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Updated: Jun 14, 2025

Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
Published on: November 10, 2017
Case report: dyslipidaemia-dramatic increase in haemoglobin A1c following statin initiation
Crystal B Chen1, Marwan Badri1, Erik Kelly1
1Lankenau Heart Institute, Lankenau Medical Center, 100 E Lancaster Avenue, 356 Medical Office Building East, Wynnewood, PA 19096, USA.
Background:
Statin therapy is associated with an increased risk of hyperglycaemia and new-onset diabetes mellitus. The absolute increase in glycosylated haemoglobin (HgbA1c, a measure of average glucose level over the past three months) is typically small; dramatic and clinically relevant increases are rare.
Case Summary:
A 52-year-old man of South Indian descent with a history of hyperlipidaemia was started on rosuvastatin 40 mg daily for primary prevention of atherosclerotic cardiovascular disease. He did not have a history of diabetes mellitus. He developed polyuria and weight loss within weeks of starting statin therapy. Laboratory assessment was notable for HgA1c of 12.4% and LDL cholesterol of 84 mg/dL. Rosuvastatin was discontinued. He was not started on antidiabetic therapy as there was suspicion that statin therapy was the culprit for his HgbA1c rise. He soon had symptom resolution, and follow-up HgA1c 3 months later was 5.5%. Two years later, patient presented to the hospital with an acute coronary syndrome. He was discharged on rosuvastatin 40 mg daily and developed polyuria 1 week later. Rosuvastatin was discontinued, and atorvastatin 40 mg daily was initiated. Antidiabetic therapy was not started. He had resolution of his symptoms; follow-up HgA1c was below the diabetes threshold.
Discussion:
Statins are associated with a small increased risk of developing diabetes mellitus. The beneficial effects of statins on cardiovascular events typically outweigh any increased risk conferred by hyperglycaemia. While high-intensity statin therapy is routinely used as initial therapy for secondary prevention, we have no documentation explaining the choice of high-intensity statin for primary prevention in this case.
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