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Drug-Induced Glucose Alterations Part 1: Drug-Induced Hypoglycemia Mays H

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Drug-Induced Glucose Alterations Part 1: Drug-Induced Hypoglycemia Mays H Pharmacy and Therapeutics Drug-Induced Glucose Alterations Part 1: Drug-Induced Hypoglycemia Mays H. Vue, PharmD, and Stephen M. Setter, PharmD, CDE, CGP Many pharmacological agents com- on Hypoglycemia has defined and monly used in clinical practice affect classified hypoglycemia based on glucose homeostasis, interfering with the severity of symptoms in patients the body’s balance between insulin, diagnosed with diabetes as outlined glucagon, catecholamines, growth in Table 2.2 In general, severe hypo- hormone, and cortisol. Drug-induced glycemia develops when a reduction serum glucose alterations manifested in blood glucose is enough to require as hyperglycemia or hypoglycemia assistance from another person and ranging from mild to moderate to actively administer carbohy- to severe symptoms either appearing drate, glucagon, or other corrective acutely or chronically, have perpetual actions.2 Severe hypoglycemia is effects on the body, particularly in a serious clinical syndrome that patients with diabetes. This article continues to be the most common and a second one that will appear in endocrine emergency faced by health the next issue of this journal review care providers and remains the drug-induced serum glucose altera- limiting factor in effective diabetes tions in a two-part series. In this management for many patients.6 article, we review pertinent clini- Hypoglycemia has been associ- cal information on the incidence of ated with a higher number of hospital drug-induced hypoglycemia and admissions, longer hospital stays, and discuss the underlying pathophysi- significant morbidity and mortality ological mechanisms involved. in patients with diabetes or hypergly- Hypoglycemia is clinically cemia.6,7 In a systemic review of 448 defined as a serum glucose con- publications describing drug-induced centration low enough to cause the hypoglycemia,8 90% of reported signs and symptoms differentiated in cases were classified as severe hypo- Table 1.1–4 Depending on the sever- glycemia in which symptoms were ity, hypoglycemic symptoms include present and required assistance by irritability, impaired concentration, someone other than the patient. neurological deficits, seizures, coma, Although hypoglycemia can be and even neuronal death.5 However, iatrogenic, in which normal body clinical manifestations vary from defenses are impaired, treatment individual to individual, and some with insulin or insulin secretagogues report hypoglycemic symptoms even (e.g., sulfonylureas [SUs] and meg- when serum glucose levels do not litinides), as monotherapy or in reflect hypoglycemia or vice versa. combination, account for a majority Although definitions of hypogly- of hypoglycemic events.3 In addition cemia differ in the literature, many to glucose-lowering agents, many trials will differentiate between commonly used non-antidiabetic hypoglycemia (asymptomatic and drugs have been reported to cause or symptomatic low serum glucose contribute to drug-induced hypogly- levels) and severe hypoglycemia. This cemia, even in individuals without article will cover and report both diabetes. Furthermore, as people when applicable. age and their number of comorbidi- The American Diabetes ties and medications increase over Association (ADA) Workgroup time, they expose themselves to an Diabetes Spectrum Volume 24, Number 3, 2011 171 Pharmacy and Therapeutics Table 1. Signs and Symptoms of Hypoglycemia3,4 Signs Symptoms Diaphoresis Neurogenic (Autonomic) Neuroglycopenic Pallor Catecholamine-mediated Acetylcholine-mediated Cognitive impairment Increased heart rate (adrenergic) (cholinergic) Behavioral changes Elevated systolic blood Irritability pressure Tremor Sweating Drowsiness Palpitations Hunger Blurred vision Anxiety/arousal Tingling Difficulty with speech Trembling Confusion Feeling faint Seizure Coma Table 2. ADA Workgroup on Hypoglycemia Definition and Classification of Hypoglycemia in People With Diabetes1,2 Type of Hypoglycemia Presentation of Symptoms Severe hypoglycemia An event requiring assistance of another person to actively adminis- ter resuscitative actions Documented symptomatic hypoglycemia An event during which typical symptoms of hypoglycemia are accompanied by a measured plasma glucose concentration ≤ 70 mg/dl Asymptomatic hypoglycemia An event not accompanied by typical symptoms of hypoglycemia but with a measured plasma glucose concentration ≤ 70 mg/dl Probable symptomatic hypoglycemia An event during which symptoms typical of hypoglycemia are not accompanied by a plasma glucose determination (but that was pre- sumably caused by a plasma glucose concentration of ≤ 70 mg/dl) Relative hypoglycemia An event during which the person with diabetes reports any of the typical symptoms of hypoglycemia and interprets those as indica- tive of hypoglycemia, with a measured plasma glucose concentration > 70 mg/dl but approaching the hypoglycemic level exponential risk for possible drug in the management of diabetes will used in the management of diabetes. interactions or cumulative adverse allow for more practical and safe Although numerous drugs can lower effects that may result in asymptom- health care practices. serum glucose concentrations, this atic or symptomatic hypoglycemia. Medications commonly used for article will review non-antidiabetic Thus, thoroughly reviewing a diabetes treatment are not discussed drugs or drug classes associated with patient’s medication history is in detail in this review because hypoglycemia used in patients with essential, and drug-associated causes hypoglycemia has been well estab- diabetes (Table 4). should always be included in the dif- lished with the use of insulin, SUs, ferential diagnosis of hypoglycemia and meglitinides as monotherapy or ACE Inhibitors until ruled out by other causes (e.g., in combination with other agents In 1985, the first case of ACE non-endocrine disease, trauma, or such as metformin, thiazolidinedio- inhibitor–induced hypoglycemia infections). nes (TZDs), exenatide, or dipeptidyl was reported with the administra- Serum glucose reductions sec- peptidase-4 (DPP-4) inhibitors. tion of captopril.11 Since then, several ondary to pharmacological agents However, metformin, TZDs, and reports and small studies have pub- are caused by multiple actions that α-glucosidase inhibitors such as lished the incidence of hypoglycemia include pharmacokinetic or phar- acarbose and miglitol, when admin- associated with ACE inhibitor use, macodynamic drug interactions istered as monotherapy at usual but the data remain controversial. or additive hypoglycemic effects doses, should have little to no risk In a small case-control study from polypharmacy. Recognition of of hypoglycemia based on their from the Netherlands,12 94 patients underlying pathophysiological mech- mechanisms of action. As a point were identified and admitted to the anisms responsible for drug-induced of reference, Table 39,10 provides the hospital with hypoglycemia, and hypoglycemia from pharmacological absolute risk of hypoglycemia for 654 control subjects were selected treatments other than those used common glucose-lowering agents from the same cohort. As many as 172 Diabetes Spectrum Volume 24, Number 3, 2011 Pharmacy and Therapeutics Table 3. Absolute Risk of Mild-to-Moderate Hypoglycemia With Commonly Used Glucose-Lowering Agents9,10 Drug Class Drug Monotherapy Combination Therapy Biguanides MET † See combinations See combinations with MET below. with MET below. Second-generation Glimepiride 0.9–1.7% + pioglitazone 13.4–15.7% sulfonylureas (SUs) + rosiglitazone 3.6–5.5% Glipizide 3% + MET 7.6–12.6% Glyburide 21.3% + MET 11.4–37.7% Meglitinides Nateglinide 1.3–3% * * Repaglinide 16–31% + MET 33% Glucagon-like pep- Exenatide 4.5–35.7% + MET 4.5–5.3% tide-1 (GLP-1) + SU 14.4–35.7% + MET + SU 19.2–27.8% + TZD 11% Liraglutide 9.7% + MET 3.6% + glimepiride 7.9% + MET + glimepiride 27.4% Thiazolidinediones Pioglitazone † + MET 4.4% (TZDs) + SU 26.7–28.8% + insulin 53.4–56.4% Rosiglitazone † + MET 3.6–5.5% + glimepiride 3.6–5.5% α-Glucosidase Acarbose † + SU or insulin 2% inhibitors Miglitol † * * DPP-4 inhibitors Sitagliptin 0.6–12.2% + MET 1.6% + glimepiride 12.2% +/- MET Saxagliptin 2.7–14.6% + MET 3.4–7.8% + glyburide 13.3–14.6% + TZD 2.7–4.1% Amylinomimetic Pramlintide 16.8% * * MET, metformin; SU, sulfonylurea; TZD, thiazolidinedione. *Risk not reported. †Absolute risk data are not available because these agents cause little to no risk of hypoglycemia when used in monotherapy and within normal dosing ranges. Although hypoglycemia risk is low in monotherapy, when given in combination with oral hypoglycemic agents or insulin, additive effects increase the risk of hypoglycemia, as shown above. 13.8% of all hospital admissions three- to fourfold increased risk of ulating hepatic glucose production. for hypoglycemia were significantly hypoglycemia. Although the exact Suppression of peripheral sympa- attributable to the use of ACE mechanism for its glucose-lowering thomimetic overactivity may also be inhibitors (odds ratio 2.8 [95% effects is unknown, the hypoth- involved in blood glucose–lowering CI 1.4–5.7]), but this was among esis involves an indirect increase in effects of ACE inhibitors.14 patients with diabetes concomitantly insulin sensitivity by increasing cir- treated with insulin or oral antidia- culating kinine, which in turn leads Alcohol/Ethanol betic agents for at least 1 year. to vasodilatation in the muscles and Hypoglycemia associated with Another small study13 determined ultimately increased glucose uptake
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