Children with asthma whose fathers have a history of the disease are at significantly greater risk for serious airway constriction than children whose father have no such history.
In reporting the results of a 5-year study, the investigators said that paternal asthma was strongly associated with childhood airway hyperresponsiveness (AHR), an exaggerated constricting response to various stimuli that characterize asthma.
Called a defining feature of asthma, AHR is directly correlated with pulmonary symptoms and disease severity, according to the authors.
The 1,041 children in the study were all participants in the Childhood Asthma Management Program (CAMP). Sponsored by the National Institutes of Health and the Canadian Institutes of Health Research, CAMP is the largest outcome study of mild to moderate asthma in children to be undertaken. The multicenter investigation, which enrolled children ages 5 to 12, was designed to determine the long-term effects of three inhaled treatments.
While other studies have demonstrated that parental history of asthma affects children, the authors of the latest study note that they are the "first to suggest that a parental history of asthma influences the natural history of airway responsiveness among children with established asthma, and that the father's history may be the predominant familial determinant of this relationship."
AHR was measured through a median logarithmic data analysis of PC20, the concentration of the bronchoconstrictor methacholine required to cause a 20 percent fall in the children's lung function test scores. (All participants took the methacholine test at the beginning of the study and yearly thereafter.)
Lower data analysis scores showed worse AHR: the results ranged from 0.84 in the 208 children who had a father with asthma to 1.13 in the 763 youngsters who did not. The correlation was even greater when both parents had asthma: 0.52 in children with two asthmatic parents and 1.17 in children without parental asthma. The researchers did not find a statistically significant correlation between maternal asthma and childhood AHR.
The study appears in the first issue for September 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
EARLY ATHEROSCLEROIS DEMONSTRATED IN SEVERE OBSTRUCTIVE SLEEP APNEA
Medical scientists detected early atherosclerosis by uncovering vascular abnormalities in 42- to 44-year-old predominately male patients who had severe obstructive sleep apnea but no overt cardiovascular disease.
In the study, the researchers investigated the functional and structural properties of the large arteries in 15 persons with mild to moderate obstructive sleep apnea (OSA), 15 individuals with severe OSA, and 12 healthy control volunteers. All groups were matched for age, sex, and body mass index.
The participants underwent a full standard overnight sleep test (polysomnography); a pulse wave velocity test, which is a noninvasive, accurate method of determining the elastic properties of the aorta and other large arteries; and an assessment with a high definition echo-tracing device to measure carotid artery thickness, diameter, and potential enlargement.
The authors said that the mechanical properties of the large arteries are important determinants of circulatory physiology in health and disease. They noted that increased arterial stiffness preceded the onset of systemic hypertension in humans and was an independent risk marker of premature artery disease, atherosclerosis, and cardiovascular disease.
In OSA, the sleeping person repeatedly stops breathing as a result of partial or complete blockage of the upper airways. This stoppage occurs long enough to decrease the amount of oxygen in the blood and brain, and to build up carbon dioxide. After a breathing pause of 10 seconds or longer, the person usually awakens enough to resume breathing. These episodes can occur numerous times during the night.
In this study, the investigators said that an important finding was the increased carotid diameter in patients with OSA. It seems that previous studies have shown that carotid artery dilation is a compensatory mechanism in the early stages of atherosclerosis.
The authors pointed out that all vascular abnormalities detected correlated significantly with the severity of the subject's OSA, which further supported the hypothesis that OSA plays an independent role in the progression of atherosclerosis.
The study appears in the first issue for September 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
For the complete text of these articles, please see the American Thoracic Society Online Web Site at http://www.atsjournals.org. For either contact information or to request a complimentary journalist subscription to ATS journals online, or if you would like to add your name to the Society's twice monthly journal news e-mail list, contact Brian Kell at (212) 315-6442, or by e-mail at bkell@thoracic.org.
Journal
American Journal of Respiratory and Critical Care Medicine