Was ist der unterschied zwischen wj pro und wj air

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Was ist der unterschied zwischen wj pro und wj air

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Was ist der unterschied zwischen wj pro und wj air

It is well established that asthma is a variable disease. Asthma can vary among individuals, and its progression and symptoms can vary within an individual's experience over time. The course of asthma over time, either remission or increasing severity, is commonly referred to as the natural history of the disease. It has been postulated that the persistence or increase of asthma symptoms over time is accompanied by a progressive decline in lung function. Recent research suggests that this may not be the case. Rather, the course of asthma may vary markedly between young children, older children and adolescents, and adults, and this variation is probably more dependent on age than on symptoms.

A prospective cohort study in which followup began at birth revealed that, in children whose asthma-like symptoms began before 3 years of age, deficits in lung growth associated with the asthma occurred by 6 years of age (Martinez et al. 1995). Continued followup on lung function measures taken at 11–16 years of age found that, compared to the group of children who experienced no asthma symptoms for the first 6 years of life, the group of children whose asthma symptoms began before 3 years of age experienced significant deficits in lung function at 11–16 years of age; however, no further loss in forced expiratory volume in 1 second (FEV1) occurred compared to children who did not have asthma (Morgan et al. 2005). The group whose asthma symptoms began after 3 years of age did not experience deficits in lung function.

A longitudinal study of children 8–10 years of age found that bronchial hyperresponsiveness was associated with declines in lung function growth in both children who have active symptoms of asthma and children who did not have such symptoms (Xuan et al. 2000). Thus, symptoms neither predicted nor determined lung function deficits in this age group.

A study by Sears and colleagues (2003) assessed lung function repeatedly from ages 9 to 26 in almost 1,000 children from a birth cohort in Dunedin, New Zealand. They found that children who had asthma had persistently lower levels of FEV1/forced vital capacity (FVC) ratio during the followup. Regardless of the severity of their symptoms, however, their levels of lung function paralleled those of children who did not have asthma, and no further losses of lung function were observed after age 9.

Baseline data from the Childhood Asthma Management Program (CAMP) study support the finding that the individual's age at the time of asthma onset influences declines in lung function growth. At the time of enrollment of children who had mild or moderate persistent asthma at 5–12 years of age, an inverse association between lung function and duration of asthma was noted (Zeiger et al. 1999). Although the analysis did not distinguish between age of onset and duration of asthma, it can be inferred that, because the average duration of asthma was 5 years and the average age of the children was 9 years, most children who had the longer duration of asthma started experiencing symptoms before 3 years of age. The data suggest that these children had the lowest lung function levels. After 4–6 years of followup, the children in the CAMP study, on average, did not experience deficits in lung growth (as defined by postbronchodilator FEV1), regardless of their symptom levels or the treatment they received (CAMP 2000). However, a followup analysis of the CAMP data showed that a subgroup of the children experienced progressive (at least 1 percent a year) reductions in lung growth, regardless of treatment group (Covar et al. 2004). Predictors of this progressive reduction, at baseline of the study, were male sex and younger age.

The CAMP study noted that when measures other than FEV1 are used to assess lung function measures over time in childhood asthma, progressive declines are observed: the FEV1/FVC ratio before bronchodilator use was smaller at the end of the treatment period than at the start in all three treatment groups; the decline in the ICS group was less than that of the placebo group (0.2 percent versus 1.8 percent) (CAMP 2000). In a comparison of lung function measures of CAMP study participants with lung function measures of children who did not have asthma, by year from ages 5 through 18, the FEV1/FVC ratio was significantly lower for the children who had asthma compared to those who did not have asthma at age 5 (mean difference 7.3 percent for boys and 7.1 percent for girls), and the difference increased with age (9.8 percent for boys and 9.9 percent for girls) (Strunk et al. 2006).

Cumulatively, these studies suggest that most of the deficits in lung function growth observed in children who have asthma occur in children whose symptoms begin during the first 3 years of life, and the onset of symptoms after 3 years of age usually is not associated with significant deficits in lung function growth. Thus, a promising target for interventions designed to prevent deficits in lung function, and perhaps the development of more severe symptoms later in life, would be children who have symptoms before 3 years of age and seem destined to develop persistent asthma. However, it is important to distinguish this group from the majority of children who wheeze before 3 years of age and do not experience any more symptoms after 6 years of age (Martinez et al. 1995). Until recently, no validated algorithms were available to predict which children among those who had asthma-like symptoms early in life would go on to have persistent asthma. Data obtained from long-term longitudinal studies of children who were enrolled at birth have generated such a predictive index. The studies first identified an index of risk factors for developing persistent asthma symptoms among children younger than 3 years of age who had more than three episodes of wheezing during the previous year. The index was then applied to a birth cohort that was followed through 13 years of age. Seventy-six percent of the children who were diagnosed with asthma after 6 years of age had a positive asthma predictive index before 3 years of age; 97 percent of the children who did not have asthma after 6 years of age had a negative asthma predictive index before 3 years of age (Castro-Rodriguez et al. 2000). The index was subsequently refined and tested in a clinical trial to examine if treating children who had a positive asthma predictive index would prevent development of persistent wheezing (Guilbert et al. 2006). The asthma predictive index generated by these studies identifies the following risk factors for developing persistent asthma among children younger than 3 years of age who had four or more episodes of wheezing during the previous year: either (1) one of the following: parental history of asthma, a physician diagnosis of atopic dermatitis, or evidence of sensitization to aeroallergens, or (2) two of the following: evidence of sensitization to foods, ≥4 percent peripheral blood eosinophilia, or wheezing apart from colds.

Accelerated loss of lung function appears to occur in adults who have asthma. In a study of adults who have asthma and who received 2 weeks of high-dose prednisone if airflow obstruction persisted after 2 weeks of bronchodilator therapy, the degree of persistent airflow obstruction correlated with both the severity and the duration of their asthma (Finucane et al. 1985).

Two large, prospective epidemiological studies evaluated the rate of decline in pulmonary function in adults who had asthma. In an 18-year prospective study of 66 nonsmokers who had asthma, 26 smokers who had asthma, and 186 control participants who had no asthma, spirometry was performed at 3-year intervals (Peat et al. 1987). Seventy-three percent of the study group underwent at least six spirometric evaluations. The slope for decline in lung function (FEV1) was approximately 40 percent greater for the participants who had asthma than for those who had no asthma. This did not appear to result from extreme measurement produced by a few participants, because fewer than 25 percent of the participants who had asthma were measured with a slope less steep than the mean for those who did not have asthma. In another study, three spirometry evaluations were performed in 13,689 adults (778 had asthma, and 12,911 did not have asthma) over a 15-year period (Lange et al. 1998). The average decline in FEV1 was significantly greater (38 mL per year) in those who had asthma than in those who did not have asthma (22 mL per year). Although, in this study, asthma was defined simply by patient report, the researchers noted that, because the 6 percent prevalence rate for asthma did not increase in this cohort as they increased in age, it is likely that the subjects who reported having asthma did indeed have asthma rather than chronic obstructive pulmonary disease (COPD). It is not possible to determine from these studies whether the loss of pulmonary function occurred in those who had mild or moderate asthma or only in those who had severe asthma. Nevertheless, the data support the likelihood of potential accelerated loss of pulmonary function in adults who have asthma.

New studies have addressed this issue since the "Expert Panel Review—Update 2002" (EPR—Update 2002). James and colleagues (2005) reanalyzed the data from the study of decline in lung function from Busselton, Australia (Peat et al. 1987), after adding a new survey in 1994–1995. Subjects (N = 9,317) had participated as adults (19 years or older) in one or more of the cross-sectional Busselton Health Surveys between 1966 and 1981 or in the followup study of 1994–1995. Using the whole data sample, James and colleagues found that subjects who had asthma showed significantly lower lung function during the whole followup period, but most of the differences were due to deficits in lung function present at the beginning of followup (when subjects were age 19). Once the effect of smoking was taken into account, the excess decline in FEV1 attributable to asthma was 3.78 mL per year for women and 3.69 mL per year for men. Although these results were statistically significant, their clinical relevance is debatable. Sherrill and coworkers (2003) reanalyzed the data from the Tucson Epidemiologic Study of Airway Obstructive Disease. A total of 2,926 subjects, with longitudinal data for lung function assessed in up to 12 surveys spanning a period of up to 20 years, were included. They found that, unlike subjects who had a diagnosis of COPD, in those who had diagnosis of longstanding asthma, FEV1 did not decline at a more rapid rate than normal. This was also true for subjects who had asthma and COPD. Griffith and colleagues (2001) studied decline in lung function in 5,242 participants in the Cardiovascular Health Study who were over age 65 at enrollment. Each participant had up to three lung function measurements over a 7-year interval. Subjects who had asthma had lower levels of FEV1 than those who reported no asthma. However, after adjustment for emphysema and chronic bronchitis, there were no significant increases in the rate of decline in FEV1 in participants who had asthma.

Taken together, these longitudinal epidemiological studies and clinical trials indicate that the progression of asthma, as measured by declines in lung function, varies in different age groups. Declines in lung function growth observed in children appear to occur by 6 years of age and occur predominantly in those children whose asthma symptoms started before 3 years of age. Children 5–12 years of age who have mild or moderate persistent asthma, on average, do not appear to experience declines in lung function through 11–17 years of age, although a subset of these children experience progressive reductions in lung growth as measured by FEV1. Furthermore, there is emerging evidence of reductions in the FEV1/FVC ratio, apparent in young children who have mild or moderate asthma compared to children who do not have asthma, that increase with age. There is also evidence of progressively declining lung function in adults who have asthma, but the clinical significance and the extent to which these declines contribute to the development of fixed airflow obstruction are unknown.