By Jeffrey Mayne, MD
Faculty Peer Reviewed
PRIMECUTS! PRIMECUTS! As the excitement of the World Cup rolls on and the din of those vuvuzela horns continues to ring heavy in your ears, the Wall Street Journal reports the horns once used to rally people in remote places, now used to champion athletes, may have lasting effects [1]. The vuvuzela is traditionally made from the horn of a kudu, a species of antelope found in Africa and was first used to communicate over long distances. Today the plastic versions have become fixtures in soccer stadiums to cheer and potentially distract players. According to a study conducted by the University of Pretoria that appeared earlier this year in the South African Medical Journal, the sound has been measured at 127 decibels, greater than the 85 decibels that could potentially put a person at risk for permanent hearing loss with extended exposure. At levels greater than 100 decibels, only minutes of exposure could be enough to cause damage according to the report. Further, Dr. McNerney of the London School of Hygiene and Tropical Medicine conducted a study ahead of the World Cup in collaboration with Ka-Man Lai at University College London and found that very high air flow with large numbers of spit droplets blown from the vuvuzela are small enough to stay suspended in the air for hours, potentially putting others at risk for infection, including the common cold, chicken pox, and rubella, among others. Professor Barry Schoub of South Africa’s National Institute for Communicable Diseases stated that with winter in the Southern Hemisphere, there’s a large caseload of respiratory diseases in the country, but that the health hazards the horn poses may not be greater than from fans shouting and screaming during a game. So rest easy FIFA and vuvuzela fans, the noise will go on!
In other news, an article published in the NEJM this week investigated the cause for nicotine addiction [2]. The study found that about 45 million Americans smoke tobacco. Of those, 70% say they would like to quit, and every year, 40% do quit for at least 1 day. Moreover, the 80% who attempt to quit on their own return to smoking within a month, and each year, only 3% of smokers quit successfully. Unfortunately, the study found that the rate at which persons become daily smokers nearly matches the quit rate, so the prevalence of cigarette smoking has declined only very slowly in recent years. The authors concluded that nicotine sustains tobacco addiction, by acting on nicotinic cholinergic receptors in the brain to trigger the release of dopamine, glutamate, and GABA, which are particularly important in the development of nicotine dependence. Nicotine addiction occurs when smokers come to rely on smoking to modulate mood and arousal, relieve withdrawal symptoms, or both. Light or occasional smokers smoke mainly for positive reinforcement in specific situations. Further, people with psychiatric or substance-abuse disorders, who account for a large proportion of current smokers, have an increased susceptibility to tobacco addiction. Finally, the study found that nicotine is metabolized primarily by the enzyme CYP2A6, and variation in the rate of nicotine metabolism contributes to differences in vulnerability to tobacco dependence and the response to smoking-cessation treatment.
In JAMA this week, Dr. Lindenauer and colleagues looked at the role of systemic corticosteroids in patients hospitalized with acute exacerbation of chronic obstructive pulmonary disease (COPD) [3]. In these patients, the optimal dose and route of administration of steroids are uncertain. The aim of the study was to compare the outcomes of patients treated with low doses of steroids administered orally to those treated with higher doses administered intravenously. This cohort study conducted at 414 US hospitals studied patients admitted with acute exacerbation of COPD in 2006 and 2007 to a non–intensive care setting who received systemic corticosteroids during the first 2 hospital days. Treatment failure was defined as the initiation of mechanical ventilation after the second hospital day, inpatient mortality, or readmission for acute exacerbation of COPD within 30 days of discharge. Length of stay and hospital costs were also considered. Of the 79,985 patients, 73,765 (92%) were initially treated with intravenous steroids, whereas 6220 (8%) received oral treatment. The authors found that 1.4% of the intravenously and 1.0% of the orally treated patients died during hospitalization, whereas 10.9% of the intravenously and 10.3% of the orally treated patients experienced the composite outcome. After multivariable adjustment, including the propensity for oral treatment, the risk of treatment failure among patients treated orally was not worse than for those treated intravenously. In a propensity-matched analysis, the risk of treatment failure was significantly lower among orally treated patients, as was length of stay and cost. Using an adaptation of the instrumental variable approach, increased rate of treatment with oral steroids was not associated with a change in the risk of treatment failure. A total of 1356 (22%) patients initially treated with oral steroids were switched to intravenous therapy later in the hospitalization. Based on the results, the study concluded that among patients hospitalized for acute exacerbation of COPD, low-dose steroids administered orally were not associated with worse outcomes than high-dose intravenous therapy.
Finally, in the Annals of Internal Medicine this week, there is a thorough review by Javier Sanz and Valentin Fuster of nine significant studies published in the field of cardiology in 2009 [4]. Among the studies reviewed is the 30-year cardiovascular risk calculator based on the Framingham data, published in Circulation by Pencina et al. Not surprisingly, a report of the JUPITER trial which demonstrated benefit in targeting statin therapy to c-reactive protein levels was included, as was the NEJM piece by Serruys et al. on coronary artery bypass surgery versus percutaneous revascularization with drug-eluting stents in patients with multivessel coronary disease. Take a look at the Annals update series: it’s a useful way to see what you may have missed in the journals over the last year.
What a week! Keep reading, enjoy the summer, and join us next week for another update on what’s hot in the journals!
Dr. Mayne if a first year resident at NYU Langone Medical Center
Peer reviewed by Barbara Porter, MD, Section Editor, Clinical Correlations
References:
1. Stewart, R. More Buzz on Vuvuzela: It’s a Health Risk, Too Horns Adds to Atmosphere at Soccer Matches and in the Streets, but Experts Warn of Harm to Hearing. [Internet]. The Wall Street Journal; 2010, June 14. http://online.wsj.com/article/SB10001424052748703280004575308663670547940.html
2. Benowitz, NL, Nicotine Addiction. N Engl J Med. 2010 June 17; 362 (24): 2295-2303. http://content.nejm.org.ezproxy.med.nyu.edu/cgi/content/full/362/24/2295
3. Lindenauer, KP, Pekow PS, et al. Association of Corticosteroid Dose and Route of Administration With Risk of Treatment Failure in Acute Exacerbation of Chronic Obstructive Pulmonary Disease. JAMA. 2010; 303 (23): 2359-2367. http://jama.ama-assn.org.ezproxy.med.nyu.edu/cgi/content/full/303/23/2359
4. Sanz, J, Fuster, V. Update in Cardiology. Annals of Internal Medicine. 2010; 152 (12): 786-791. http://www.annals.org.ezproxy.med.nyu.edu/content/152/12/786.full