Proposed ABCD-3P-PQRST characterization system for asthma phenotypes, genotypes, and endotypes
| ABCD | 3P modela | PQRST | |
|---|---|---|---|
| Asthmaticsymptoms | Paroxysmal (< 1 month) Persistent (1–6 months) Permanent (> 6 months) | Precipitating factors | Exertion (during, after), allergens, odors, drugs, tobacco smoke |
| Qualitative description | Cough, wheezing, chest tightness, dyspnea | ||
| Reversibility to bronchodilator | Absolute change, percent change | ||
| Severity | Mild intermittent, mild, moderate, severe, or very severe persistent | ||
| Type | Onset (adulthood or childhood), race and ethnicity, gender (male or female, prepubertal, adult, postmenopausal) | ||
| Biomarkers | Predominant cells | Effector cells: eosinophils, neutrophils, mast cells, mixed cellularity, paucicellular Lymphocytes: T-helper 1 (Th1), Th2, Th17, regulatory T lymphocyes, natural killer cells | |
| Predominant cytokines, immunoglobulins, molecules | Interleukin (IL) 4, IL-5, IL-9, IL-13, IL-33, periostin; interferon gamma, IL-15, IL-17, IL-18, IL-21, IL-22; immunoglobulin E or G; nitric oxide | ||
| Predisposing genotype | Specific gene polymorphisms, mutations | ||
| Conditions associated | Prenatal risk factors | Maternal smoking, diet, nutrition, antibiotic use, stress | |
| Postnatal risk factors | Early-life wheezing, breastfeeding, early tobacco smoke exposure, viral infections, vitamin D deficiency, contact with animals, occupational exposures | ||
| Pathogenically linked conditions | Atopy, allergic rhinitis, chronic rhinosinusitis, nasal polyposis, obstructive sleep apnea, gastroesophageal reflux disease, obesity, bronchiectases | ||
| Drugs used | Anticholinergics (short-acting and long-acting), beta-2 adrenergic agonists (short-acting and long-acting), corticosteroids (inhaled, oral), leukotriene pathway-modifying agents (eg, leukotriene receptor agonists, lipooxygenase inhibitors), phosphodiesterase inhibitors (eg, theophylline, rofl umilast), cromolyn, nedocromil, mast cell stabilizers, anti–IL-5 agents (eg, mepolizumab, benralizumab, reslizumab), anti–IL-13 agents (eg, lebrikizumab, tralokinumab), anti-IgE (eg, omalizumab), anti-tumor necrosis factor alpha (golimumab) | ||
↵a 3P model for disease persistence should be characterized clinically, functionally, and biologically (eg, including exhaled gas concentration of nitric oxide).