Version May 2024
| Category | Agents | Mechanism* |
| Anti-infectives | ||
| Fluoroquinolones | Gatifloxacin¶ (not available in United States), moxifloxacin | Altered insulin secretion. Association with moxifloxacin is rare. |
| HIV antiretrovirals | Protease inhibitors Nucleoside reverse transcriptase inhibitors (NRTIs) | Increased peripheral insulin resistance. Part of antiretroviral-associated metabolic syndrome. |
| Other anti-infectives | Pentamidine | Altered pancreatic beta cell function. Following initial hypoglycemic effect, beta cell destruction can occur. |
| Antipsychotics | ||
| First-generation | Chlorpromazine¶, perphenazine, other phenothiazines | Mechanism not established. Appears to involve increased insulin resistance and diminished insulin secretion. |
| Second-generation | Clozapine¶, iloperidone, olanzapine¶, paliperidone, quetiapine, risperidone | Mechanism not established. Appears to involve increased insulin resistance and diminished insulin secretion. |
| Cardiovascular | ||
| Beta blockers | Atenolol, metoprolol, propranolol[1] | Decreased insulin sensitivity (moderate effect). Carvedilol does not appear to impair glucose tolerance. Refer to UpToDate topic on treatment of hypertension in patients with diabetes mellitus. |
| Hypolipidemic | Niacin (nicotinic acid)¶, statins | Niacin – Altered hepatic glucose metabolism, probably greater with extended-release form. Statins – Evidence of impaired glucose tolerance due to statins is conflicting, and overall risk appears low. |
| Thiazide diuretics | Hydrochlorothiazide, chlorthalidone, chlorothiazide, indapamide | Reduced total-body potassium, decreased insulin secretion, and increased insulin resistance[2]. Infrequent with low dosages (ie, hydrochlorothiazide ≤25 mg or equivalent). Potassium supplementation may decrease thiazide-associated glucose intolerance. |
| Vasodilators | Diazoxide | Reduced insulin secretion and sensitivity, increased hepatic glucose production. |
| Vasopressors | Epinephrine¶, norepinephrine[3] | Activation of glycogenolysis, increased hepatic gluconeogenesis, stimulation of glucagon and cortisol, inhibition of insulin secretion. |
| Gonadotropin-releasing hormone agonists | Class effect in males receiving androgen deprivation therapy for metastatic prostate cancer | Refer to UpToDate topic on side effects of androgen deprivation therapy. |
| Glucocorticoids, systemic* NOTE: Glucocorticoids are a particularly common cause of clinically significant drug-induced hyperglycemia | Class effect | Multifactorial, including increased hepatic glucose production, increased insulin resistance, increased expression of peroxisome proliferator activated gamma receptors (PPAR-gamma). Refer to UpToDate topic on major side effects of systemic glucocorticoids. |
| Hormones, growth | Somatropin, tesamorelin | Increased counterregulatory responses. Refer to UpToDate topics on treatment of growth hormone deficiency and treatment of HIV-associated lipodystrophy. |
| Immune checkpoint inhibitors | ||
| Programmed cell death receptor 1 (PD-1) inhibitors | Nivolumab, pemprolizumab, cemiplimab | PD-1 and PD-L1 inhibitors overcome immune suppression of cytotoxic T cells in the tumor milieu; CTLA-4 inhibitors overcome immune suppression of cytotoxic T cells in secondary lymphoid tissues. Immune checkpoint inhibitors promote activation of cytotoxic T cells that act "off target" to attack and destroy islet cells. |
| Programmed cell death ligand 1 (PD-L1) inhibitors | Atezolizumab, avelumab, durvalumab | |
| Cytotoxic T-lymphocyte associated protein 4 (CTLA-4) inhibitors | Iipilimumab, tremelimumab | |
| Immunosuppressants | Cyclosporine (cyclosporin), sirolimus, tacrolimus | Decreased insulin synthesis and release. Refer to UpToDate topic on new-onset diabetes after transplant in kidney transplant recipients. |
* Degree or incidence of hyperglycemia is generally related to dose.
¶ Among agents listed, these have been more frequently associated with hyperglycemia and/or diabetes mellitus.آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
