Prostate cancer is the leading cancer diagnosis and second leading cause of cancer-related mortality for men in the United States. Due to the increased prevalence of prostate cancer in men older than 50 years, men at risk for prostate cancer represent the same population of men who are at greatest risk for metabolic syndrome, diabetes mellitus, and coronary artery disease (CAD). In addition to risk factors for CAD that are applicable to the general population, men with prostate cancer can be at increased risk for CAD due to long-term androgen deprivation therapy (ADT) administered as treatment for prostate cancer. Men undergo ADT by medical (drug therapy) or surgical (castration) means. Luteinizing hormone-releasing hormone (LHRH) agonists are the primary drug therapies used for ADT. Commercially available LHRH agonists are goserelin, histrelin, leuprolide, and triptorelin. Body composition changes, hyperlipidemia, insulin resistance, metabolic syndrome, and acute coronary syndrome are all reported adverse effects of ADT, which are consequences of reduced levels of circulating testosterone. Metabolic and body composition changes associated with ADT arise within months of beginning medical ADT and persist after discontinuation of therapy. To better understand the increased risk of metabolic syndrome, diabetes, and heart disease in patients undergoing ADT for prostate cancer, we performed a MEDLINE search (1986-2008) to identify pertinent studies and reports. Additional citations were obtained from the articles retrieved from the literature search. We found that the increased risk for serious cardiovascular disease becomes evident within months of beginning ADT. Pharmacists should provide counseling to these patients on primary disease prevention. Men receiving ADT should be monitored routinely for signs and symptoms of metabolic syndrome, diabetes, and CAD. Healthy lifestyle practices should be encouraged, and physical therapy should be considered for these patients.

BackgroundHyponatremia (HN) occurs commonly in patients with acute heart failure and confers a worse prognosis. Current HN treatment varies widely, with no consensus. This study recorded treatment practices currently used for patients hospitalized with acute heart failure and HN.Methods and ResultsData were collected prospectively from 146 US sites on patients hospitalized with acute heart failure and HN (serum sodium concentration [Na+] ≤130 mEq/L) present at admission or developing in the hospital. Baseline variables, HN treatment, and laboratory values were recorded. Of 762 patients, median [Na+] was 126 mEq/L (interquartile range, 7) at baseline and increased to 130 mEq/L at discharge. Fluid restriction was the most commonly prescribed therapy (44%), followed by no specific HN treatment beyond therapy for congestion (23%), isotonic saline (5%), tolvaptan (4%), and hypertonic saline (2%). Median rate of change in [Na+] varied by treatment (0.5 [interquartile range, 1.0] to 2.3 [8.0] mEq/L/d) and median treatment duration ranged from 1 (interquartile range, 1) to 6 (5) days. Fluid restriction and no specific HN treatment resulted in similar changes in [Na+], and were least effective in correcting HN. Few patients (19%) had [Na+] ≥135 mEq/L at discharge.ConclusionsThe most commonly used treatment approaches for HN (fluid restriction and no specific treatment) in acute heart failure increased [Na+] minimally, and most patients remained hyponatremic at discharge.

Parenteral and transdermal anticholinergic medications are useful for the reduction of noisy respirations in hospitalized hospice patients. Difficult administration makes oral and sublingual products less desirable for use in this population.

Amiodarone has been reported to cause asymptomatic increases in liver function tests in 15-55% of patients. Clinically apparent, symptomatic hepatic disease occurs less frequently, but patients have been reported to have hepatomegaly, jaundice, cirrhosis, or chronic active hepatitis. Less well recognized is the fact that amiodarone has been attributed to six deaths. We cared for a patient with amiodarone hepatotoxicity, which led us to review the literature associated with this serious condition.

Lisinopril is a synthetic, nonsulfhydryl, angiotensin-converting enzyme inhibitor. Its bioavailability is approximately 25% and is not affected by food. Hepatic metabolism is not required for pharmacologic effect, which occurs 1 hour after administration. Peak serum concentration and effect are delayed, occurring 6-8 hours after a single dose and lasting for at least 24 hours. The drug is eliminated primarily by the kidneys. The elimination half-life is 12.6 hours and is prolonged in renal impairment. Lisinopril 10-80 mg once a day is effective in lowering blood pressure in all grades of essential and renovascular hypertension. It is as effective as hydrochlorothiazide, atenolol, metoprolol, and nifedipine. Combining lisinopril with hydrochlorothiazide produces a greater degree of blood pressure reduction. Patients with congestive heart failure have demonstrated immediate and prolonged beneficial hemodynamic effects and increased exercise tolerance. Lisinopril is well tolerated. Clinically significant drug interactions have not been reported, but caution should be used when lisinopril is administered with diuretics, nifedipine, or agents that may increase concentrations of potassium. The usual initial oral dosage of lisinopril is 10 mg once a day (range 20-40 mg/day). Lower dosages may be necessary in patients with renal impairment or congestive heart failure, elderly persons, and those receiving diuretics.