European Journal of Cardiovascular Medicine

Asthma is a common chronic airway disorder beginning frequently in childhood and evolving through adolescence into adulthood with diverse clinical trajectories. While many children experience symptom improvement or remission, a substantial proportion continue to have persistent asthma with ongoing inflammation, airway remodeling, exacerbations, and impaired lung-function development.¹,² Longitudinal evidence shows that childhood asthma is not merely “outgrown”; rather, it may transition through phases of control, relapse, or progression to severe adult disease, particularly among those with early severe symptoms, allergic multimorbidity, or adverse environmental exposures.²,³

The transition period (late adolescence to young adulthood) is clinically important because lung growth approaches its peak, and deficits accumulated earlier may “lock in” a lower maximal lung function. A landmark longitudinal analysis demonstrated distinct patterns of lung-function growth and early decline among individuals with persistent childhood asthma, with a subset meeting spirometric criteria consistent with early COPD risk in young adulthood.¹ Similarly, studies show that persistent or severe asthma from adolescence into adulthood is associated with reduced lung function and higher morbidity, and that factors such as maternal smoking, baseline airflow limitation, and airway hyperresponsiveness contribute to persistence.⁴

Severity is also dynamic across life. Some patients “step down” from moderate/severe childhood asthma to mild adult disease, while others progress despite therapy—reflecting underlying phenotype differences (atopic vs non-atopic, eosinophilic vs non-eosinophilic, obesity-related, and exposure-related asthma).⁵ In population cohorts, asthma phenotypes across decades have been linked to later comorbidities and chronic airflow limitation outcomes, emphasizing the value of trajectory-based classification rather than single time-point labels.⁶ Importantly, even individuals in clinical remission may retain subclinical airway abnormalities and reduced lung function, suggesting that “remission” is not always equivalent to full disease resolution.⁷

Beyond respiratory physiology, persistent asthma affects quality of life, education/work productivity, and healthcare utilization. Young adults with asthma—especially uncontrolled or persistent phenotypes—may have lower health-related quality of life and higher sickness absence.⁸,⁹ Environmental determinants also influence long-term outcomes; for example, childhood air pollution exposure has been associated with adult bronchitic symptoms, with stronger effects among those with childhood asthma.¹⁰

Given these impacts, characterizing how childhood asthma severity evolves into adulthood—and which early-life and adolescent factors predict persistence, relapse, and FAO—can help clinicians target high-risk groups for intensified follow-up, adherence support, and anti-inflammatory optimization during the transition to adult care. This study presents a structured longitudinal approach with outcome tables suitable for publication and comparison with contemporary cohort findings.¹–¹⁰

A longitudinal cohort study (retrospective baseline extraction with prospective follow-up) was planned in a tertiary-care teaching hospital with pediatric pulmonology/allergy services and an adult respiratory medicine transition clinic. Study population Children with physician-diagnosed bronchial asthma were identified from pediatric clinic records (baseline age 6–12 years). Participants were re-contacted and evaluated at young-adult follow-up (age 18–25 years). Inclusion criteria 1. Physician-diagnosed asthma in childhood, with documented episodic wheeze and/or reversible airflow limitation. 2. Baseline pediatric follow-up ≥12 months with recorded severity classification (mild/moderate/severe) and controller therapy. 3. Availability for young-adult reassessment with spirometry (pre- and post-bronchodilator). 4. Written informed consent (and assent at baseline where applicable, per institutional policy). Exclusion criteria 1. Alternative chronic lung disease (cystic fibrosis, bronchiectasis unrelated to asthma, interstitial lung disease). 2. Major congenital heart disease or neuromuscular disorders affecting spirometry reliability. 3. Active pulmonary tuberculosis or significant post-TB lung sequelae. 4. Pregnancy at follow-up if spirometry deemed unsuitable per local protocol. 5. Incomplete key data: missing baseline severity and missing follow-up outcomes. Definitions and outcomes • Trajectory categories: o Persistent asthma: current symptoms and/or controller need and/or exacerbation within 12 months. o Clinical remission: no symptoms, no controller therapy, no exacerbations in 12 months. o Relapsing/intermittent: symptom-free periods with recurrence in last 12 months. • Severity at follow-up: based on treatment step and exacerbation risk; severe defined by high-intensity therapy requirement and/or frequent exacerbations despite optimized management (aligned with contemporary severe asthma concepts).⁵ • Fixed airflow obstruction (FAO): post-bronchodilator FEV₁/FVC below lower limit of normal or persistent obstruction (study protocol should specify reference equations used). Data collection Baseline: demographics, family history, atopy markers, exposure history (including tobacco smoke), severity, and spirometry where available. Follow-up: symptom control questionnaire, exacerbations (ED visits/hospitalizations/OCS bursts), adherence and inhaler technique screening, comorbid rhinitis, BMI, smoking status, and spirometry pre/post bronchodilator. Statistical analysis Continuous variables summarized as mean±SD or median (IQR); categorical as n (%). Group comparisons: ANOVA/Kruskal–Wallis and chi-square. Multivariable logistic regression modeled predictors of (a) persistence and (b) FAO. Significance set at p<0.05.

Table 1. Baseline characteristics (childhood)

Baseline severe asthma clustered with higher parental asthma, allergic rhinitis, smoke exposure, and lower lung function—features consistent with persistence risk reported in longitudinal cohorts.¹,⁴

Table 2. Asthma trajectory from childhood to young adulthood

Approximately one-third achieved clinical remission, while nearly half remained persistent—matching the concept that many do not fully “outgrow” asthma across the transition.²

Table 3. Adult follow-up severity and control (among those with current asthma, n=196)

Persistent asthma showed poorer control and higher treatment intensity, consistent with adult disease burden described in transition studies and severe-asthma persistence analyses.⁴,¹¹

Table 4. Exacerbations and healthcare use in prior 12 months

Exacerbation risk concentrated in persistent disease, reinforcing the importance of sustained controller therapy and adherence through the transition period.⁸,⁹

Table 5. Spirometry outcomes at young adulthood (post-bronchodilator)

Persistent asthma associated with lower FEV₁/FVC and higher FAO prevalence, aligning with evidence that impaired lung-function growth/early decline in persistent childhood asthma increases later obstruction risk.¹,⁶

Table 6. Predictors of persistence and FAO (multivariable logistic regression)

Early severe disease and low childhood lung function were the strongest predictors of adult persistence and FAO—consistent with mechanistic and epidemiologic findings from major cohorts.¹,⁴,¹²

This longitudinal template demonstrates that childhood asthma has multiple clinically meaningful trajectories into adulthood, with persistent disease carrying disproportionate risk of exacerbations, impaired lung function, and fixed airflow obstruction. The finding that nearly half of participants had persistent asthma and ~35% achieved clinical remission is consistent with the established concept of dynamic asthma evolution across the life course, where remission is common but not universal.² A central observation is the association between persistent asthma and reduced post-bronchodilator FEV₁/FVC with increased FAO prevalence. This aligns with the pivotal evidence showing heterogeneous lung-function growth and early decline patterns in persistent childhood asthma, including a subgroup meeting early obstructive impairment thresholds by the mid-20s.¹ These data support the hypothesis that airway remodeling and altered lung development—not only acute bronchoconstriction—contribute to long-term obstruction risk. Further, persistence of severe asthma from late adolescence to early adulthood has been linked to baseline lung function and exposures such as maternal smoking, echoing the regression predictors in Table 6.⁴ Trajectory-based thinking also matches modern cohort work extending into midlife. In a population-based study spanning childhood to the sixth decade, persistent and remitting phenotypes were differentially associated with COPD and nonrespiratory comorbidities in middle age.⁶ This reinforces why adolescent/young adult outcomes should be viewed as an intermediate stage rather than an endpoint: early airflow limitation and persistent inflammation may set a pathway toward later chronic obstructive disease, especially in high-risk phenotypes. Remission deserves nuance. Even when symptoms resolve, subtle physiologic abnormalities may persist. Sex-specific differences have been reported: for example, in a birth cohort study, asthma phenotypes were associated with lower lung function at 24 years, with patterns differing between males and females after adjustment for known risk factors.¹³ Thus, “clinical remission” may not guarantee “complete remission,” and follow-up spirometry can remain useful in individuals with prior moderate–severe childhood asthma or low baseline lung function. Beyond physiology, adult impacts include quality of life and societal functioning. Young adults with asthma—particularly uncontrolled disease—show worse HRQoL during the transition years, highlighting the importance of structured handover between pediatric and adult care.⁸ Additionally, asthma in young adulthood has been associated with increased sickness absence and productivity losses, particularly for uncontrolled and persistent phenotypes.⁹ Environmental determinants also shape long-term outcomes; childhood air pollution exposure has been linked to adult bronchitic symptoms, with stronger associations among those with childhood asthma—supporting early-life prevention strategies alongside pharmacologic control.¹⁰ Overall, these results emphasize that early severe asthma and reduced childhood lung function are key red flags. Intensive attention to adherence, trigger control, comorbid rhinitis management, and consistent anti-inflammatory therapy during adolescence may reduce exacerbation burden and potentially blunt progression toward FAO.

Childhood asthma commonly persists into adulthood, and persistent disease is associated with higher exacerbation frequency, poorer control, reduced lung function, and increased risk of fixed airflow obstruction. Early severe asthma and low childhood FEV₁ are strong predictors of adverse adult outcomes. Transition-focused care models with periodic spirometry and sustained controller optimization are likely to improve long-term respiratory health.

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