1 . Type 2 diabetes mellitus (T2DM)
| A) | | is anticipated to increase as the U.S. population ages. |
| B) | | appears to be occurring at a lower rate in younger adults. |
| C) | | is diagnosed most often in those with a body mass index (BMI) less than 30 kg/m2 than in those with a higher BMI. |
| D) | | All of the above |
EPIDEMIOLOGY OF TYPE 2 DIABETES
Several causes for the extreme increase in incidence of T2DM
in the late 20th century have been noted. First, the U.S. population is expanding annually,
resulting in an increase in the number of people with T2DM [10]. Second, rising rates of overweight and
obesity correlate with the rising incidence of T2DM, as these factors have a positive
association [5,11]. Rates of obesity were 15% in 1980, 23% in
1994, 31% in 2000, 35% in 2011–2012, and more than 42% in 2017–2018 [5,12,13].Among those with
diabetes, 89.8% of patients are overweight or obese, with 45.8% being obese (body mass index
[BMI] >30 kg/m2 to ≤39.9 kg/m2) and
16.2% being classified as severely obese (BMI >40 kg/m2) [1,6]. Third, because T2DM disproportionately affects elderly individuals,
rising rates of T2DM are anticipated to reflect the steadily growing population of adults 65
years of age and older [10,14]. It has also been observed that T2DM
appears to be occurring at a greater frequency in younger adults. Between 1988–1994 and
1999–2000, the mean age at diagnosis of T2DM decreased from 52 years to 46 years, and in
2015, more than one-half of new cases were among adults 45 to 64 years of age [5,15]. Rates of incidence, both increasing and decreasing, can be attributed
to changing diagnostic criteria, improved physician recognition of T2DM, and increased
public awareness, making additional research necessary to determine if changes in incidence
rates are due to prevention and treatment strategies or if the rates reflect a shifting
trend toward earlier onset of T2DM [15].
2 . Within the United States, which racial/ethnic group reports the largest percentage of T2DM?
| A) | | Alaska Natives |
| B) | | Asian Americans |
| C) | | Non-Hispanic whites |
| D) | | American Indians in certain areas of the Southwest |
EPIDEMIOLOGY OF TYPE 2 DIABETES
T2DM is marked by a number of disparities among affected
groups, most notably within specific racial and ethnic populations. For example, while the
number of non-Hispanic whites in the United States with T2DM far exceeds the number of
non-Hispanic blacks with this condition, the percentage of non-Hispanic blacks with T2DM
(11.5%) is significantly greater than that of non-Hispanic whites (7.2%) (Figure
1) [1,16]. Hispanic Americans also appear to
be disproportionately affected by T2DM, with studies indicating rates of T2DM to be
significantly higher in this population compared to non-Hispanic whites (11.8% and 7.2%,
respectively) [1]. Asian Americans have a
slightly higher rate (8.9%) compared to non-Hispanic whites (7.2%) [1]. In addition, the group reporting the
largest percentage of T2DM, at 14.5% of the total adult population, is American Indians and
Alaska Natives, with rates ranging from 6.0% among Alaska Natives to as high as 22.2% among
American Indians located in certain areas of the Southwest [1]. Increasing numbers of members of high-risk minority groups in the
United States contribute to the overall projected rise of T2DM [8]. Therefore, targeting these populations for
prevention, intervention, and education is a strategy that can be employed to mitigate the
impact of T2DM across the nation.
3 . Obesity increases the risk of T2DM by affecting
| A) | | cellular metabolism. |
| B) | | serum free fatty acids. |
| C) | | adipocyte hormone production. |
| D) | | All of the above |
PATHOPHYSIOLOGY OF TYPE 2 DIABETES
A number of predisposing risk factors have been attributed to
the development of T2DM, most notably obesity, which affects cellular metabolism, serum free
fatty acids, and adipocyte hormone production (Figure 2)
[17,18,19]. Other environmental
factors, including poor diet (evidenced by increased caloric intake as well as decreased
food quality) and decreased activity, amplify these effects, as can certain medications and
ongoing stress [17,20]. However, these factors alone are not
adequate to initiate T2DM; certain genetic characteristics must also be present. To date, a
large number of loci possessing common variants have been implicated in diabetes
susceptibility, aided in great part by genome-wide association—a hypothesis-generating
approach directed at linking new loci with a disease or trait of interest (in this instance,
T2DM) [21]. The exact combination of genetic
and environmental factors that generates T2DM is as yet unknown, but research continues to
elucidate potential contributors.
4 . The term "pancreas plasticity" refers to the ability of the pancreas to adapt
| A) | | beta-cell mass to glucose load. |
| B) | | beta-cell function to glucose load. |
| C) | | beta-cell mass to insulin demand. |
| D) | | beta-cell function to insulin demand. |
PATHOPHYSIOLOGY OF TYPE 2 DIABETES
Impaired insulin secretion is a key mechanism in the
development of T2DM. The framework for this process is built on the understanding that
insulin is secreted from beta cells and hyperglycemia occurs when beta-cell secretion of
insulin is inadequate respective to the glucose load [22]. In healthy individuals, glucose ingestion (and resultant increase in
plasma glucose concentration) triggers the production and release of insulin by pancreatic
beta cells [22]. In those with T2DM, insulin
response to glucose declines as a result of a functional beta-cell deficiency [23]. This defect has been demonstrated by
findings that islet function appears to be approximately 50% of normal at the time of
diagnosis and is supported by data from the United Kingdom Prospective Diabetes Study
(UKPDS), in which patients who achieved beta-cell function greater than 55% with
sulfonylurea monotherapy were less likely to require additional therapy to maintain glycemic
targets [24]. Thus, it is now understood
that insulin sensitivity is inversely and proportionally related to beta-cell function [24]. These processes are further exacerbated
when the inability of the pancreas to adapt beta-cell mass to insulin demand (referred to as
pancreas plasticity) results in a decrease in functional beta-cell mass [17]. Studies have revealed an approximate 40%
reduction in beta-cell mass in patients with impaired glucose tolerance and a 60% reduction
in beta-cell mass in patients with T2DM compared to healthy individuals [24].
5 . Which of the following most accurately describes the incretin effect?
| A) | | Reduced or absent effects of GLP-1 and GIP, resulting in reduced pancreas plasticity |
| B) | | Enhanced effect of GLP-1 and GIP, resulting in increased postprandial insulin secretion |
| C) | | Severely reduced or absent effects of GLP-1 and GIP, resulting in impaired insulin regulation |
| D) | | Enhanced effect of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), resulting in reduced beta-cell mass |
PATHOPHYSIOLOGY OF TYPE 2 DIABETES
Incretin hormones, hormones released from gut endocrine cells
during meals, also play a significant role in insulin secretion [25]. Glucagon-like peptide-1 (GLP-1) and
glucose-dependent insulinotropic polypeptide (GIP) may be responsible for as much as 70% of
postprandial insulin secretion in healthy individuals, but demonstrate severely reduced or
even absent effects in those with T2DM, often referred to as the incretin effect. This
incretin effect is believed to contribute to the impaired insulin regulation and glucagon
secretion that are the hallmarks of T2DM, and studies have demonstrated that improved
glycemic control in patients with T2DM partially restores the impaired action of GLP-1 and
GIP [17].
6 . The process by which insulin is unable to decrease plasma glucose levels and stimulate glucose uptake is typically described as
| A) | | incretin effect. |
| B) | | insulin resistance. |
| C) | | hepatic glucose output. |
| D) | | impaired insulin secretion. |
PATHOPHYSIOLOGY OF TYPE 2 DIABETES
Another central mechanism of T2DM is insulin resistance,
which is characterized by the failure of insulin to decrease plasma glucose levels through
hepatic glucose suppression and stimulation of glucose uptake in skeletal muscle and adipose
tissue [22]. Consequently, inefficient
glucose utilization is replaced by cellular utilization of fats and proteins. Factors that
contribute to insulin resistance are complex and may include defective insulin-mediated cell
signaling pathways, decreased muscle glycogen syntheses, and reduced numbers of skeletal
muscle, liver, and adipose tissue insulin receptors (particularly in obese individuals). In
many cases, insulin resistance may be the earliest detectable marker for T2DM [22]. Patients who transition from normal
glucose tolerance to T2DM typically experience a 40% decrease in insulin sensitivity, which
is further accentuated by chronic hyperglycemia and elevated free fatty acids.
7 . Which of the following is potentially the earliest detectable marker for T2DM?
| A) | | Insulin resistance |
| B) | | The incretin effect |
| C) | | Pancreas plasticity |
| D) | | Increased hepatic glucose output |
PATHOPHYSIOLOGY OF TYPE 2 DIABETES
Another central mechanism of T2DM is insulin resistance,
which is characterized by the failure of insulin to decrease plasma glucose levels through
hepatic glucose suppression and stimulation of glucose uptake in skeletal muscle and adipose
tissue [22]. Consequently, inefficient
glucose utilization is replaced by cellular utilization of fats and proteins. Factors that
contribute to insulin resistance are complex and may include defective insulin-mediated cell
signaling pathways, decreased muscle glycogen syntheses, and reduced numbers of skeletal
muscle, liver, and adipose tissue insulin receptors (particularly in obese individuals). In
many cases, insulin resistance may be the earliest detectable marker for T2DM [22]. Patients who transition from normal
glucose tolerance to T2DM typically experience a 40% decrease in insulin sensitivity, which
is further accentuated by chronic hyperglycemia and elevated free fatty acids.
8 . According to the American Diabetes Association, a diagnosis of T2DM can be confirmed in patients
| A) | | who have a fasting plasma glucose of 125 mg/dL or less. |
| B) | | whose glycated hemoglobin (A1c) level is 6.5% or higher. |
| C) | | with a BMI of at least 25 kg/m2 and A1c level greater than 4%. |
| D) | | who have a two-hour plasma glucose greater than 100 mg/dL during an oral glucose tolerance test. |
DIAGNOSIS OF TYPE 2 DIABETES
According to the ADA, a diagnosis of T2DM can be confirmed in
patients whose A1c level is 6.5% or higher. T2DM can also be diagnosed with FPG ≥126 mg/dL,
two-hour PG ≥200 mg/dL during an OGTT, or random plasma glucose ≥200 mg/dL in patients with
classic symptoms of hyperglycemia or hyperglycemia crisis [28]. Prediabetes—a condition in which glucose levels are below diagnosis
criteria but higher than a normal range—can also be diagnosed in those with FPG 100–125
mg/dL, two-hour PG 140–199 mg/dL in OGTT, or A1c level of 5.7% to 6.4%, although the World
Health Organization and several other diabetes groups define prediabetes at a FPG of 110
mg/dL [28].
9 . As a simple rule, to induce weight loss, patients' caloric intake should be reduced by how many calories from the current level?
| A) | | 100–300 daily. |
| B) | | 300–500 daily. |
| C) | | 500–1,000 daily. |
| D) | | 1,000–1,250 daily. |
TREATMENT OPTIONS IN TYPE 2 DIABETES
As a simple rule, to induce weight loss, patients' caloric
intake should be reduced by 500–1,000 calories per day from the current level. This
reduction will produce the recommended weight loss of one to two pounds per week in most
patients [35].
10 . Which drug class works to reduce fasting plasma glucose levels through inhibition of hepatic gluconeogenic gene expression?
| A) | | Insulin |
| B) | | Biguanides |
| C) | | Secretagogues |
| D) | | Thiazolidinediones (TZDs) |
TREATMENT OPTIONS IN TYPE 2 DIABETES
Biguanides, specifically metformin, are the most widely
used first-line T2DM medication. Both the AACE/ACE and the ADA/EASD recommend metformin as
first-line therapy in most patients with T2DM, except where contraindicated [29,30]. Biguanides inhibit expression of hepatic gluconeogenic genes, thereby
reducing fasting plasma glucose levels [2]. Metformin offers several benefits, including an oral route of administration (to be
dosed once or twice daily) and a weight-neutral, non-hypoglycemia-inducing side-effect
profile [30]. Metformin may also provide
some cardiovascular benefit, although a meta-analysis does not support this claim [30,40]. In addition, generic formulations of metformin are available, which
may be preferred in patients who are unable to afford the cost of this agent due to high
co-pays or lack of prescription insurance [2].
11 . All of the following statements regarding glinides are TRUE, EXCEPT:
| A) | | They are long-acting secretagogues. |
| B) | | They are intended to be taken with food. |
| C) | | They are associated with modest weight gain. |
| D) | | They decrease postprandial glucose levels only. |
TREATMENT OPTIONS IN TYPE 2 DIABETES
The various secretagogues have different profiles.
Sulfonylureas are relatively long-acting secretagogues that can decrease both fasting
plasma and postprandial glucose levels, whereas glinides are short-acting secretagogues
that decrease postprandial glucose levels only [2]. These oral agents are intended to be taken with meals; the morning
meal if dosed daily, or the morning and evening meals (or bedtime with food) for
twice-daily dosing [2]. Both types of
secretagogues are associated with modest weight gain and risk of hypoglycemia, although
glinides may carry a lower risk of the latter [29]. In addition, some studies have suggested these agents may be
associated with a secondary failure rate in excess of other T2DM drugs resulting from
exacerbation of islet dysfunction [30].
The central benefit of secretagogues is cost. These agents have generic equivalents, and
many are available in combination with other drugs, such as metformin or the TZD
pioglitazone [2].
12 . All of the following statements regarding dipeptidyl peptidase-4 (DPP-4) inhibitors are TRUE, EXCEPT:
| A) | | DPP-4 inhibitors require the presence of insulin for efficacy. |
| B) | | DPP-4 inhibitors are typically used as second- or third-line therapy. |
| C) | | DPP-4 inhibitors produce an estimated 1.5- to 4-fold increase in active postprandial GLP-1 levels. |
| D) | | DPP-4 inhibitors are associated with increased incidence of nausea and vomiting compared to GLP-1 agonists. |
TREATMENT OPTIONS IN TYPE 2 DIABETES
DPP-4 inhibitors (alogliptin, saxagliptin, linagliptin,
sitagliptin) also target GLP-1 and the incretin effect. But unlike GLP-1 agonists, DPP-4
inhibitors restrict DPP-4 to prevent enzymatic inactivation of endogenous GLP-1, thereby
prolonging the availability of endogenous GLP-1 and increasing GLP-1 concentrations in the
gastrointestinal tract [2]. By inhibiting
more than 80% of DPP-4 activity over a 24-hour period, these agents produce an estimated
1.5-to 4-fold increase in active postprandial GLP-1 levels, resulting in increased insulin
and amylin secretion from beta cells and decreased glucagon secretion and liver glucose
production [2]. DPP-4 inhibitors offer
many benefits, including oral route of administration (with or without food), low
hypoglycemia risk, a weight-neutral profile, and a potential cardiovascular benefit [2]. They are also associated with a lower
incidence of nausea and vomiting compared to GLP-1 agonists. However, like TZDs, DPP-4
inhibitors require the presence of insulin (either endogenous or exogenous) for efficacy
[2]. These second-or third-line drugs
are often used in combination with other agents; they have been studied and are often used
with metformin, pioglitazone, sulfonylureas, and basal insulin [2].
13 . Which form of insulin therapy is typically offered first in patients who fail to respond to other antidiabetes medications?
| A) | | Basal |
| B) | | Bolus |
| C) | | Prandial |
| D) | | Basal/bolus |
TREATMENT OPTIONS IN TYPE 2 DIABETES
Exogenous insulin works much like endogenous insulin in
that it causes cells in the liver, muscle, and fat tissue to take up glucose from the
blood and store it as glycogen. Due to the progressive nature of T2DM, injectable or
inhaled insulin therapy is typically required at some point in the disease course, with
the goal of creating as normal a glycemic profile as possible without causing unacceptable
weight gain or hypoglycemia [30]. Basal
insulin is usually offered first when insulin therapy becomes necessary, as this approach
offers relatively uniform insulin coverage over a 24-hour period, with peakless
time-action curves producing a more consistent effect [29,30].
Intermediate-acting, long-acting, and insulin detemir formulations are available, with the
latter two offering a slightly lower risk for overnight hypoglycemia and weight
gain.
14 . According to guidelines, which strategy should be initiated first to reduce A1c in most patients with T2DM (unless otherwise contraindicated)?
| A) | | Insulin |
| B) | | Lifestyle modification |
| C) | | Metformin monotherapy |
| D) | | Metformin/TZD/sulfonylurea combination therapy |
TREATMENT OPTIONS IN TYPE 2 DIABETES
The ACE, the AACE, and the ADA have each provided guidelines
for the step-wise selection of therapies for T2DM (Figure
3 and Figure 4) [28,29,30,31]. Lifestyle modification (e.g., healthy
diet, weight control, increased physical activity) is recommended as a first step in
glycemic control, although a consensus statement from the AACE/ACE states that lifestyle
optimization efforts should not delay needed pharmacotherapy in higher risk individuals
[29]. The AACE/ACE emphasize that
minimizing risk of weight gain and promoting weight loss in patients with adiposity-based
chronic disease should be a high priority [29].
15 . Which organization recommends therapies other than metformin for first-line treatment in some individuals with T2DM?
| A) | | American Diabetes Association (ADA) |
| B) | | American College of Physicians (ACP) |
| C) | | American Association of Clinical Endocrinologists (AACE)/ American College of Endocrinology (ACE) |
| D) | | None of the above |
TREATMENT OPTIONS IN TYPE 2 DIABETES
Should pharmacotherapy become necessary, metformin should be
the initial drug of choice, although an AACE/ACE algorithm denotes that TZDs, sulfonylureas,
DPP-4 inhibitors, GLP-1 agonists, or alpha-glucosidase inhibitors (AGIs) can be used alone
or together for therapeutic initiation depending on the presenting A1c level and with
consideration of other factors [29]. Two-or
three-drug combinations with metformin plus other oral antidiabetes drugs are recommended
when first-line therapy is deemed inadequate, with all organizations agreeing that insulin
should be reserved for failure of triple combination therapy. To measure efficacy, all
groups recommend regular assessment of A1c. Although target A1c levels vary slightly
according to organization, all agree that elevated A1c indicates treatment inadequacy and
warrants treatment escalation.
16 . Which organization recommends an A1c target of 6.5% or lower unless contraindicated?
| A) | | ADA |
| B) | | ACP |
| C) | | AACE |
| D) | | European Association for the Study of Diabetes (EASD) |
ISSUES SURROUNDING TIGHT GLYCEMIC CONTROL
The AACE recommends an A1c target level of ≤6.5% unless
contraindicated by specific factors, such as age and hypoglycemia risk [29]. This goal is different than that set forth
by the ADA and EASD, which recommend a target A1c of <7.0% [30]. In addition, in 2018, the ACP
controversially recommended a target A1c of 7% to 8% for most patients with diabetes [60,61]. The recommendation for tight glycemic control by the AACE is based on
data from numerous older trials. The Diabetes Control and Complications Trial, the
Epidemiology of Diabetes Interventions and Complications Study, and the UKPDS trial data
between 1993 and 2008 are supportive of an A1c target of ≤6.5%, as are findings from the 2000
Kumamoto Study and the Steno-2 trial by Gaede et al. [62,63,64,65,66,67,68,69,70]. Although some of these trials are relatively
dated, further evidence was provided by three landmark trials: the Action to Control
Cardiovascular Risk in Diabetes (ACCORD) study, the Action in Diabetes and Vascular disease
(ADVANCE) trial, and the VA Diabetes Trial (VADT) [71,72,73]. In these studies, lower A1c levels
correlated with reduced incidence of microvascular and sometimes macrovascular
complications.
17 . According to the Action in Diabetes and Vascular disease (ADVANCE) trial, intensive glycemic control was associated with
| A) | | improvements in blood pressure. |
| B) | | a non-significant trend towards lower cumulative mortality. |
| C) | | a beneficial effect on macrovascular and microvascular complications (collectively). |
| D) | | All of the above |
ISSUES SURROUNDING TIGHT GLYCEMIC CONTROL
Of these studies, the ADVANCE trial provides a particularly
strong rationale for tight glycemic control, as it was designed specifically to evaluate the
effect of intensive glycemic control on death from cardiovascular disease, nonfatal myocardial
infarction or nonfatal stroke, and new or progressing neuropathy or retinopathy [59,72]. More than 11,000 patients with T2DM were enrolled in this trial, with a
median age of 67 years, a median duration of T2DM of 8 years, and a mean A1c of 7.5% upon
study entry. Patients were required to have a history of major macrovascular or microvascular
disease or at least one risk factor for macrovascular disease. Outcomes of this study revealed
no adverse effects of intensive glycemic therapy (with an A1c target of ≤6.5%). In fact, tight
glycemic control was associated with a non-significant trend toward lower cumulative mortality
and a beneficial effect on macrovascular and microvascular complications (when assessed
collectively) [59]. Both intensive and
standard glycemic control groups also experienced improvements in blood pressure and
low-density lipoprotein cholesterol levels.
18 . Patients in the ADVANCE trial may have benefitted more from intensive glycemic control than in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial because
| A) | | Patients in the ADVANCE trial had fewer comorbidities than in the ACCORD trial. |
| B) | | A1c was reduced over a greater period of time in the ADVANCE trial compared to the ACCORD trial. |
| C) | | The ADVANCE trial occurred much more recently than the ACCORD trial, and patients therefore had access to more effective A1c-lowering therapy. |
| D) | | None of the above |
ISSUES SURROUNDING TIGHT GLYCEMIC CONTROL
Alternatively, some data challenge the importance of tight
glycemic control in T2DM. In the VADT study, no beneficial effect of intensive glycemic
control was observed when the entire study population was taken into consideration [59]. In fact, a deleterious effect was observed
in association with tight glycemic control in patients who had T2DM for 15 years or more. This
is suggestive of a potential "window of opportunity" early in the disease course for intensive
control that closes over time [59]. Moreover,
in the ACCORD study, the intensively treated group experienced a number of negative effects,
including a three-fold increased risk of hypoglycemia and severe hypoglycemia and excessive
weight gain—a well-known risk factor for increased mortality [59]. However, it is important to note that in the
ACCORD trial, a 1.4% reduction in A1c was achieved within four months in the intensive control
group [59]. The more gradual reduction in A1c
observed in the ADVANCE trial may have influenced the apparent beneficial effect of intensive
glycemic control on outcomes [59]. Still, in
the ADVANCE trial, much like in the ACCORD study, excessive weight gain (and associated
morbidity and mortality) was positively correlated with intensive glycemic control. Likewise,
in a 2011 meta-analysis of 14 clinical trials involving approximately 28,600 patients with
T2DM, intensive glycemic control did not appear to significantly impact the relative risk of
all-cause or cardiovascular mortality, and study authors were unable to find sufficient
evidence for the beneficial effect of intensive control on microvascular outcomes [77]. Given the severe risk of hypoglycemia that
was found to accompany intensive glycemic control (with a 30% increased relative risk),
authors concluded that intensive glycemic control does not appear to reduce all-cause
mortality and that data fail to clearly demonstrate a benefit on cardiovascular mortality,
non-fatal myocardial infarction, or microvascular complications. Other questions remain
regarding the benefit of intensive glycemic control in T2DM, including duration of follow-up
required to demonstrate beneficial effects, extent of influence glycemic control has on
outcomes (given the numerous risk factors in T2DM), and extent of influence glycemic control
has on pre-existing macrovascular outcomes [59].
19 . Which of the following is TRUE regarding T2DM treatment nonadherence?
| A) | | Adherence to medication is highest when first prescribed and decreases over time. |
| B) | | Anticipated patient nonadherence dissuades many providers from initiating insulin therapy. |
| C) | | Patients are significantly more nonadherent to insulin compared to oral antidiabetes agents. |
| D) | | None of the above |
THE ROLE OF ADHERENCE IN ACHIEVING TREATMENT GOALS
As with many chronic diseases, medication adherence is a
significant barrier to optimal outcomes in T2DM. Adequate adherence to T2DM therapies, which
is typically defined as collecting and/or taking >80% of prescribed medication, appears to
vary significantly, although the vast majority of studies on this topic report some level of
nonadherence among most patients with T2DM. An estimated 36% to 93% of individuals with T2DM
are believed to practice inadequate adherence to oral antidiabetic agents, a considerably
broad percentage [80]. Insulin nonadherence is
similarly indefinite, reported to affect between 19% and 46% of patients with T2DM [81,82]. Paradoxically, anticipated patient nonadherence actually dissuades a
significant number of providers from initiating insulin [83]. Research suggests that nonadherence is a relatively immediate response in
many patients with T2DM. Rather than tapering off medication over a substantial period of
time, evidence suggests that patients often fail to fill second or additional prescriptions,
and many discontinue medication within a year of prescription, actions suggestive of causative
factors beyond simple medication fatigue [84].
The consequences of medication nonadherence are significant, ultimately resulting in hundreds
of billions of dollars in additional economic cost and increased risk of mortality among
nonadherent individuals compared to adherent patients with T2DM [82,85,86]. To reduce the
personal and societal burden of nonadherence to antidiabetes medication, it is important that
healthcare professionals understand the factors that contribute to suboptimal compliance, as
well as strategies to overcome these barriers (Table 3).
20 . Which of the following strategies can help to reduce treatment complexity?
| A) | | Avoidance of pen devices |
| B) | | Prescribing loose-pill combination therapy |
| C) | | Prescribing oral fixed-dose combination therapy |
| D) | | Prescribing twice-daily dosing (versus once-daily dosing) |
THE ROLE OF ADHERENCE IN ACHIEVING TREATMENT GOALS
STRATEGIES FOR OVERCOMING BARRIERS TO MEDICATION ADHERENCE IN T2DM
| Barrier | Strategy |
|---|
| Oral and Non-Insulin Therapies |
| Fear of side effects |
| Attempt to balance therapeutic efficacy and tolerability. | | Utilize agents associated with fewer side effects. | | Discuss side effects before starting. | | Provide education regarding the symptoms and treatment of
hypoglycemia. |
|
| Treatment complexity |
| Utilize oral fixed-dose combination therapy. | | Reduce dosing frequency whenever possible. |
|
| Insulin Therapy |
| Fear of side effects |
| Attempt to balance therapeutic efficacy and tolerability. | | Utilize agents associated with fewer side effects. | | Discuss side effects before starting. |
|
| Needle anxiety/treatment complexity |
| Discuss developments that have improved ease and comfort of
injections. | | Utilize pen devices. | | Tailor therapy to patients' needs utilizing optimal formulations. |
|
| Negative patient attitude |
| Provide education regarding the importance of insulin in maintaining
glycemic control. | | Dispel beliefs that insulin therapy is punishment or an indication of
failure. |
|
| Other Barriers |
| Medication cost | Work with managed care programs and patient financial profile to ensure easy
access to medication. |
| Clinical inertia | Improve patient-provider communication to obtain feedback on adherence. |
