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Drug-Induced Hyperglycemia
Beatriz Luna, PharmD, BCPS;
Mark N. Feinglos, MD, CM
JAMA. 2001;286:1945-1948.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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INTRODUCTION
It is well recognized that certain classes of drugs can cause clinically significant elevations in glucose concentrations. Historically, the agents implicated have included  -blockers, thiazide diuretics, corticosteroids, niacin, pentamidine, and others.1-2 Of recent interest are the increasing numbers of reported cases of new-onset diabetes mellitus (DM) in patients receiving treatment with protease inhibitors (PIs) or atypical antipsychotic agents. In most cases the mechanisms by which hyperglycemia occurs are not fully understood, although several possible theories have been proposed for each drug class.1-2
Elevated blood glucose concentrations can have significant consequences especially in high-risk populations. In the setting of hyperglycemia, granulocyte activity may be impaired, compromising the normal immunologic response and the host's capacity to resist infection.3-4 Hyperglycemia also directly inhibits the development of granulation tissue, impairing the wound healing process.5-6 Some evidence suggests that hyperglycemia, even in the nondiabetic range, can . . . [Full Text of this Article]
Thiazide Diuretics and  -Blockers
Protease Inhibitors
Atypical Antipsychotics
Conclusion
Author Affiliations: Department of Internal Medicine, Campbell University School of Pharmacy, Buies Creek, NC, and Durham Regional Hospital, Duke University Health System, Durham, NC (Dr Luna); Department of Internal Medicine, Division of Endocrinology, Metabolism and Nutrition, Duke University Medical Center, Durham, NC (Dr Feinglos).
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