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Cannabidiol (CBD) oil has been gaining popularity as a natural alternative for numerous disease states. CBD is a phytocannabinoid obtained from the Cannabis sativa plant. Unlike its relative tetrahydrocannabinol (THC), CBD does not activate CB1 receptors in the brain and therefore lacks psychotropic effects (1). Instead, this substance is thought to work on the G-protein coupled receptor, endothelial cannabinoid receptor, and serotonin-1A receptors, among others. Diabetes is the seventh leading cause of death and affects >30 million people in the United States (2). CBD has been investigated, mostly in animal models, for its ability to help treat diabetes. It is theorized that cannabis has desirable effects on hyperglycemia through its anti-inflammatory and antioxidant properties (3). The endocannabinoid system modulates food intake and energy homeostasis by activating cannabinoid receptors. Modulation of these receptors with CBD has the possibility to reduce body weight and A1C in people with diabetes. In one study using mouse models, CBD was shown to significantly reduce the incidence of diabetes in these mice (4). This was shown by a significant decrease in pancreatic islets production of destructive insulitis and inflammatory cytokine production. The potential to use CBD as a method to treat diabetes reveals the need for studies and case reports. The following case illustrates the initiation of CBD in a patient with type 2 diabetes. A 62-year-old Hispanic obese man (weight 113 kg, BMI 39 kg/m2) with a history of type 2 diabetes for 11 years began taking CBD oil to control his blood glucose in place of insulin degludec. Initiation of this product was independent of his clinician’s recommendation and based on the patient’s personal review of information that suggested CBD was beneficial for people with type 2 diabetes. As shown in Table 1, the week before the patient’s initiation of CBD, …

Hypoglycemia has been a barrier to A1C attainment in people with diabetes (1). It is well known that a glucocentric approach with intensive control reduces microvascular complications, but at what cost? Worse clinical outcomes, increased risk of severe hypoglycemia, and heavier treatment burden can result from aggressive efforts to lower A1C (2). People with diabetes also tend to experience more stress as a result of fear of hypoglycemia, higher costs of care, and increased prevalence of polypharmacy—especially for those with type 2 diabetes of longer duration. New medication classes (e.g., sodium–glucose cotransporter 2 inhibitors and glucagon-like peptide 1 receptor agonists) are providing impetus for replacing the glucocentric treatment paradigm with an individualized multifactorial approach (2). Traditional glucagon kits have long been available for the ambulatory treatment of patients with hypoglycemia. However, these kits have disadvantages. Their complicated multistep injection procedure can be difficult to perform. Additionally, the use of glucagon must be taught to the family members, friends, or caregivers because it is administered by someone else when a person with diabetes is unconscious or otherwise incapacitated by severe hypoglycemia (3). For these reasons, glucagon is undertaught and underutilized (3). Two new glucagon formulations offer potentially easier delivery. The purpose of this article is to review all available glucagon formulations, discussing the associated literature and possible new directions for the treatment of hypoglycemia. The American Diabetes Association has adopted a three-level classification of hypoglycemia. Level 1 is a glucose concentration

Gastroparesis is characterized by delayed gastric emptying in the absence of mechanical obstruction. This complication is associated with uncontrolled diabetes, contributing to approximately one-third of all gastroparesis cases (1–3). Gastroparesis is more prevalent in patients with type 1 diabetes than in those with type 2 diabetes (4). The 10-year cumulative incidence of diabetic gastroparesis has been estimated to be 5.2% in patients with type 1 diabetes and 1% in those with type 2 diabetes (5,6). The prevalence of diabetes-associated gastrointestinal symptoms is 5–12% (7,8). In a study by Jung et al. (9) conducted in Olmsted County, MN, the prevalence of gastroparesis was about 5% in patients with type 1 diabetes and 1% in type 2 diabetes (9). In the same study, the age-adjusted incidence rate of gastroparesis was 2.4/100,000 person-years in men and 9.8/100,000 person-years in women (9). Gastroparesis, a form of autonomic neuropathy, is most commonly seen in people who have had diabetes for >10 years and who have already developed other microvascular complications (10). Once the symptoms from gastroparesis begin, they typically persist and are stable over 12–25 years; this is true even when blood glucose levels have been controlled (11). The most common symptoms are early satiety, nausea, bloating, abdominal pain, and vomiting. In terms of prognosis, a recent study published by Chang et al. (12) found no association between delayed gastric emptying and increased mortality over a 25-year period. Although there is no evidence to date that diabetic gastroparesis increases mortality, this complication substantially impairs all aspects of life (13). Although still not fully elucidated, the suggested pathophysiology of diabetic gastroparesis includes poor glycemic control, sympathetic vagal neuropathy, Cajal interstitial cell abnormalities, and loss of neuronal nitric oxide synthase (nNOS) (3,14). The loss of interstitial cells …

Glucagon-like peptide 1 (GLP-1) receptor agonists are a safe and effective treatment option for patients with type 2 diabetes (1). Selective activation of the GLP-1 receptor causes glucose-dependent insulin secretion, resulting in a very low risk of hypoglycemia (2). The additional mechanism of slowing gastric emptying has resulted in reliable weight loss with this class of antihyperglycemic medications (3). In addition, multiple agents in this drug class (semaglutide, liraglutide, and dulaglutide) have been proven to reduce the risk of cardiovascular events (4). Furthermore, the possibility of once-weekly dosing for glycemic control in type 2 diabetes has been realized with some GLP-1 receptor agonists (semaglutide, exenatide extended-release, and dulaglutide) as a result of albumin binding that decreases renal clearance and protects against metabolic degradation by the dipeptidyl peptidase-4 enzyme (2). Poor adherence to pharmacologic therapy is well documented in patients with type 2 diabetes and is linked to inadequate glycemic control (based on the American Diabetes Association’s general A1C goal of 10%) and injection-site reactions (>1%) (1,7). General injection-site reactions (e.g., erythema, pain, or rash) have been reported with all of the commercially available GLP-1 receptor agonists (i.e., exenatide, lixisenatide, liraglutide, dulaglutide, and semaglutide) (8–13). However, post-marketing reports have revealed that exenatide extended-release, specifically, may cause more alarming injection-site …

Individuals with type 1 diabetes represent only ∼6% of all patients with diabetes in the United States and require characteristically complex treatment modalities (1). Autoimmune pancreatic β-cell destruction ultimately results in an absolute insulin deficiency, the presence of autoimmune markers, and little to no residual C-peptide (2,3). Additionally, pancreatic α-cell dysfunction is present, resulting in excess glucagon in both the fasting and postprandial states, and the gastric emptying rate is altered in many patients. Exogenous insulin serves as the foundation of therapy for type 1 diabetes and is commonly delivered via a multiple-dose regimen or an insulin pump. The two most common adverse effects associated with insulin use are hypoglycemia and weight gain. Recent data suggest that 68% of people with type 1 diabetes are overweight or obese and that severe hypoglycemia occurs at a rate of 9–20% (4). The latter complication is considered a limiting factor to achieving glycemic targets in the type 1 diabetes population. Indeed, the average A1C for adults ≥18 years of age with type 1 diabetes in the United States was 7.9% in 2015, a value well above the target of 7% recommended by the American Diabetes Association for most adult patients. Further complicating matters, diabetic ketoacidosis (DKA) occurs at a rate of 10% per year in some age-groups (4). Overall, these data suggest a need for adjunctive therapies for type 1 diabetes that reduce the risk for hypoglycemia and weight gain. While β-cell dysfunction is clearly a therapeutic focus for all types of diabetes, multiple other pathways of hyperglycemia present opportunities for alternate treatment modalities that may assist in achieving glycemic targets (5). The ideal pharmacotherapy regimen for a patient with type 1 diabetes would not only target the β-cell dysfunction, but also decrease blood glucose through hyperglycemic pathways independent of β-cell …

Canagliflozin is a member of the sodium–glucose cotransporter 2 (SGLT2) inhibitor class and is approved by the U.S. Food and Drug Administration (FDA) for use in patients with type 2 diabetes as an adjunct to diet and exercise to improve glycemic control. Canagliflozin works by inhibiting SGLT2 in the proximal renal tubules, causing a reduction of filtered glucose reabsorption, lowering of the renal threshold for glucose, and increasing urinary glucose excretion (1). The American Diabetes Association (ADA) Standards of Medical Care in Diabetes—2017 (2) and the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE) (3) recommend SGLT2 inhibitors as add-on to metformin for patients with type 2 diabetes uncontrolled after 3 months of metformin use. The ADA lists the SGLT2 inhibitors as investigational agents for patients with type 1 diabetes because of the risk of diabetic ketoacidosis (DKA). Despite concerns for DKA in patients with type 2 diabetes treated with an SGLT2 inhibitor, a clinical review by an expert panel found that DKA occurred infrequently and recommended no change to their labeling (4). Although SGLT2 inhibitors are not FDA-approved for use in patients with type 1 diabetes, providers have prescribed these agents for off-label use in this patient population. Glycemic variability may be problematic in patients with type 1 diabetes; therefore, adding an SGLT2 inhibitor can assist in not only improving glycemic control but also reducing glycemic fluctuations. Although adding an SGLT2 inhibitor to insulin may increase the risk of hypoglycemia, the potential to reduce the need for increasing insulin doses may moderate this effect. Patients with type 1 diabetes uncontrolled with insulin therapy who are overweight/obese and have hypertension may benefit from the addition of an SGLT2 inhibitor because these medications help to lower A1C values and can reduce both weight and blood pressure. Several studies have …

Glucagon-like peptide 1 (GLP-1) receptor agonists are relatively new additions to the treatment options available for type 2 diabetes. These agents provide glycemic control by increasing glucose-dependent insulin secretion, decreasing inappropriate glucagon secretion, slowing gastric emptying, and increasing satiety (1). The GLP-1 receptor agonists are an attractive treatment option because they are associated with weight loss and have a low risk of hypoglycemia. However, their use is limited in some patients because of gastrointestinal adverse effects (nausea, vomiting, diarrhea), cost, and their subcutaneous route of administration (1). There are currently six GLP-1 receptor agonists approved for use in the United States: exenatide (Byetta), 2005; liraglutide (Victoza), 2010; exenatide XR (Bydureon), 2012; albiglutide (Tanzeum), 2014; dulaglutide (Trulicity), 2014; and lixisenatide (Adlyxin), 2016. Many differences exist within this class of medications, including efficacy and safety profiles, dosing schedules, and preparation and administration requirements, making product selection and use potentially confusing for both health care professionals (HCPs) and patients. Dosing schedule is one important consideration when comparing GLP-1 receptor agonists. Whereas three of the GLP-1 receptor agonists are available in multi-use, disposable pen devices and are given either twice daily (exenatide) or once daily (liraglutide and lixisenatide), the other three GLP-1 receptor agonists are once-weekly formulations available in single-use, disposable pen devices (albiglutide [2], dulaglutide [3], and exenatide XR [4]). Once-weekly products may offer the advantage of better adherence and ease of use compared to once- or twice-daily medications. In clinical studies, adherence to treatment and treatment satisfaction significantly increased with once-weekly GLP-1 receptor agonists compared to once- or twice-daily GLP-1 receptor agonists (5–7). In comparing efficacy and safety of the once-weekly agents, meta-analyses and head-to-head trials demonstrate that dulaglutide showed the greatest reduction in A1C compared with other once-weekly GLP-1 receptor agonists, …

Diabetes is a major worldwide epidemic with >415 million individuals living with the disease. This number is expected to grow to a staggering 642 million by 2040 (1). According to the American Diabetes Association, diabetes affects 29.1 million Americans, or 9.3% of the population. Diabetes management in the United States presents several challenges: 20% of individuals with diabetes remain undiagnosed, 1.4 million new cases are diagnosed annually, and one-third of adults with diabetes are not at the general recommended A1C goal of

Obtaining complete medication histories is imperative to treating patients effectively and avoiding unintended medication consequences. Health care providers (HCPs) receive training and learn skills to help elicit complete medical information, including but not limited to medication use, but the system falls short in some instances (1,2). In these instances, undocumented medication use can complicate patients’ treatment. Examples encompass confounding of the differential diagnosis and unforeseen medication interactions. The potential for unintended medication consequences can be increased by omissions in reporting usage of herbal, homeopathic, or over-the-counter (OTC) treatments. Although warnings about the risks of self-medicating, such as possible variability of medication effects from one person to another, date back for decades, this practice has become increasingly common (3,4). Self-medication through the use of old prescriptions or OTC products has the potential to pose problems, but self-medication via prescription sharing with other individuals—often family members or friends—is especially problematic. This practice can be dangerous because it can remain undetected for long periods of time and may be accompanied by a wide range of effects. Prescription medications are intended to be used under the supervision of licensed HCPs. The sharing of prescription medications among individuals removes pharmacists and other HCPs from the medication use process, resulting in the loss of education and instruction regarding the safe use of medications and increasing the potential for adverse effects (5,6). A survey distributed to patients in community pharmacies in New Zealand showed that, among prescription sharers, about half of prescription borrowers received written instructions with the medication, and about half of prescription lenders gave verbal instructions with the medication (7). That leaves many individuals with no instructions at all, and those who do receive instructions cannot be certain that they have received correct information because the source is not …

Diabetes is a complex, chronic medical condition affecting 29.1 million people in the United States (9.3% of the population) and is projected to affect one in three Americans by 2050 if the current trend continues (1). Diabetes management can be challenging, often requiring multiple therapeutic agents as the disease progresses. Current guidelines recommend metformin as first-line pharmacological therapy for the treatment of type 2 diabetes. Multiple second-line options are available for patients whose A1C goal is not achieved with monotherapy, and selection should be based on patient- and drug-specific factors. Sodium–glucose cotransporter 2 (SGLT2) inhibitors, the newest U.S. Food and Drug Administration (FDA)–approved oral antidiabetic agents, are among these options for patients with type 2 diabetes. Canagliflozin, dapagliflozin, and empagliflozin are the currently available SGLT2 inhibitors in the United States (2,3). Sodium–glucose cotransporter 1 (SGLT1) is predominantly located in the small intestine, but is also expressed in the kidneys, trachea, heart, and colon (4,5). In the kidneys, SGLT1 is primarily located in the S3 segment of the proximal convoluted tubule (PCT) (4). SGLT2 is expressed in the kidneys and primarily located in the S1 and S2 segments of the PCT (4,5). In normoglycemic adults, about 180 g of glucose (Figure 1) is filtered per day in the glomerulus, and most is reabsorbed (4,6). In people with diabetes, reabsorption of glucose is increased compared to people without diabetes (7,8). SGLT1 and SGLT2 are located in the apical membrane and facilitate the transport of glucose with sodium from the renal tubular lumen into the cells (Figure 2) (4). FIGURE 1. Structures of glucose, phlorizin, canagliflozin, dapagliflozin, and empagliflozin. FIGURE 2. Cotransport of glucose and sodium by SGLT1 and SGLT2 in the PCT. Phlorizin (Figure 1), an O -glucose derivative/ O -glycoside, was discovered in …

Latent autoimmune diabetes in adults (LADA) is considered a subgroup of type 1 diabetes and is often misdiagnosed because of a lack of both awareness and standardized diagnostic criteria (1–3). LADA is characterized by adult-onset diabetes and circulating autoimmune antibodies; thus, patients may present clinically with characteristics of both type 1 and type 2 diabetes (2–5). Typically, the clinical features of type 1 diabetes seen in LADA include a lower BMI compared to what is typical in type 2 diabetes and autoimmunity against one or more of the following antibodies: islet cell autoantibodies (ICA), autoantibodies to glutamic acid decarboxylase (GAD), tyrosine phosphatase–related islet antigen 2 (IA-2), and insulin autoantibodies (IAA) (4,5). The characteristics of type 2 diabetes that may present in LADA include older age at onset and insulin resistance or deficiency. Characteristics of LADA tend to include an intermediate level of β-cell dysfunction between those in type 1 and type 2 diabetes, faster decline of C-peptide compared to type 2 diabetes, and a level of insulin resistance that is comparable to type 1 diabetes (4). β-Cell decline is variable in LADA, as measured by C-peptide levels (5–7). Although it has a closer pathophysiological relationship to type 1 diabetes, LADA is often misdiagnosed and treated as type 2 diabetes (2–5). This results in insufficient glycemic control and harm to patients. It is imperative to establish distinct practice guidelines for the diagnosis and treatment of LADA and for providers to recognize this clinical scenario as one that requires special testing to establish a proper diagnosis and thus improve patient safety and treatment efficacy. The similarities between type 1 diabetes, type 2 diabetes, and LADA can make diagnosis difficult (Table 1). There are, however, other characteristics for this population that may …

Underserved Hispanic patients are particularly vulnerable to problems associated with controlling diabetes. Hispanics not only are more susceptible to developing diabetes, but also have higher A1C values (1) and more severe diabetes-related complications. Hispanic Americans are 2.6 times more likely to start treatment for diabetes-related end-stage renal disease and have a 50% higher mortality rate than non-Hispanic whites (2). According to the Hispanic Community Health Study/Study of Latinos, the prevalence of diabetes in the United States is 10.2% in South Americans, 13.4% in Cubans, 17.7% in Central Americans, 18% in Puerto Ricans and Dominicans, and 18.3% in Mexicans (3). Total yearly costs in 2010 for Hispanics with diabetes totaled $49.8 billion and are estimated to reach $109.9 billion in 2025 because of an expected 111% increase in diabetes cases (4). Many diabetes patients, including Hispanics, are overwhelmed by the high treatment burden of self-care demands (5). A retail pharmacy survey of individuals in five states found that many individuals with diabetes lack a focused management plan and may also be confused about specific health care issues (6). One particular obstacle is nonadherence to diabetes treatments. Hispanic patients have exhibited nonadherence behaviors related to their diabetes treatment, including medication nonadherence (7,8). Nonadherence is very costly (9), and savings of $5 billion annually are possible with improved medication adherence on the part of non-Hispanic and Hispanic patients alike. This could result in 341,000 fewer hospitalizations and 700,000 fewer emergency room visits (10). One tactic to mitigate nonadherence has been to involve pharmacists in diabetes management, particularly in primary care settings, where diabetes is a common diagnosis (11). Studies demonstrating the benefit of pharmacists in diabetes care and of their expertise in medication management highlight their importance as interdisciplinary team members (12–17). Including pharmacists in team-based …

Diabetes has been increasing in prevalence over the years, and nearly 30 million Americans (9.3%) now have diabetes (1). This disease burden on the population also translates to increased prevalence rates of diabetes complications. Diabetes is associated with several eye complications, including cataracts and glaucoma (2). However, the most common eye disorder associated with diabetes is diabetic retinopathy (DR), which is the leading cause of blindness among U.S. adults (2,3). During the 2005–2008 time period, >4 million adults ≥40 years of age with diabetes had retinopathy, including diabetic macular edema (DME) and proliferative diabetic retinopathy (PDR), which can lead to vision loss (1). The management of systemic disorders is vital to preventing diabetic eye complications (4). Specifically, the management of diabetes, hypertension, and hyperlipidemia has been associated with reduced or delayed onset and progression of DR (5–11). However, even with adequate control of these metabolic conditions, people with diabetes may still be at risk for developing retinopathy. Adequate eye screening is therefore important for the early detection and treatment of visual complications (4). Screening recommendations call for a dilated, comprehensive eye examination within 5 years after diabetes diagnosis for people with type 1 diabetes and immediately after diagnosis for those with type 2 diabetes (12). Laser therapy has been the mainstay of treatment for DR and DME. Primarily, laser photocoagulation treatment has been used to prevent vision loss and to delay progression of retinopathy (13). The associated adverse effects of laser therapy, including night and peripheral vision loss, are generally preferred to eventual blindness. When laser treatment is not feasible, vitreous surgery becomes an option and has been shown to be beneficial for PDR and DME (4). Research has supported the intravitreal administration of steroids, whose anti-inflammatory and antiangiogenic effects are beneficial in …

There are 29.1 million people in the United States living with diabetes (1). Except in cases with contraindications, annual influenza vaccination is recommended for all people with diabetes to reduce morbidity, mortality, and health care costs associated with influenza illness (2,3). There were 12 influenza vaccines available for the 2016–2017 influenza season. These vaccines were categorized into inactivated or live, quadrivalent or trivalent, and high-dose or standard-dose formulations (2). Common adverse reactions of pain, soreness, fever, muscle aches, fatigue, redness, or swelling may occur after intramuscular vaccine administration (4). Hyperglycemia is not noted as an adverse reaction in vaccine package inserts; however, reports of its occurrence have been documented in the Vaccine Adverse Event Reporting System (VAERS) (5). Since 1991, there have been 946 reports of hyperglycemia with all available vaccines and 361 reports of hyperglycemia with all types of influenza vaccines. When looking specifically at the trivalent influenza vaccine, there have been 235 reported cases, with 70.6% reported during the first 4 days after vaccine administration (5). In light of these reports, a literature search was performed to obtain more information about acute hyperglycemia after vaccine administration. The search was performed with the advanced search option in PubMed using the terms "hyperglycemia,” “blood sugar,” “blood glucose,” “vaccines,” “influenza vaccine,” “diabetes,” and “immunizations.” The search failed to yield any literature reports specifically related to blood glucose …

Just a few years shy of a century ago, a group of Canadian researchers discovered a viable method of extracting insulin, filling a large and critical gap in the therapeutic treatment of diabetes (1). Since then, insulin and its associated delivery devices have become an integral part of the care and management of patients living with diabetes. Shortly after the first insulin injection was successfully delivered, vials of insulin became available commercially. At this time, large glass syringes were used to administer insulin, and each injection required sterilization of the syringe, as well as sharpening of the syringe needle with a pumice stone. Through the years, insulin syringes modernized, but it was not until the 1970s that an alternate delivery system—the insulin pump, used in continuous subcutaneous insulin infusion (CSII) regimens—became available. Fifteen years later, the first insulin pen was introduced to the marketplace, providing evidence that, as time progresses, there is no shortage of innovation in the diabetes arena. The first two rapid-acting inhaled insulins on the market—Exubera in 2006 and Afrezza in 2014—represented yet another innovation milestone. In theory, inhaled insulin completely eliminated the psychological barriers associated with subcutaneous insulin delivery, such as needle phobia and incorrect injection technique. However, in October 2007, Pfizer withdrew Exubera from the market, and in January 2016, Sanofi withdrew from a $925 million marketing agreement with MannKind for Afrezza; both removals were due to poor sales volume. Although patients and providers have been searching for years for alternatives to injecting insulin, Exubera has already failed, and Afrezza’s destiny is uncertain. In 2006, Exubera was the first inhaled insulin approved by the U.S. Food and Drug Administration (FDA). It showed noninferiority in efficacy with regard to A1C lowering in both type 1 diabetes (2) and type 2 diabetes (3) compared to mixed regular/NPH …

The growing incidence and prevalence of diabetes has made a significant impact on the development of diabetic kidney disease (DKD) (1). DKD is among the most frequent complications of diabetes; indeed, diabetes accounts for ∼50% of all cases of end-stage renal disease (ESRD) in developed countries (2). Patients often have comorbid diabetes and chronic kidney disease (CKD). Although intensive glycemic management has been shown to delay the onset and progression of increased urinary albumin excretion and reduced estimated glomerular filtration rate (eGFR) in diabetes patients (3), conservative dose selection and adjustment of antidiabetic medications is necessary to balance glycemic control with safety. A1C has limitations related to its precision and interpretation in the CKD population (4), with erythrocyte turnover being a major cause of A1C imprecision in this population. Red blood cell survival times become shorter as eGFR falls, resulting in a reduction in measured A1C. Treatment with erythrocyte-stimulating agents lowers A1C further, perhaps because of changes in hemoglobin concentrations (5,6). Observational data support the notion that higher A1C levels in nondialysis diabetes patients with CKD stages 3–5 (eGFR levels

Exercise, as part of lifestyle modification, is known to be the first line of therapy for patients with type 2 diabetes (1), and, dating back as far as 1000 AD, Greek physicians prescribed exercise as a way to improve health (2). Regular exercise provides many physiological and psychological benefits, including improvements in glycemic control (in most individuals), insulin sensitivity, blood pressure, lipid profile, muscular strength, and bone mineral density. In addition, exercise reduces total daily insulin requirements in people on insulin therapy, risk for coronary artery disease, body weight, percentage of body fat, stress, and depression and improves individuals’ sense of well-being and quality of life (3–5). Given all the health benefits it provides, exercise truly can be considered “medicine.” Despite being advised to participate in exercise as an essential part of diabetes management, only 39% of adults with diabetes are physically active (6), and many face barriers to becoming and staying physically active. Brazeau et al. (7) found four main barriers to physical activity in patients with type 1 diabetes: fear of hypoglycemia, work schedule, loss of control over diabetes, and low fitness level. Fear of hypoglycemia is the major barrier and biggest challenge for people treated with insulin. Exercise can cause profound changes in glucose homeostasis and may lead to hypoglycemia. Some hypoglycemia symptoms such as sweating and fatigue are similar to the physical sensations of normal exertion, which can make it difficult for patients to distinguish between the two (7). Given that an excessive decrease in blood glucose is a primary clinical concern and barrier to being physically active for people with diabetes, it is important to consider potential interactions between antihyperglycemic medications and exercise to minimize the risk of hypoglycemia. This article provides a brief overview of medication management considerations in people with …

The association between inpatient hyperglycemia and adverse patient outcomes is well documented.1–7 Thus, focus on inpatient glycemic control has increased in the past decade. However, optimal glycemic targets remain controversial, and significant barriers to optimal glycemic control persist. After publication of the initial van den Berghe trial in surgical intensive care patients,1 several professional organizations published guidelines supporting near-normal glycemic targets.8,9 Subsequent trials documented an increased risk for hypoglycemia with tight glycemic control, suggesting that more modest glycemic targets may be optimal.10–13 The Normoglycemia in Intensive Care Evaluation–Survival Using Glucose Algorithm Regulation (NICE-SUGAR) study,14 a large, randomized trial involving > 6,100 medical and surgical patients, documented higher 90-day mortality rates in patients managed with tight glycemic control than in those receiving conventional glucose management. Although hypoglycemia was more common among patients in the intensive treatment group, the association of hypoglycemia with an increased hazard ratio for death was similar in the two groups, suggesting that hypoglycemia contributed to the excess mortality in the intensively treated group.15 The increased risk for hypoglycemia and mortality with tight glycemic control does not justify ignoring glycemic control, but it does justify setting more moderate targets. The American Diabetes Association (ADA), the American Association of Clinical Endocrinologists (AACE), the Surviving Sepsis Campaign, and the Institute for Healthcare Improvement all updated their guidelines for glycemic control in 2009 in response to data from NICE-SUGAR.16–18 All four sets of guidelines recommend initiating insulin therapy in patients with persistent hyperglycemia (blood glucose > 180 mg/dl). After insulin is initiated, the target blood glucose range should be 140–180 mg/dl for the majority of patients. However, a more stringent goal of 110–140 mg/dl may be appropriate for certain patients, provided it can be achieved without …