The MVA risk in this large cohort of unselected patients with OSA suggests a need for accurate tools to identify individuals at risk. Sleep apnea severity (e.g., apnea-hypopnea index) failed to identify patients at risk.

Carbonic anhydrase inhibition reduces apnoeic events in sleep disordered breathing. Zonisamide inhibits carbonic anhydrase, and induces weight loss in obese patients. This study explored the relative influence of these two properties, which may both alleviate obstructive sleep apnoea (OSA). Continuous positive airway pressure (CPAP) was used as a standard care comparator.47 patients with moderate-to-severe OSA and a body mass index of 27-35 kg?m -2 were randomised to receive either zonisamide, placebo or CPAP for 4 weeks. The open extension phase (20 weeks) compared CPAP and zonisamide. Polysomnography, biochemistry and symptoms were evaluated.At 4 weeks, zonisamide reduced apnoea/hypopnoea index (AHI) by a mean¡SD 33¡39% and oxygen desaturation index by 28¡31% (p50.02 and 0.014, respectively; placebo adjusted). The mean compliance adjusted reduction of AHI after zonisamide and CPAP was 13 and 61%, respectively, (p50.001) at 24 weeks. Body weight was marginally changed at 4 weeks, but reduced after zonisamide and increased after CPAP at 24 weeks (-2.7¡3.0 kg versus 2.3¡2.0 kg, p,0.001). Zonisamide decreased bicarbonate at 4 and 24 weeks. Side-effects were more common after zonisamide.Zonisamide reduced OSA independent of body weight potentially by mechanisms related to carbonic anhydrase inhibition. The effect was less pronounced than that obtained by CPAP. @ERSpublicationsThe carbonic anhydrase inhibitor zonisamide reduces sleep apnoea, but the effect is inferior to CPAP treatment

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SUMMARYObstructive sleep apnea is associated with increased motor vehicle accident risk, and improved detection of patients at risk is of importance. The present study addresses potential risk factors in the European Sleep Apnea Database and includes patients with suspected obstructive sleep apnea [n = 8476, age 51.5 (12.5) years, body mass index 31.0 (6.6) kg m À2 , 82.4% driver's licence holders]. Driving distance (km year À1), driver's licence type, sleep apnea severity, sleepiness and comorbidities were assessed. Previously validated risk factors for accident history: Epworth Sleepiness Scale ≥16; habitual sleep time ≤5 h; use of hypnotics; and driving ≥15 000 km year À1 were analysed across European regions. At least one risk factor was identified in male and female drivers, 68.75 and 51.3%, respectively. The occurrence of the risk factors was similar across Europe, with only a lower rate in the eastern region (P = 0.001). The mean number of risk factors increased across classes of sleep apnea severity. Frequent driving was prevalent [14.0 (interquartile range 8.0-20.0) 9 10 3 km year À1 ] and 32.7% of drivers had severe obstructive sleep apnea [apnea-hypopnea index 50.3 (38.8-66.0) n h À1 ]. Obesity, shorter sleep time and younger age were associated with increased traffic exposure (P ≤ 0.03). In conclusion, the risk factors associated with accident history were common among European patients with suspected obstructive sleep apnea, but varied between geographical regions. There was a weak covariation between occurrence of risk factors and clinically determined apnea severity but frequent driving, a strong risk factor for accidents, was over-represented. Systematic evaluation of accident-related risk factors is important to detect sleep apnea patients at risk for motor vehicle accidents. IN TROD UCTI ONObstructive sleep apnea (OSA) leads to hypoxaemia, autonomic activation and sleep fragmentation. The condition affects at least 24% of male and 9% of female adults (Punjabi, 2008;Young et al., 1993). Daytime consequences of OSA include excessive daytime sleepiness (EDS) (Stoohs et al., 1994) and cognitive impairment (Mitler, 1993) in many, but not all, OSA patients.Risk factors (RFs) for motor vehicle accidents (MVA) include driving exposure and experience, road and weather conditions, traffic density and time of day (Horne and Reyner, 1995;Pack, 1995;Stutts et al., 2003). The linked human factors include circadian timing, time on task, cumulative sleep deficit and presence of comorbidities such as metabolic, neurological or cardiovascular disease

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Background: Risk factors for obstructive sleep apnea (OSA) are male gender, obesity and abnormalities in neck soft tissue mass. OSA is associated with both growth hormone (GH) excess and severe GH deficiency in adults. Adults with abdominal obesity have markedly suppressed GH secretion. Aim: To study the effect of GH treatment on OSA in abdominally obese men with impaired glucose tolerance. Patients and Methods: Forty men with abdominal obesity and glucose intolerance were randomized in a prospective, 12-month double-blind trial to receive either GH or placebo. The treatment groups had similar BMI and waist circumference. Overnight polysomnography and computed tomography to assess muscle and fat distribution in the neck and abdomen were performed at baseline and after 12 months. Results: GH treatment increased insulin-like growth-factor-1 from (mean [SD]) 168 (72) to 292 (117) μg/L, the apnea-hypopnea index from (n/h) 31 (20) to 43 (25) and oxygen-desaturation index from (n/h) 18 ( 14) to 29 (21) (p = 0.0001, 0.001, 0.002). Neck transverse diameter, circumference and total cross-sectional area (p = 0.007, 0.01, 0.02) increased, while abdominal visceral adipose tissue (p = 0.007) was reduced. No between-group differences in total sleep time, REM sleep, NREM sleep, and time spent in supine position were found. The Epworth sleepiness scale score was unchanged. Conclusions: GH treatment increased the severity of OSA in abdominally obese men. The possible mechanism appears to be reflected by the GH-induced increase of measures of neck volume. The present results, to some extent, argue against that low GH/IGF-I activity is a primary cause of OSA in abdominally obese men.

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Obstructive sleep apnea-hypopnea and related clinical features in population-based sample of subjects aged 30-70 yr. Am J Respir Crit Care Med 163:685-689 7. Gami AS, Pressman G, Caples SM et al (2004) Association of atrial fibrillation and obstructive sleep apnea. Circulation 110:364-367 8. Gus M, Goncalves SC, Martinez D et al (2008) Risk of obstructive sleep apnea by Berlin Questionnaire, but not daytime sleepiness, is associated with resistant hypertension: a case-control study.