Risk Factors For Persistent Asthma Research Articles

Class III Obesity as a Risk Factor for Persistent Asthma.

The burden of asthma remains steady with no decline observed in the past few decades. Obesity prevalence has been steadily increasing with a rate of 41.9% in the United States between 2017-2020. Obesity is an inflammatory chronic condition that may partially contribute to the burden and severity of asthma. This study aimed to examine whether the association between obesity and asthma varies with the categories of obesity (class I, II, and III) and persistent asthma (mild, moderate, and severe asthma). We hypothesized that subjects with elevated body mass index (BMI) are more likely to be diagnosed with persistent asthma than subjects without obesity with asthma. As a retrospective and cross-sectional study, this study used a total of 1,977 records of subjects with asthma (age ≥ 19 y) hospitalized in Nevada between 2016-2021. BMI and persistent asthma were evaluated as the main exposure and outcome of interest. Logistic regression was used to estimate the magnitude of the association between obesity and persistent asthma. Among the selected subject records, subjects with obesity were more likely to be diagnosed with persistent asthma compared to subjects without obesity (odds ratio 1.50 [CI 1.10-2.05]). Subgroup analyses revealed that subjects with class III obesity (BMI ≥ 40) were more likely than subjects without obesity to be diagnosed with mild persistent asthma (odds ratio 2.21 [CI 1.18-4.16]) and severe persistent asthma (odds ratio 1.74 [CI 1.12-2.70]). Obesity was identified as a risk factor for persistent asthma, particularly class III obesity. This in turn increases the potential for greater health care utilization and economic burden. Public health and clinical interventions are necessary among those with comorbid asthma and obesity.

Year in review 2017: Chronic obstructive pulmonary disease and asthma.

Year in review 2017: Chronic obstructive pulmonary disease and asthma.

Inhaled steroid inhibits development of total and mite IgE

Serum levels of total immunoglobulin E (IgE) and allergen-specific IgE are related to asthma severity and risk factors for persistent asthma in childhood wheezing. Inhaled corticosteroids (ICS) have been the most effective therapy in children with asthma, as well as in adults. The serum levels of total and mite specific IgE in children with asthma and the effects on IgE levels of beclomethasone dipropionate (BDP) treatment on IgE levels in asthmatic children were investigated. First, a cross-sectional study of 255 children with asthma was carried out to measure IgE levels. Children under three years of age with asthma who were negative for Df-specific IgE were then treated with BDP or disodium cromoglycate (DSCG) as controls for one year. Serum IgE levels, numbers of eosinophils in peripheral blood and clinical variables were determined before and after treatment. After one-year DSCG treatment, the total IgE levels increased significantly, whereas the levels remained the same during BDP treatment. Five of 22 (23%) patients in the DSCG-treated group became positive for Df-specific IgE; however, only one of 13 (8%) in the BDP-treated group became positive. Taken together, ICS therapy may modulate the levels of total IgE and allergen-specific IgE.

Association of wheezing phenotypes with fractional exhaled nitric oxide in children.

Asthma comprises a heterogeneous group of disorders characterized by airway inflammation, airway obstruction, and airway hyperresponsiveness (AHR). Airway inflammation, which induces AHR and recurrence of asthma, is the main pathophysiology of asthma. The fractional exhaled nitric oxide (FeNO) level is a noninvasive, reproducible measurement of eosinophilic airway inflammation that is easy to perform in young children. As airway inflammation precedes asthma attacks and airway obstruction, elevated FeNO levels may be useful as predictive markers for risk of recurrence of asthma. This review discusses FeNO measurements among early-childhood wheezing phenotypes that have been identified in large-scale longitudinal studies. These wheezing phenotypes are classified into three to six categories based on the onset and persistence of wheezing from birth to later childhood. Each phenotype has characteristic findings for atopic sensitization, lung function, AHR, or FeNO. For example, in one birth cohort study, children with asthma and persistent wheezing at 7 years had higher FeNO levels at 4 years compared to children without wheezing, which suggested that FeNO could be a predictive marker for later development of asthma. Preschool-aged children with recurrent wheezing and stringent asthma predictive indices also had higher FeNO levels in the first 4 years of life compared to children with wheezing and loose indices or children with no wheeze, suggesting that FeNO measurements may provide an additional parameter for predicting persistent wheezing in preschool children. Additional large-scale longitudinal studies are required to establish cutoff levels for FeNO as a risk factor for persistent asthma.

Environmental Risk Factors for Persistent Asthma in Lucknow

To identify the risk factors for persistent asthma among common environmental exposures, like ambient air pollutants and second hand smoke, animals, place of residence, decreased ventilation, dust, as well as history of allergic conditions like rhinitis, dermatitis and family history of asthma in children. This hospital-based, cross-sectional study was conducted after institutional ethical clearance. Children aged 1-12 y with asthma were recruited after parental consent. Children were classified into asthma severity categories according to GINA 2002 and level of control categories according to GINA 2009 guidelines. Adjusted logistic regression analysis was used to identify factors associated with persistent asthma. From August 2008 through October 2010, 205 asthmatic children were recruited of which 73 (35.60 %) had intermittent and 132 (64.40 %) had persistent asthma. Asthma was controlled in 19 (9.26 %), partly controlled in 90 (43.90 %) and uncontrolled in 96 (46.82 %). Patients with persistent asthma were more likely to have uncontrolled asthma (OR = 8.28; 95 % CI: 2.43-31.01; p < 0.001). Adjusting for age, sex, socioeconomic status and place of residence, persistent asthma was associated with residence within 1.5 km from heavy traffic (OR = 4.58; 95%CI: 2.18-9.59; p < 0.001) and father smoking indoors >5 cigarettes or "bidi"/day (OR = 17.76; 95 % CI: 1.85-170.76; p = 0.01). Since patients with persistent asthma are more likely to have uncontrolled asthma and since persistent asthma is associated with residence closer to heavy traffic and exposure to second hand smoke, minimizing exposures to these may help in better asthma control.

Febrile respiratory illnesses in infancy and atopy are risk factors for persistent asthma and wheeze

Severe viral respiratory illnesses and atopy are risk factors for childhood wheezing and asthma. The aim of this study was to explore associations between severe respiratory infections and atopy in early childhood with wheeze and asthma persisting into later childhood. 147 children at high atopic risk were followed from birth to age 10 yrs. Data on all respiratory infections occurring in infancy were collected prospectively and viral aetiology ascertained. Atopy was measured by skin prick tests at 6 months, and 2 and 5 yrs. History of wheeze and doctor-diagnosed eczema and asthma was collected regularly until 10 yrs of age. At 10 yrs, 60% of the cohort was atopic, 25.9% had current eczema, 18.4% current asthma and 20.4% persistent wheeze. 35.8% experienced at least one lower respiratory infection (LRI) associated with fever and/or wheeze in first year of life. Children who had wheezy or, in particular, febrile LRI in infancy and were atopic by 2 yrs, were significantly more likely to have persistent wheeze (RR 3.51, 95% CI 1.83-6.70; p<0.001) and current asthma (RR 4.92, 95% CI 2.59-9.36; p<0.001) at 10 yrs. Severe viral respiratory infections in infancy and early atopy are risk factors for persistent wheeze and asthma. The strongest marker of the asthmatogenic potential of early life infections was concurrent fever. The occurrence of fever during respiratory illnesses is an important marker of risk for wheeze and asthma later in childhood, suggesting it should be measured in prospective studies of asthma aetiology.

Predicting the Long-Term Course of Asthma in Wheezing Infants Is Still a Challenge

Background. In recurrent wheezing infants, it is important to identify those likely to remain asthmatic in order to propose appropriate long-term management. Objective. To establish predictive factors for persistent asthma at adolescence in a population of recurrent wheezing infants. Methods. Retrospective study of 227 infants. Inclusion criteria were age under 36 months, a history of at least three wheezing episodes assessed via a doctor-led ISAAC questionnaire and a standardized allergy testing programme. At 13 years, active asthma was assessed by questionnaire. Results. Risk factors for asthma persisting into adolescence were allergic sensitization to multiple airborne allergens (OR 4.6, CI-95% (1.9–11.2) P = 0.001), initial atopic dermatitis (OR 3.4, CI-95% (1.9–6.3) P < 0.001), severe recurrent wheezing (OR 2.3, CI-95% (1.3–4.2) P = 0.007), and hypereosinophilia ≥470/mm3 (OR 2.2, CI-95% (1.07–4.7) P = 0.033). Conclusion. While it is still difficult to predict the long-term course of asthma, atopy remains the major risk factor for persistent asthma.

Suivi de nourrissons asthmatiques parisiens et auvergnats jusqu’à l’adolescence. Réflexions pour un suivi personnalisé

The evaluation of long-term prognosis of asthma in infants is a key issue given its frequency. The persistence of asthma in adolescence is multifactorial. Main objective of the study To compare the frequency of asthma in adolescence according to the geographical origin of children. Secondary objective Identify key risk factors for persistence. Design Retrospective, transversal, conducted in two university hospitals (centre for asthma, hôpital Trousseau, Paris, unit of paediatric pneumology and allergology, CHU-Estaing, Auvergne, Clermont-Ferrand). Inclusion criteria Children aged under 36 months old with infant asthma as defined by the HAS and which standardized investigation has been performed. Asthma symptoms were recorded after the age of 12. Two hundred and twenty patients were enrolled (148 in Clermont-Ferrand, 79 in Paris). Results There is no difference in the follow-up (persistent asthma in adolescence) according to the geographical origin of patients (32.26% in Clermont-Ferrand vs 25% in Paris, P = 0.27). The children followed in Auvergne are more sensitized at the adolescence that Parisians (26.16% for two inhalant sensitizations vs 11.11% in Paris, P = 0.03). Risk factors for persistent asthma in both groups are [1] sensitizations for multiple allergens (OR 4.6), history of atopic dermatitis (OR 3.4), the initial severity (OR 2.3) and eosinophilia greater than 470/mm 3 (OR 2.2). Coexistence of allergic rhinitis is significantly associated with severity of current asthma. Conclusions Atopic dermatitis and the multi-allergen sensitization are risk factors for the follow-up. Living in a heavily urbanized or not does not alter significantly the long-term, with the exception of allergen sensitization.

Factors Associated with Asthma Severity in Children: A Case–Control Study

Objective. To investigate factors associated with the severity of childhood asthma. Methods. We conducted a case–control study in a group of Brazilian children (2–12 years old) with diagnosis of asthma attending the pediatric pulmonology clinic of a teaching hospital. The study sample consisted of cases (children with persistent asthma) and controls (children with intermittent asthma). Data were collected through an interview with the child's parent or caretaker using a standard questionnaire. Association between asthma severity and studied variables was assessed by calculating odds ratios (OR) and 95% confidence interval (95% CI) through logistic regression test. Results. 171 children were included in this study, of which 104 (61%) had persistent asthma and 67 (39%) had intermittent asthma. Onset of the disease before 2 years of age, paternal educational level lower than 9 years, and low household income (≤1 minimum wage per month) were independent risk factors for persistent asthma, with adjusted OR (95% CI) of 2.56 (1.01–6.48), 2.49 (1.04–5.99), and 4.36 (1.06–17.87), respectively. Regular consumption of fruits during the last 30 days was inversely associated with the risk of having persistent asthma, with an adjusted OR (95% CI) of 0.19 (0.04–0.97). Conclusions. Early onset of the disease, low paternal education, and low household income are independent risk factors for persistent childhood asthma. Regular consumption of fruits appears to be a protective factor against more severe asthma in children.

Do risk factors for persistent asthma modify lung function in infants and young children with recurrent wheeze?

There is very limited information on how the risk of persistent asthma in recurrent wheezing (RW) infants modifies their lung function early in life. The aim of this study is to compare lung function of RW infants and young children with a positive or negative asthma predictive index (API), an index previously used to anticipate asthma persistence into childhood and adolescence. Two groups of RW infants and young children were recruited in two centres in Spain (Palma de Mallorca and Murcia). Lung function was measured according to the thoracho-abdominal compression technique (RCT), and values of the maximal flow at functional residual capacity (V'FRC) were expressed as Z-scores. Other variables included in the study, as independent factors, were: gender, age, length, weight, and parental smoking habits together with information regarding API. Expressed as mean +/- SD, API+ RW infants (n = 50; age in months 11.9 +/- 4.9) had a lower V'FRC Z-score than API- RW ones (n = 41; age in months 12.3 +/- 6.2; -2.01 +/- 0.79 vs. -1.64 +/- 0.77, P = 0.026, respectively). Centre and tobacco exposition did not have an effect on lung function. Among RW infants and young children, those having a positive API have a significant lower lung function as measured by V'FRC at an early age.

Predictable Factors for the Persistence of Asthma from Infancy to Late Childhood

RATIONALE: It is difficult to accurately predict the outcome of early-onset asthma started prior to 2 years of age. We tried to find possible risk factors for persistent asthma to allow better control of the illness from infancy to late childhood.

Risk Factors for Persistent Asthma on the Breathmobile Population in San Bernardino County, California

Risk Factors for Persistent Asthma on the Breathmobile Population in San Bernardino County, California

REPLY

We thank Sears et al. for their comments on our annotation.1 They point out that they have never suggested that the children should not be breast-fed on the basis of their findings and neither did we suggest that they had recommended such a course. Indeed, we were well aware of, and referred to, their previous statement on this issue.2 A point of concern is that others who are less well informed might misinterpret the conclusion in their Lancet paper3 that breast-feeding ‘may even increase the risk’ of atopy and asthma. There is considerable community concern concerning allergic disease and such statements have the potential to influence mothers and practitioners to make a decision not to breast-feed. Sears et al. agree that there are protective effects against allergic disease in early life quote, ‘studies with outcomes examined over the first few years of life generally indicate that breast-feeding protects against early childhood wheezing and to some extent atopic dermatitis’. We also agree with their conclusion that breast-feeding has not been shown to have preventative effects on asthma and atopy in later life. Thus, the issue is whether one regards those positive benefits on allergic disease in early life as one rationale for recommending breast-feeding as we have done, or emphasize the lack of a proven protective effect in later life as advocated by Sears et al. It is perhaps not surprising that any benefits from breast-feeding with regard to allergic disease are most prominent in early life as in later life, other environmental considerations come into play. However, a significant issue from their Lancet paper was their suggestion that breast-feeding might increase the risk of atopic disease. This controversial suggestion obviously demands close examination. Sears et al. address possible discrepancies between the data provided in their original Lancet publication3 and that provided on the same cohort in their article in the New England Journal of Medicine.4 The fact remains that the statistic (P for trend) that they chose to examine influences on severity of asthma in the latter publication did not show any adverse effect of breast-feeding. In their list of the independent risk factors for persistent asthma in adulthood, they listed allergy to house dust mites, smoking, airway hyperresponsiveness and female sex but not breast-feeding.4 In this correspondence, they provide additional analysis of their New England Journal of Medicine figures stating that the prevalence of breast-feeding was significantly higher among those with persistent, relapsing or remitting asthma (56.8% vs 48.3%, P = 0.038) at 26 years of age. However, when examining whether breast-feeding protects against or promotes the development of long-term asthma, it seems illogical to include the category of asthma in remission in the persisting category, particularly as from their paper the remission may have occurred from 11 years of age. Examination of their data on the effect of breast-feeding on persisting, relapsing and intermittent asthma as compared to transient asthma never wheezed, and asthma in remission indicates that the prevalence of breast-feeding in the group with ongoing symptoms is 50.7% and in the remission, transient or never wheezed group 52.6% (P = 0.67). On face value this does not support the suggestion that breast-feeding may increase the risk of asthma in adult life. With respect to some of the additional points raised by Sears et al., they again refer to the Tucson cohort,5 which suggests that breast-feeding may exacerbate asthma outcomes in later life, without acknowledging the very small numbers involved. The issue as to whether mothers who have children with atopic eczema in early life, and thus choose to prolong breast-feeding, is not resolved by their statement that ‘as atopic eczema is very rare before age 4 weeks, this should not have impacted the decision to breast-feed’. A recent population-based study indicates that, of those infants who manifest eczema by 6 months of age, eczema was present in 40% at 4 weeks of age.6 The importance of studies such as that of Sears et al., which have examined the long-term influence of breast-feeding on atopic disease, should be acknowledged and we did so in the final paragraph of our annotation.1 However, the suggestion that breast-feeding may increase the risk of atopy or asthma in later life is far from proven.

Asthma update: epidemiology and pathophysiology.

1. Margaret F. Guill, MD* 1. *Professor of Pediatrics; Chief, Pediatric Pulmonology, Medical College of Georgia, Augusta, Ga After completing this article, readers should be able to: 1. Characterize asthma, including its prevalence in the United States. 2. Describe the interaction of immunologic mechanisms producing airway inflammation and hyperreactivity in asthma. 3. Discuss the major risk factor for persistent asthma in young children. This is the first of a two-part article on asthma. Readers should consider both parts for a complete review. Asthma continues to be the leading serious chronic illness among children, responsible for 10 million lost school days each year and costing more than $12 billion per year. Asthma is not a series of episodic events over time, but a state of airway inflammation and hyperresponsiveness that has variable manifestations within a given patient and between individuals. In this first of two articles, we review the epidemiology and pathophysiology of asthma. The second part reviews diagnosis, classification of severity, and management of asthma. The Expert Panel of the National Asthma Education and Prevention Program defined asthma in its 1997 report as a “chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular mast cells, eosinophils, T-lymphocytes, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli.” Although convoluted and a bit difficult to follow, this definition captures the chronic and inflammatory nature of asthma, its pathophysiology involving multiple cell types, and the variable nature of its manifestations. According to the National Center for Health Statistics, the prevalence of asthma in children younger than 18 years of age …

Asthma phenotypes in childhood: lessons from an epidemiological approach.

Asthma is a heterogenous disease with variable signs and symptoms among patients. It also presents significant individual variability over time. Recently, some important population-based studies that followed children from birth or from early childhood into adulthood have shed new light on how we understand this syndrome. Three phenotypes have been identified in children with asthma: transient wheezing, non-atopic wheezing of the toddler and pre-school-aged child and IgE-mediated wheezing. Transient wheezing is associated with symptoms that are limited to the first 3-5 years of life, decreased lung function, maternal smoking during pregnancy and exposure to other siblings or children at daycare centres. There is no association between transient wheezing and family history of asthma or allergic sensitisation. Children wheezing with respiratory syncytial virus in the first years of life are more likely to be wheezing up to 13 years of age; this is independent of atopy (non-atopic wheezers) and is not related to atopic sensitisation. Wheezing associated with evidence of allergic sensitisation has been identified as the 'classic' asthma phenotype. Early allergic sensitisation is a major risk factor for persistent asthma.

Risk of asthma in children with exposure to mite and cat allergens

Allergic sensitisation has been identified as a risk factor for persistent asthma. But it is unclear whether the onset of asthma is increased by exposure to allergens early in life or prevented by avoidance. Pearce and colleagues1 recently reviewed the studies on this topic and concluded that there is no evidence that allergen exposure in early life is a major risk factor for the development of asthma in children. Two longitudinal studies had been carried out, both among children with a family history of atopy.

A Reexamination of Risk Factors for Ventilatory Impairment

Previous cross-sectional analyses of data from the Tucson Epidemiological Study of Airways Obstructive Diseases have shown significant relationships of ventilatory impairment to a variety of risk factors, including smoking, chronic productive cough, a history of childhood respiratory illnesses, atopy, blood eosinophilia, and serum immunoglobulin E (IgE). In the present report, we reexamine these relationships in subjects 40 to 74 yr of age to determine the effect of excluding known asthmatics who, as a group, have markedly impaired lung function. After exclusion of asthmatics, atopy, eosinophilia, and IgE no longer appear to be significant risk factors for ventilatory impairment, and nonasthmatic nonsmokers show almost no remaining ventilatory impairment. In current smokers, quantitative relationships of FEV1 to pack-years of cigarette consumption and to chronic productive cough are changed little by excluding asthmatics. In nonasthmatic ex-smokers, however, age at quitting smoking adds significantly to prediction of FEV1 after accounting for pack-years. Young ex-smokers closely resemble nonsmokers, but they become increasingly similar to current smokers as their age at quitting increases. A history of respiratory trouble before 16 yr of age continues to appear to increase susceptibility to smoking effects, even after exclusion of asthmatics. But, as in previous studies, the possible bias of preferential recall of childhood illnesses by impaired subjects limits interpretations of this observation. On the other hand, present findings suggest that such factors as atopy, eosinophilia, and elevated serum IgE may well be risk factors for persistent asthma, but they have no relationship to nonasthmatic forms of chronic obstructive pulmonary disease (COPD).(ABSTRACT TRUNCATED AT 250 WORDS)