Peripheral vascular disease or peripheral arterial disease presents as diminished
or absent foot pulses, intermittent claudication, skin ulcers, gangrene, or amputation.
People with diabetes are 2 to 10 times more likely to experience symptoms of
peripheral arterial disease than those without diabetes, and half of all nontraumatic
amputations in the United States are performed in patients with diabetes. In one study
that followed Type 2 patients for 7 years, 5.5% had an amputation. The prevalence of
this condition increases with age, duration of diabetes, and the presence of risk
factors such as hypertension or smoking.
Signs and symptoms of peripheral arterial disease include leg pain, which is
relieved by rest; cold feet; nocturnal leg pain, which is relieved by dangling the feet
over the bed or walking; absent pulses; loss of hair on the foot and toes; and
gangrene. Treatment of this condition includes elimination and treatment of risk
factors such as smoking, dyslipidemia, hypertension, and hyperglycemia; antiplatelet
therapy; exercise, which is the mainstay of therapy; and revascularization surgery.
DRUG-INDUCED ALTERATIONS IN GLUCOSE
Persons with diabetes are likely to take more drugs in their lifetime than any other
group of patients. Patients with Type 2 diabetes present with a constellation of
chronic conditions, including hypertension, dyslipidemia, and CVD, all of which will
likely require drug therapy. Drugs to manage depression, intermittent infections, and
neurologic and ophthalmologic conditions also are commonly prescribed. Because
we know that the actions of drugs are complex and that for every desired effect there
are several other unwanted effects, each time a drug is added to the regimen of
someone with diabetes it is important to assess the patient’s situation to determine
whether a potential exists for a drug–drug or drug–disease interaction or whether the
benefit of the newly prescribed drug is likely to outweigh its risks. With the
availability of online drug information databases to assist in assessment of drug–drug
and drug–disease interactions, a detailed listing of drugs that can exacerbate
hyperglycemia and hypoglycemia is not provided. Below, a few case examples are
illustrated. Some medications that can have significant hyperglycemic effects include
atypical antipsychotics, protease inhibitors, corticosteroids, immunosuppressants
(e.g., tacrolimus, cyclosporine), niacin (higher doses), gonadotropin-releasing
hormone agonists (used in men for prostate cancer), and pentamidine (can also cause
299,300 Patients should be monitored closely for a medication’s
possible effect on the BG levels.
QUESTION 1: A.L., a 37-year-old obese woman with systemic lupus erythematosus, has been taking 60
mg/day of prednisone for 6 months. During this period, her weight has increased by 30 lb and she has
diabetes clinic, where her predinner and bedtime BG values were found to be 140 to 160 mg/dL and FBG
contribute to diabetes mellitus? How should A.L. be treated?
The term steroid diabetes was first used to describe the hyperglycemia and
glycosuria seen in patients with Cushing syndrome. Now, it is associated more
commonly with exogenously administered glucocorticoids and has been a side effect
of parenteral, oral, and even topical therapy. Corticosteroids are one of the most
common drug groups that unmask latent diabetes or aggravate preexisting disease,
and they may produce hyperglycemia and overt diabetes in individuals who are not
Corticosteroids increase hepatic gluconeogenesis, suppress insulin secretion, and
decrease tissue responsiveness to insulin.
300 The primary effect is impaired glucose
disposal after meals, resulting in daytime hyperglycemia, and by morning, the glucose
levels normalize. Although steroid-induced diabetes generally is mild and rarely
associated with ketonemia, a wide spectrum of severity may be encountered—from
after months to years of chronic therapy. The effect generally is considered dose-
dependent and usually is reversible on discontinuation of the drug.
A.L. exhibits many symptoms that can be attributed to supraphysiologic doses of
corticosteroids: truncal obesity, depression, acneiform rash, and diabetes. Mildly
elevated glucose levels in obese individuals, as in A.L.’s case, sometimes can be
controlled by diet, but may require treatment with a short-acting insulin secretagogue
or rapid-acting insulin before meals.
300 A person with diabetes whose BG is
increased by use of a glucocorticoid should modify treatment appropriately to restore
glycemic control. It is important to anticipate the need to modify insulin or other
antidiabetic therapy because corticosteroid doses are increased or decreased.
regimen and has been taking pseudoephedrine 30 mg QID for 7 days and Robitussin DM 10 mL QID (which
sympathomimetics and cough preparations in patients with diabetes.
Over-the-counter drug products, such as decongestants and diet aids, which
contain sympathomimetics, carry warning labels that caution against their use in
patients with diabetes. Standard sugar- and ethanol-containing cough preparations
also carry such warning labels. However, clinically significant drug-induced glucose
intolerance probably is very infrequent. It is well established that parenterally
administered epinephrine increases BG concentrations secondary to increased
glycogenolysis and gluconeogenesis. Other sympathomimetics generally do not have
as potent an effect on BG as epinephrine, and their use usually does not pose a
practical problem in diabetic patients. Furthermore, the effects of sympathomimetics
on BP must be considered in many patients with diabetes. Therefore, antihistamines
or occasional use of nasal sprays for severe congestion may be needed.
In summary, pseudoephedrine or the cough preparation may be aggravating R.C.’s
glycemic control, although at these low-to-normal therapeutic doses, it is quite
unlikely. The stress related to R.C.’s underlying cold is more likely to be impairing
his glucose tolerance than these low doses of sympathomimetic agents or the small
amounts of sugar contained in the cough syrup.
QUESTION 1: C.F., a 22-year-old woman with newly diagnosed Type 1 diabetes, enjoys a glass or two of
insulin? Is alcohol contraindicated in C.F. or any person with diabetes?
Clinicians often are reluctant to permit the use of alcoholic beverages in patients
with diabetes. However, barring contraindications that are similar in the nondiabetic
and diabetic patient alike (e.g., alcoholism, hypertriglyceridemia, gastritis,
pancreatitis, pregnancy), a person with diabetes can safely enjoy a moderate alcohol
intake as long as certain precautions are taken. For an in-depth discussion, the reader
is referred to two comprehensive reviews of alcohol and diabetes,
which are summarized in the following list:
Drink in moderation. The ADA defines this as a daily intake of one drink for adult
women and two drinks for adult men (one drink is defined as 5 ounces of wine,
12 ounces of beer, or 1.5 ounces of distilled liquor). The patient should be aware
of his/her own sensitivity to the intoxicating effects of ethanol and adjust
Avoid drinks that contain large amounts of sugar, such as liqueurs, sweet wines, and
sugar-containing mixes. Instead, consider dry wines, light beers, and distilled
spirits. Not only does the simple sugar content add an additional source of
glucose and calories to the diet, but ethanol ingested with simple sugar-containing
mixers enhances reactive hyperglycemia.
Remember to count the calories in alcohol (calories = [0.8] × [proof] × [ounces]);
substitute 1 ounce of alcohol for two fat exchanges.
Be aware that the symptoms of alcohol intoxication and hypoglycemia are similar. If
hypoglycemia is mistaken for intoxication by others, appropriate and potentially
life-saving treatment can be delayed.
The authors acknowledge Lisa A. Kroon and Craig Williams for their contributions
to this chapter in earlier editions.
A full list of references for this chapter can be found at
http://thepoint.lww.com/AT11e. Below are the key references and websites for this
chapter, with the corresponding reference number in this chapter found in parentheses
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