation integrase strand transfer inhibitor, may induce acute hyperglycemia in patients with metabolic risk factors, though this was not reported in clinical trials. We describe a patient who developed severe hyperglycemia shortly after starting a BIC-containing antiretroviral therapy (ART).
CASE REPORT: A 36-year-old patient with virologically suppressed HIV, obesity, and prediabetes developed severe hyperglycemia, HbA1c 12.8% and nonfasting blood glucose of 685 mg/dL, without ketoacidosis within 2 months after switching to a BIC-containing ART requiring hospitalization and insulin therapy. Glycemia improved after discontinuation of BIC, suggesting a direct cause and effect with BIC. There were no significant changes in body weight, HIV viral load, or CD4+ T-cell count during this period, as well as a negative evaluation for secondary causes of hyperglycemia.
DISCUSSION: Acute hyperglycemia from BIC was not associated with weight changes and was reversible with no long-term effects on pancreatic beta-cell function. Incorporating metabolic monitoring (glycemia, weight, and lipid profile) and patient education for BIC into clinical practice, and utilizing a multidisciplinary team, can reduce the risk of acute hyperglycemia and glycemia-related hospitalization.
CONCLUSION: Patients starting a BIC-containing ART who have a history of obesity and/or dysglycemia should be educated and monitored for risk of developing acute hyperglycemia, which can be reversed upon BIC discontinuation.
CASE REPORT: A 36-year-old patient with virologically suppressed HIV, obesity, and prediabetes developed severe hyperglycemia, HbA1c 12.8% and nonfasting blood glucose of 685 mg/dL, without ketoacidosis within 2 months after switching to a BIC-containing ART requiring hospitalization and insulin therapy. Glycemia improved after discontinuation of BIC, suggesting a direct cause and effect with BIC. There were no significant changes in body weight, HIV viral load, or CD4+ T-cell count during this period, as well as a negative evaluation for secondary causes of hyperglycemia.
DISCUSSION: Acute hyperglycemia from BIC was not associated with weight changes and was reversible with no long-term effects on pancreatic beta-cell function. Incorporating metabolic monitoring (glycemia, weight, and lipid profile) and patient education for BIC into clinical practice, and utilizing a multidisciplinary team, can reduce the risk of acute hyperglycemia and glycemia-related hospitalization.
CONCLUSION: Patients starting a BIC-containing ART who have a history of obesity and/or dysglycemia should be educated and monitored for risk of developing acute hyperglycemia, which can be reversed upon BIC discontinuation.