Asthma

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Description

  • A heterogeneous disease characterized as chronic inflammation of the airway
  • Patient may experience symptoms-free periods alternating with sporadic flare-up (exacerbations) brought on by triggers (e.g., exercise, allergens, weather changes, viral respiratory infections).
  • There are many different asthma phenotypes, with the most common including allergic asthma, nonallergic asthma, adult-onset, asthma with fixed airflow limitation, asthma of obesity, and cough variant asthma.
  • Asthma severity is assessed retrospectively from treatment required to control symptoms.
    • Mild: well controlled with step 1 or 2 treatment (i.e., with as-needed ICS-formoterol alone or with low-intensity maintenance controller treatment)
    • Moderate: well controlled with step 3 or 4 treatment (i.e., low- or medium-dose inhaled corticosteroids [ICS] long-acting β-agonists [LABA])
    • Severe: remains “uncontrolled” with optimized treatment with high-dose ICS-LABA or that requires high-dose ICS-LABA to prevent it from becoming “uncontrolled”

Epidemiology

Incidence

The yearly incidence rate of asthma in United States ~3.8/1,000 at-risk adults and 12.5/1,000 at-risk children (1). Incidence varies by demographic group.

Prevalence

Asthma affects 262 million individuals worldwide.

  • In 2021, 7.7% of the U.S. population had asthma (2).
  • African Americans are three times more likely to die from asthma.
  • Asthma affects about 10% of children ages 5 to 18 years in the United States.
  • Obesity is associated with increased prevalence and incidence of asthma.
  • Rate of asthma deaths is largest among those ages ≥65 years.

Etiology and Pathophysiology

Asthma is defined by airway hyperresponsiveness. Several theorized contributory mechanisms, including inflammatory cell infiltration and degranulation, subbasement fibrosis, mucus hypersecretion, epithelial injury, significant smooth muscle hypertrophy and hyperreactivity, and angiogenesis lead to reversible bronchospasm, which lead to intermittent airway obstruction.

Genetics

Broadly, there is a genetic association between asthma and genes that are involved in the production of inflammatory cytokines (e.g., interleukin [IL]-13 and IL-4) that lead to IgE production, recruitment of inflammatory cells (e.g., eosinophils, basophils, T cells) and the differentiation of T cells into Th2 cells. The subsequent inflammation leads to increased airway hyperresponsiveness. The immunotherapies lebrikizumab, tralokinumab, and dupilumab target these cytokine signaling pathways.

Risk Factors

  • Genetic predisposition, sex, obesity, preterm or small for gestational age (SGA)
  • Environmental: viral infections, animal and airborne allergens, tobacco smoke exposure, e-cigarette use, pollution, stress
  • Aspirin or NSAIDs hypersensitivity

General Prevention

  • Avoidance of environmental tobacco exposure during pregnancy and first year of life (1)
  • Encourage vaginal delivery and breastfeeding (1).
  • Avoid use of broad-spectrum antibiotics during first year of life (1).
  • Avoid allergens and triggers in new-onset asthma.

Commonly Associated Conditions

  • Atopy: eczema, allergic conjunctivitis, allergic rhinitis
  • Obesity (associated with higher asthma rates)
  • Gastroesophageal reflux disease (GERD)
  • Obstructive sleep apnea (OSA)

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