Clinical Briefs
May 15, 2014
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.Zinc for the Common Cold
Source: Das RR, Singh M. JAMA 2014; 311:1440-1441.
The mechanism by which zinc could impact the common cold is fairly straightforward: rhinovirus (the cause of the common cold) uses the ICAM-1 nasal epithelial cell receptor to latch on, and zinc ions block this. Since our bodies already usually have plenty of zinc on-board, the question is whether supplemental zinc can have an impact. In a JAMA clinical evidence synopsis, Das and Singh review 14 clinical trials of zinc in adults (n = 1781) and three in children.
Overall, common cold duration in adults was 7.5 days on placebo and 6.75 days when zinc supplementation was started within 24-48 hours of symptom onset, so folks got better about 1 day sooner. Disappointingly, symptom severity during illness was not alleviated.
Although not studied in adults, use of zinc as common cold prophylaxis in children has shown more impressive efficacy. When zinc supplements were provided at the onset of cold season, there was a 38% reduction in symptomatic colds compared to placebo (61.8% vs 38.2%). Whether similar benefits could be observed in adults has not been demonstrated.
Many persons find zinc lozenges unpalatable, so whether the 1-day reduction in symptoms is worth the effort may be a personal decision. Guidelines from the American Academy of Family Physicians support the use of zinc within 24 hours of cold onset.
A Potential Key to Which Smokers Will Develop COPD
Source: Petersen H, et al. Chest 2014; 145:695-703.
In the best of all worlds, we would convince smokers that they need to quit and assist them in that process. Even though smoking is associated with diverse risk in multiple anatomic compartments, it is lung disease that the public most commonly associates with smoking. Yet, we have to acknowledge that only a minority (20-25%) of smokers incur problems like chronic obstructive pulmonary disease (COPD). Is there a way to identify which smokers are most likely destined to develop COPD, thereby garnering an additional motivational tool — especially since so many smokers see consequences as either "it won’t happen to me" or "it’s a long, long way off"?
Petersen et al studied ever smokers (n = 809) who were free of spirometric abnormalities at baseline with periodic spirometry (q 18 months) for a mean of 6 years. Concordant with current guidelines, the metric utilized to quantify lung function was post-bronchodilator FEV1. One premise of the investigation was that study subjects who exhibited the most rapid rate of decline in FEV1 would also be most likely to develop COPD. Study subjects were categorized by rate of decline as rapid decline (≥ 30 mL/year), normal (0-29.9 mL/year), and no decline (unchanged from baseline). At the conclusion of the mean follow-up of 6 years, about one-third of the subjects fell into each of these categories.
As hypothesized by the authors, subjects who experienced rapid decline were approximately twice as likely to develop COPD. Another interesting insight from this trial was an evaluation of the association of various medications with outcomes. Seven different medication classes were addressed that were being used by these patients: angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, beta-blockers, CCBs, statins, insulin, and oral hypoglycemic agents. ACE inhibitors were associated with a 45% lesser incidence of rapid decline, but no other statistically significant associations with other medications were demonstrated. The authors posit that salutary effects of ACE inhibitors upon development of COPD are related to anti-inflammatory activity of this class.
These data suggest that we may be able to identify smokers destined to develop COPD by rate of decline in FEV1.
While You’re Fixing OSA with CPAP, Are You Fixing BP Too?
Source: Fava C, et al. Chest 2014;145: 762-771.
The association between obstructive sleep apnea (OSA) and hypertension is well established, with putative mechanisms including hypoxia-induced sympathetic activation, as well as renin-angiotensin-aldosterone activation. One would hope, then, that if OSA is causing the elevation in blood pressure (BP) — rather than just being an innocent bystander, or for instance being associated through a common comorbidity such as obesity — treatment of OSA might reduce BP.
Fava et al performed a systematic review and meta-analysis of randomized, controlled trials that reported data on BP in patients treated by continuous positive airway pressure (CPAP) for OSA (n = 2566). Overall, when compared to no treatment, OSA treatment was associated with a statistically significant reduction in BP, which was particularly prominent during the night (3.8/1.8 mmHg reduction). Although at first blush this degree of BP lowering might not seem that important, CPAP treatment trials are characterized by three limitations: 1) they are short term — most are 3 months or less, 2) the fact that patients entered a CPAP trial does not guarantee full compliance with the CPAP, and 3) less than half of the patients had hypertension, so we would anticipate a very small change in BP in a non-hypertensive population. Indeed, in subgroup analysis it is demonstrated that trials with longer duration and among patients with better compliance, BP reductions were greater.
Recognition that OSA is associated with resistant hypertension, coupled with the knowledge that CPAP treatment of OSA improves BP, bolsters both the therapeutic rationale for CPAP and inclusion of OSA screening as a component of evaluation for patients with resistant hypertension.
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