Clinical Briefs
By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville
Dr. Kuritzky is a retained consultant for Boehringer Ingelheim, Daiichi Sankyo, Forest Pharmaceuticals, Janssen, Lilly, Novo Nordisk, Pfizer, and Sanofi.
Is There a Difference Between Dutasteride and Finasteride for Male Pattern Baldness?
Source: Harcha WG, et al. J Am Acad Dermatol 2014;70:489-498.
In the united states, the two approved pharmacologic agents for treatment of male pattern hair loss are topical minoxidil (Rogaine) and systemic finasteride 1 mg/d (Propecia). The mechanism by which finasteride enhances hair growth is related to its activity as a 5-alpha-reductase inhibitor (5-ARI), which prevents the conversion of testosterone in the skin to its active derivative dihydrotestosterone (DHT). Since DHT is believed to be the primary culprit inducing male pattern hair loss, diminution of its activity results in reduced hair loss and allows better unrestrained hair regrowth.
The 5-ARI activity of finasteride is designated as type 2. Because there are multiple 5-ARI isoenzymes (types 1, 2, and 3), the potential role of dutasteride — which is active at both type 1 and type 2 tissue sites — is of interest. Indeed, dutasteride is already approved in Korea for treatment of male pattern baldness.
A placebo-controlled, randomized, head-to-head (no pun intended, honest) trial compared hair growth in men with male pattern baldness treated with finasteride 1 mg/d vs dutasteride 0.02-0.5 mg/d for 6 months (n = 917).
At the end of the trial, although both active agents were superior to placebo, there was a significant difference favoring dutasteride for both absolute hair count as well as hair width compared to finasteride. Dutasteride may become a viable alternative to finasteride for male pattern hair loss.
Best Management of Superficial Thrombophlebitis in the Lower Extremities
Source: Di Nisio M, et al. JAMA 2014; 311:729-730.
The consequences of superficial thrombophlebitis (STBP) of the lower extremities are not as well recognized as those of deep venous thrombosis (DVT). Similarly, there is some uncertainty among clinicians about best management. Choosing treatment wisely is important because untreated STBP can extend to DVT; indeed, even treated STBP can progress or recur in as many as 10% of patients.
Although other consequences are important (extension of STBP, recurrence), the most concerning sequel of STBP is DVT. Although trials of fondaparinux found a significant reduction in risk for DVT when administered for 45 days (an 85% risk reduction), data from studies with low-molecular-weight heparin (LMWH) and nonsteroidal anti-inflammatory drugs (NSAIDs) did not confirm venous thromboembolism risk reduction.
LMWH and NSAIDs provided lower rates of STBP recurrence than placebo, but based on equivocal results for VTE reduction, fondaparinux should be the preferred treatment.
Is There a Role for Pregabalin in Restless Legs Syndrome?
Source: Allen RP, et al. N Engl J Med 2014;370:621-631.
The impact of restless legs syndrome (RLS) can range from nuisance symptomatology requiring modest interruption of sleep to major decrements in quality of life for the patient and/or bed partner. Although dopaminergic medications have become the mainstay of therapy, they are sometimes associated with "augmentation;" a worsening of symptom intensity, symptom frequency, or increase in areas of the body involved with symptoms, over long-term treatment. Since there is no known cure for RLS, many patients require lifelong treatment, necessitating alternatives in the event that RLS augmentation occurs. To complicate the picture further, not everyone agrees that augmentation is a pharmacologically related issue; instead, the worsening of symptoms over time may simply reflect disease progression in susceptible individuals.
Allen et al performed a randomized, double-blind trial to compare the initial success rate for RLS symptoms (over 12 weeks) as well as frequency of augmentation over an additional 40 weeks of treatment with either pregabalin (300 mg/d), pramipexole (0.25 or 0.5 mg/d), or placebo (n = 719).
Both active treatments were effective in reducing RLS symptoms, although only higher dose pramipexole (0.5 mg) and pregabalin were statistically significantly superior to placebo. For the endpoint of augmentation, pregabalin was superior to both placebo and pramipexole 0.5 mg.
The underlying assumptions prompting treatment choices for RLS presume dopaminergic deficits. Since pregabalin has no known dopaminergic activity, and was found to be as effective as the dopaminergic treatment (pramipexole), the current understanding of the pathophysiologic basis for RLS has been challenged.
