Clinical Briefs

By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is an advisor for Endo, Kowa, Pricara, and Takeda.

Zoledronic Acid Treatment of Osteoporosis in Men

Source: Boonen S, et al. Fracture risk and zoledronic acid therapy in men with osteoporosis. N Engl J Med 2012; 367:1714-1723.

When hearing the word osteoporosis, most clinicians think “pink,” as if the disorder only affected women. To the contrary, 30% of hip fractures occur in men, and the post hip-fracture mortality in men is higher than women. Although the dataset about preferred treatments is less robust for men than women, trials of oral bisphosphonates have been shown to provide meaningful fracture risk reduction for men and women.

Zoledronic acid (ZOL) is a parenterally administered bisphosphonate that has been previously demonstrated to provide significant reduction in osteoporotic fractures in women. For treatment of osteoporosis, ZOL is administered as a single intravenous dose, repeated in 1 year.

Boonen et al performed a placebo-controlled randomized trial in osteoporotic men (n = 1199). As in most osteoporosis trials, calcium (1000-1500 mg/d) and vitamin D (800-1200 IU/d) supplements were administered in both the treatment and placebo arms of the study. The primary outcome variable of the study was new vertebral fractures.

At the end of the 2-year study, men who had received ZOL enjoyed a 67% relative risk reduction in new vertebral fractures (1.6% vs 4.9%), as well as improved bone mineral density. There were no serious drug-related adverse events. Risk for osteoporotic vertebral fracture in men is promptly and effectively reduced by zoledronic acid.


Relapsing Lyme Disease: Fact or Fiction?

Source: Nadelman RB, et al. Differentiation of reinfection from relapse in recurrent Lyme disease. N Engl J Med 2012;367:1883-1890.

A characteristic dermatologic manifestation of the acute phase of Lyme disease (LYME) is erythema migrans. With appropriate antibacterial treatment of LYME, the etiologic bacterium Borrelia burgdorferi is typically eradicated, and further disease progression is prevented. Untreated LYME can induce repetitive episodes of erythema migrans, as can LYME treated with antibiotics to which B. burgdorferi is not susceptible. In an individual patient, it may be difficult to differentiate disease relapse from new infection with a different strain of B. burgdorferi.

Genotyping of B. burgdorferi surface proteins allows determination of specific bacterial subtypes. Nadelman et al performed such analysis on patients (n = 17) who had experienced two episodes of erythema migrans. Each of the patients had received appropriate antibacterial treatment.

The second episode of erythema migrans was not caused by the same strain of B. burgdorferi in any of the patients, indicating that in each circumstance the patient had suffered reinfection rather than relapse. Whereas clinicians may have suspected relapse in patients with repeated episodes of LYME, it appears that reinfection with a new strain is more likely to be responsible.


Hypertension and Gout

Source: McAdams-DeMarco MA, et al. Hypertension and the risk of incident gout in a population-based study: The atherosclerosis risk in communities cohort. J Clin Hypertens 2012;14:675-679.

Gout and hypertension are often seen together. Indeed, there has been a substantial degree of discussion about the potential for elevated levels of uric acid to cause hypertension. The “storyline” remains incomplete, however, because of the observational nature of the data, confounders like thiazide diuretics (which of course elevate uric acid in treated hypertensives), and renal insufficiency, which is common in hypertension and is also associated with elevated uric acid. If uric acid is ultimately proven to increase the incidence of hypertension, it will still remain to be determined whether lowering urate can reduce hypertension safely and effectively.

The Atherosclerosis Risk in Communities study (ARIC) study population provides a dataset for evaluating the association between gout and hypertension. Adults (n = 15,792) from four different metropolitan areas were followed for approximately 10 years.

There was a strong relationship between gout and hypertension. Participants with hypertension were almost two to three times as likely to develop gout, even after adjustment for confounders. For instance, when results were evaluated only among persons not taking thiazide diuretics, a positive association between hypertension and gout was still found. The authors posit that the relationship between hypertension and gout is mediated through blood pressure-induced renal damage that leads to increased levels of uric acid.