By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is a consultant for Abbott, AstraZeneca, Boehringer Ingelheim, Daiichi, Sankyo, Forest Pharmaceuticals, Lilly, Novo Nordisk, Takeda.
Coenzyme Q10 for Peyronie's disease
Source: Safarinejad MR. Safety and efficacy of coenzyme Q10 supplementation in early chronic Peyronie's disease. Int J Impot Res 2010;22:298-309.
Peyronie's disease is an uncommon penile fibrotic disorder that most commonly affects young and middle-aged men. It is characterized by pain, deformity, or decreased capacity for intromission as a result of penile angulation. In contrast to chordee, the congenital abnormality in which ventral penile tissue defects prevent full expansion of the underside of the penis, resulting in a downward curvature upon erection, Peyronie's disease is an acquired fibrosis of the penis, which results in thickened penile plaques that prevent full erection. In whatever area of the penis such fibrotic plaques occur, that area will be unable to achieve full dilation and erection, resulting in angulation of the penis. There is no uniformly effective treatment for Peyronie's disease, although surgical correction is often effective.
Fibrotic plaque analysis in Peyronie's disease has demonstrated early oxidative inflammation, followed by creation of fibrotic scar. Since coenzyme Q10 has been shown to have antioxidant capacity, a clinical trial of its efficacy in early Peyronie's was intuitively appealing.
Men with early Peyronie's disease (n = 186) were randomized to coenzyme Q10 300 mg/day or placebo for 24 weeks. At trial end, there was a statistically significant reduction in plaque size, penile curvature, and improvement in sexual function in the active treatment group. Because coenzyme Q10 is a very well tolerated intervention with no known serious adverse effects (there were no reported drug-related adverse events or discontinuations), it offers a promising alternative for persons with Peyronie's disease.
Impact of using A1c to diagnose pre-diabetes
Source: Mann DM, et al. Impact of A1c screening criterion on the diagnosis of pre-diabetes among U.S. adults. Diabetes Care 2010;33:2190-2195.
The dramatic increase in type 2 diabetes (DM2) seen in the last decade is predictably going to become even more evident: Although 24 million Americans currently have DM2, more than twice as many have pre-diabetes (p-DM2). Historically, persons with p-DM2 who are untreated progress to frank DM2 at a rate of 7%-10% per year.
Until 2010, p-DM2 was diagnosed based upon the presence of either impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or both. Since 2010, the ADA has indicated that an A1c of 5.7%-6.4% qualifies as p-DM2. This tool has been welcomed by the primary care community because it does not require fasting, and can be obtained during any routine office visit. The limitation of A1c, however, is that it does not necessarily capture all the persons who would have been identified had either a fasting blood glucose or postprandial glucose (or both) been obtained; data from NHANES indicate that a substantial number of persons with IFG will not have an abnormal A1c, and vice versa. For instance, of 51.7 million NHANES subjects with IFG, only 23 million have an A1c that meets p-DM2 criteria.
All of the diagnostic markers for p-DM2 are used in an effort to identify the pathophysiologic derangements at a point in time where intervention might change disease progression. IFG, IGT, and A1c identify overlapping, but not identical, populations. Because clinicians will commonly have access to fasting glucose levels obtained concomitantly with other labs (e.g., CMP), it appears that few cases of p-DM2 will be missed by utilizing an A1c measurement.
Should tiotropium be a maintenance asthma medication?
Source: Peters SP, et al. Tiotropium bromide step-up therapy for adults with uncontrolled asthma. N Engl J Med 2010;363:1715-1726.
Traditional maintenance pharmacotherapy for persistent asthma includes inhaled corticosteroids (ICS), leukotriene modulators, andwhen used concomitantly with ICSlong-acting beta agonists (LABA). Except for the acute care setting, anticholinergic treatment, like tiotropium (TIO) has been generally thought of as a treatment for COPD rather than asthma.
Peters et al performed a double-blind, crossover trial in asthmatics (n = 210) who were poorly controlled on ICS alone. As add-on treatment, patients were randomized to tiotropium (ICS + TIO), the long-acting beta agonist salmeterol (ICS + LABA), or a doubling of ICS (ICS + ICS).
ICS + TIO was found to be superior to ICS + ICS for morning peak expiratory flow (the primary endpoint of the trial). ICS + TIO was demonstrated to be non-inferior to ICS + LABA for morning peak expiratory flow, prebronchodilator FEV1, and proportion of asthma-controlled days (the secondary endpoint of the trial). These results support the consideration of TIO as a maintenance medication for asthma when used in conjunction with ICS. Because the study duration was brief (14 weeks), the durability of anticholinergic treatment for asthmafor instance, is TIO useful in preventing asthma exacerbations?remains to be determined.