Allergic Bronchopulmonary Aspergillosis (ABPA) is an allergic disease of the lungs. It happens when your immune system becomes overly sensitive to a common mold called Aspergillus fumigatus. You breathe in tiny mold spores every day. In most people, the body clears them without trouble. In people with asthma or cystic fibrosis (CF), the immune system can overreact. It releases many allergy chemicals (like IgE and cytokines). This causes swelling in the airways, thick sticky mucus, coughing, wheeze, and sometimes brown “mucus plugs.” Over time, repeated flares can damage the airways and cause bronchiectasis (airway widening and scarring). Doctors confirm ABPA using symptoms, allergy blood tests to Aspergillus, high total IgE, chest imaging, and sometimes sputum tests. Recent guidelines suggest a total IgE of ≥500 IU/mL (by modern assays) plus other criteria for diagnosis. Treatment aims to calm the allergic inflammation, reduce fungus growth in the airways, prevent flares, and protect lung function. PMC
Allergic bronchopulmonary aspergillosis (ABPA) is an allergic disease of the lungs. It happens when a person’s airways become oversensitive to a common mold called Aspergillus fumigatus. The mold does not invade healthy lung tissue like a true infection. Instead, it colonizes mucus inside the bronchial tubes and repeatedly triggers the immune system. This allergic reaction (mainly IgE-mediated, with other immune pathways also involved) causes swelling of the airways, thick sticky mucus, and “plugging” of the bronchi. Over time, repeated flares can damage and widen the central airways (central bronchiectasis). People with asthma or cystic fibrosis (CF) get ABPA more often than others. Diagnosis uses a combination of symptoms, blood allergy tests, and chest imaging; a widely used international guideline recommends a total IgE ≥500 IU/mL plus evidence of A. fumigatus sensitization, together with typical clinical and radiologic features. PMC+2ERS Publications+2
Other names
ABPA (short form).
Hinson–Pepys disease (historic term).
Allergic bronchopulmonary mycosis (ABPM) when the same process is due to molds other than Aspergillus (ABPA is the Aspergillus subtype of ABPM). Wikipedia+1
How ABPA develops
You breathe in tiny Aspergillus spores every day. In most people, the lungs clear them. In some people—especially those with asthma or CF—the spores stick to airway mucus and colonize it. The immune system then reacts strongly to Aspergillus proteins (antigens), making high levels of IgE, IgG, and eosinophils. This causes coughing, wheeze, brown mucus plugs, and sometimes fleeting (moving) lung shadows on scans. Over time, repeated inflammation leads to central bronchiectasis and, in some, dense “high-attenuation” mucus on CT scans (a very specific clue for ABPA). PMC+2PMC+2
Types
Clinicians use a few simple labels. You may see more than one apply to the same person:
Serologic ABPA (ABPA-S): Blood tests and symptoms fit ABPA, but CT does not yet show bronchiectasis. Think of this as an early or milder radiologic form. ScienceDirect+1
ABPA with central bronchiectasis (ABPA-CB): Typical ABPA features plus widening of the central bronchi on high-resolution CT (HRCT). ScienceDirect
ABPA with high-attenuation mucus (ABPA-HAM): CT shows very dense mucus (often >70 Hounsfield units); this is highly specific and often signals more severe disease. Chest Journal
ABPA in asthma and ABPA in cystic fibrosis: Same disease mechanism, different patient groups; clinicians call this out because screening thresholds and care pathways can differ. Cystic Fibrosis Foundation
(Older staging language): Some texts still mention “acute,” “remission,” “exacerbation,” “steroid-dependent,” and “fibrotic” stages. Newer guidelines focus more on clear diagnostic criteria and phenotypes (S, CB, HAM) rather than fixed stages. PMC
Causes
ABPA has one root cause—a strong allergic response to A. fumigatus in the bronchi. The items below are practical contributors that raise risk or help set off flares:
Asthma: The strongest predisposing condition; airways are already inflamed and mucus-prone. PMC
Cystic fibrosis: Thick mucus and impaired clearance make colonization easier. Cystic Fibrosis Foundation
Frequent Aspergillus exposure at home or work: Damp buildings, compost, farming, or construction can increase the airborne spore load. (General risk context.) PMC
Atopy (personal or family allergy history): People with eczema, allergic rhinitis, or multiple aeroallergen sensitivities are more prone to IgE-mediated reactions. PMC
Poor mucus clearance: Any reason for impaired mucociliary function (e.g., CF, chronic bronchitis) helps spores persist. PMC
Bronchiectasis (existing): Damaged, widened airways trap mucus and organisms, setting the stage for colonization and allergy. PMC
Corticosteroid-dependent or poorly controlled asthma: Frequent inflammation and mucus plugging increase colonization risk. PMC
High humidity or damp environments: Moisture supports mold growth and higher spore counts. (Environmental contributor.) PMC
Genetic predisposition (e.g., certain HLA patterns, CFTR variants in CF): Genetic background can shape immune responses and mucus properties. PMC
Air pollution and smoke exposure: Irritants inflame airways and impair clearance. (General airway risk.) PMC
Sinus disease with fungal colonization: Post-nasal drainage seeds the lower airways. PMC
Prior lung infections that left scarring: Scarred bronchi clear mucus less effectively. PMC
Occupational dusts (grain, wood, compost): Often carry fungal spores and organic particles. PMC
Warm climates: Some regions have higher environmental mold burdens year-round. (Epidemiologic contributor.) PMC
Frequent antibiotic use that alters airway microbiome: May favor fungal overgrowth in mucus. (Hypothesized contributor in reviews.) PMC
Structural airway anomalies (congenital or acquired): Pockets where mucus pools promote colonization. PMC
Imbalanced immune responses (Th2-skewed): Strong IgE/eosinophil tendency to fungi. PMC
Repeated Aspergillus sensitization without early recognition: Ongoing exposure deepens the allergic cycle. PMC
Co-sensitization to multiple molds: Broader fungal allergy can amplify airway inflammation. PMC
Inadequate ventilation at home/work: Traps moisture and spores indoors. (Environmental contributor.) PMC
(Note: Many items above are risk contributors; the necessary element is airway colonization by Aspergillus with a strong allergic response.)
Common symptoms
Wheezing: Musical, whistling sounds from narrowed, inflamed airways. Often worse at night or with exertion. American Thoracic Society
Chronic cough: Usually productive. The cough tries to clear thick, sticky mucus. PMC
Brown mucus plugs: Classic clue. Mucus may be thick, rubbery, and brown; sometimes you see brown flecks. American Thoracic Society+1
Shortness of breath (breathlessness): From swollen airways and mucus blocking airflow. American Thoracic Society
Chest tightness or pain with breathing: From bronchospasm and coughing. Allergy & Asthma Network
Recurrent “asthma attacks” despite usual inhalers: Flares that seem out of proportion to typical asthma. American Thoracic Society
Fever that comes and goes: Low-grade fevers can occur during flares. American Thoracic Society
Fatigue and exercise intolerance: Breathing effort and inflammation make you tired. American Thoracic Society
Coughing up blood (hemoptysis): Can happen when inflamed airway surfaces bleed. Seek care urgently if significant. American Thoracic Society
Weight loss or poor appetite during bad flares: Inflammation and breathlessness reduce intake. PMC
Night cough or early-morning cough: Mucus shifts with position and triggers cough. PMC
Sinus symptoms (stuffy, drippy nose): Upper airway allergy often accompanies ABPA. PMC
Crackles on breathing exam: Air moving through mucus produces extra sounds. PMC
Episodes of “pneumonia” that seem to move around on X-rays: These are “fleeting” infiltrates from mucus plugging, not classic bacterial pneumonia. NCBI
Anxiety related to breathlessness: Breathlessness can be scary; anxiety may worsen symptoms. (Clinical context note.) PMC
Diagnostic tests
A) Physical examination
General check and vital signs
Your clinician looks for fever, fast breathing, or low oxygen levels. These suggest an active flare or severe airway blockage. Physical exam cannot diagnose ABPA alone but guides urgency and next steps. PMCChest listening (auscultation) and percussion
Wheezes, crackles, and dull or hyper-resonant note help locate mucus plugging or air trapping. Findings often change as mucus moves, which is typical in ABPA flares. PMCENT and skin allergy check
Doctors look for nasal polyps or allergic rhinitis and other atopic signs because ABPA commonly coexists with atopy. PMC
B) Manual/bedside allergy & airway tests
Skin prick test with A. fumigatus antigen
A tiny drop of allergen is placed on the skin with a small prick. A quick “wheal and flare” means your immune system is sensitized to Aspergillus. This is a screening test; positive results must be confirmed with blood tests and imaging. Merck Manuals+1Intradermal skin test (if prick test is negative but suspicion stays high)
A small amount is injected just under the skin. It is more sensitive but less specific, so doctors rely on the full picture, not this test alone. Merck ManualsPeak expiratory flow (PEF) monitoring
A handheld meter measures how fast you can blow air out. Variable daily readings support asthma activity; big ups and downs despite regular care make ABPA more likely and prompt lab/imaging work-up. (Adjunct test.) PMCGross sputum plug inspection
Seeing rubbery, brownish plugs is a clinical red flag for ABPA and may prompt targeted testing. (Microscopy and culture are lab steps described below.) PMC
C) Laboratory and pathological tests
Total serum IgE
This is a cornerstone test. An IgE ≥500 IU/mL strongly supports ABPA when combined with other findings; it’s also used to track response after treatment (IgE usually falls from its personal peak). ERS Publications+1A. fumigatus–specific IgE (blood)
Confirms true sensitization to the mold. High levels plus elevated total IgE strongly support the diagnosis. Component-resolved assays (e.g., Asp f1, f2) can add precision in some labs. JAci OnlineA. fumigatus–specific IgG (precipitins)
Shows ongoing immune exposure to the fungus. Doctors may order ELISA for IgG or older “precipitin” tests. It helps distinguish ABPA from simple asthma with mold sensitization. Merck ManualsPeripheral eosinophil count
Eosinophils are allergy-type white cells. High counts support the diagnosis (especially when not on systemic steroids). Not specific by itself. PMCSputum microscopy and culture
Lab looks for Aspergillus hyphae and tries to grow the mold. Positive results support colonization but are not mandatory for diagnosis. PMCAllergen component testing (if available)
Blood tests for specific Aspergillus components can improve accuracy in tough cases or research settings. JAci OnlineSerial IgE tracking
After treatment begins, repeating total IgE helps monitor trend. A sustained drop suggests control; a new rise may signal relapse. (Guideline-endorsed use of IgE trend.) PMC
D) Electrodiagnostic & physiology monitoring
Spirometry with bronchodilator response
Typically shows airway obstruction (low FEV1/FVC) and significant improvement after a bronchodilator. This pattern is common in asthma and ABPA; spirometry helps quantify severity and track recovery. PMCFractional exhaled nitric oxide (FeNO)
FeNO is a breath test for eosinophilic airway inflammation. High values support an allergic/eosinophilic pattern and help follow response to anti-inflammatory therapy. (Adjunctive, not diagnostic alone.) PMCPulse oximetry (± exercise oximetry)
A fingertip sensor measures blood oxygen at rest and with walking. Low readings suggest significant airway blockage or mucus plugging needing urgent care. PMC
E) Imaging tests
Chest X-ray
May show “fleeting” patchy opacities that move location between episodes. Classic signs include the “finger-in-glove” pattern and “tram-track” lines caused by mucus-filled, inflamed bronchi. X-ray is a quick, first-line tool. NCBIHigh-resolution CT (HRCT) chest
Key test to detect central bronchiectasis (widened, thick-walled central bronchi), mucus impaction, and air-trapping. HRCT clarifies type (serologic vs with bronchiectasis) and baseline damage. PMCHigh-attenuation mucus (HAM) assessment on CT
When the plugged mucus appears very dense (often >70 Hounsfield units), it is highly specific for ABPA and often marks more severe disease. Radiologists explicitly look for this sign. Chest Journal+1
Non-pharmacological treatments (therapies & other measures)
Each item includes a short description, purpose, and mechanism (how it helps).
Education & written action plan
Description: A simple, written plan that says what to do when symptoms rise or peak flow falls.
Purpose: Catch flares early and act fast.
Mechanism: Lowers delay to treatment; reduces steroid bursts and hospital visits by guiding self-management.Allergen and mold avoidance
Description: Reduce indoor dampness; fix leaks; keep home humidity under 50%; use exhaust fans; avoid compost piles, damp basements, and hay barns.
Purpose: Cut exposure to Aspergillus spores.
Mechanism: Fewer spores → less immune activation → fewer flares.HEPA air filtration
Description: Room air purifiers with true HEPA filters in bedroom/living areas.
Purpose: Lower airborne particles, including spores.
Mechanism: Mechanical filtration reduces inhaled triggers.Dehumidifiers in damp rooms
Description: Keep relative humidity 40–50%.
Purpose: Make mold growth harder.
Mechanism: Aspergillus grows in moisture; drier air slows growth.Regular airway clearance (Active Cycle of Breathing/Autogenic Drainage)
Description: Daily sessions to loosen and move mucus.
Purpose: Reduce mucus plugging and infections.
Mechanism: Changes in lung volumes shear mucus from airway walls and move it outward.Oscillating PEP device (e.g., Flutter®, Acapella®)
Description: You exhale through a small handheld device that vibrates and adds back-pressure.
Purpose: Help clear thick secretions.
Mechanism: Oscillations + positive pressure open small airways and dislodge mucus.Postural drainage
Description: Positioning to let gravity drain different lung segments.
Purpose: Clear mucus from stubborn areas.
Mechanism: Gravity assists movement of secretions toward larger airways.Nebulized sterile saline (0.9%–3%) before airway clearance
Description: Inhale saline mist before clearance sessions.
Purpose: Hydrate mucus so it moves easier.
Mechanism: Water moves into mucus layer; viscosity drops.Pulmonary rehabilitation / aerobic training
Description: Structured walking or cycling 3–5 days/week.
Purpose: Improve stamina, breathlessness, and quality of life.
Mechanism: Better cardiorespiratory fitness and ventilatory efficiency.Breathing retraining (diaphragmatic & pursed-lip breathing)
Description: Slow, belly-focused inhalation and gentle, prolonged exhalation.
Purpose: Ease dyspnea and reduce dynamic air-trapping.
Mechanism: Lowers respiratory rate; keeps airways from collapsing during exhale.Nasal hygiene & saline rinses (if sinus disease)
Description: Daily isotonic saline irrigation.
Purpose: Reduce post-nasal drip and cough triggers.
Mechanism: Washes out allergens and mucus; decreases upper-airway inflammation.Vaccinations kept up to date (influenza, pneumococcal)
Description: Annual flu shot and pneumococcal vaccines as indicated.
Purpose: Prevent infections that can trigger ABPA flares.
Mechanism: Immune priming lowers risk of viral/bacterial infections that worsen asthma.Sleep optimization (7–9 hours, consistent schedule)
Description: Regular, good-quality sleep.
Purpose: Better immune regulation and symptom control.
Mechanism: Sleep deprivation raises inflammatory cytokines; good sleep lowers them.Stress reduction (mindfulness/CBT/yoga)
Description: Simple daily practice of relaxation or guided breathing.
Purpose: Reduce anxiety-driven dyspnea and improve adherence.
Mechanism: Lowers sympathetic drive and hyperventilation tendency.Trigger diary & peak-flow monitoring
Description: Record symptoms, peak flows, exposures, and medication doses.
Purpose: Personalize triggers and spot early drops in lung function.
Mechanism: Data trends prompt early action per plan.Nutrition coaching (anti-inflammatory pattern)
Description: Emphasize whole foods, lean protein, fruits/vegetables, omega-3 sources.
Purpose: Support immunity and muscle mass; reduce systemic inflammation.
Mechanism: Nutrients and fiber modulate inflammatory pathways and gut-lung axis.Hydration routine
Description: Regular fluids unless restricted by another condition.
Purpose: Thins secretions.
Mechanism: Improves mucociliary clearance.Smoking/vape avoidance & secondhand smoke reduction
Description: Complete avoidance.
Purpose: Protect airway lining and cilia.
Mechanism: Smoke paralyzes cilia, thickens mucus, and amplifies inflammation.Environmental remediation
Description: Professional cleaning of visible mold, safe removal of moldy carpets/drywall.
Purpose: Reduce home spore burden.
Mechanism: Fewer reservoirs → fewer exposures.Adherence support tools
Description: Pillboxes, phone reminders, family support.
Purpose: Keep long treatments on track.
Mechanism: Reduces missed doses that can lead to relapse.
Drug treatments
Always follow your specialist’s plan. Doses below are common examples, not personal medical advice. Many ABPA medicines interact (especially azoles). Doctors often check liver tests and drug levels.
Oral glucocorticoid: Prednisolone (anti-inflammatory steroid)
Dose & time: Often ~0.5 mg/kg/day for 2–4 weeks, then taper over ~3–6 months, adjusted to IgE, symptoms, and imaging.
Purpose: First-line for acute ABPA to control the allergic flare and stop lung damage.
Mechanism: Suppresses Th2-allergic inflammation and eosinophils; quickly reduces swelling and mucus.
Side effects: Weight gain, mood change, high glucose, bone loss, infection risk—monitoring needed. Strong guideline-supported first-line therapy. PMC+1Itraconazole (triazole antifungal)
Dose & time: 200 mg twice daily with food for ~16 weeks; drug-level monitoring when available.
Purpose: Reduce Aspergillus burden and downstream allergic drive; steroid-sparing.
Mechanism: Blocks fungal cell membrane synthesis (ergosterol).
Side effects: Liver enzyme elevation, GI upset; strong interactions (CYP3A4). RCTs show effectiveness; sometimes used up front if steroid risk is high. PubMedVoriconazole (triazole antifungal)
Dose & time: Often 200 mg twice daily; adjust for weight, levels, and liver function.
Purpose: Alternative to itraconazole when not tolerated or ineffective.
Mechanism: Similar antifungal effect with good airway penetration.
Side effects: Photosensitivity, vision changes, liver toxicity; monitor levels. (Guideline-supported alternate azole.) PMCPosaconazole (triazole antifungal)
Dose & time: Delayed-release tablets commonly 300 mg daily after 300 mg twice on day 1; level monitoring.
Purpose: Another alternative in azole-intolerant/resistant cases.
Mechanism: Broad triazole activity; reduces fungal load.
Side effects: GI upset, liver enzyme rise; drug interactions. PMCIsavuconazole (triazole antifungal)
Dose & time: Loading then 200 mg daily; specialist use.
Purpose: Option if others fail or cause adverse effects.
Mechanism: Ergosterol synthesis inhibition.
Side effects: Liver toxicity, interactions; limited ABPA-specific data but considered in practice. PMCInhaled corticosteroids (ICS) (e.g., budesonide, fluticasone)
Dose & time: Medium–high dose per asthma guidelines, daily.
Purpose: Control background asthma; reduce wheeze and rescue inhaler use.
Mechanism: Local anti-inflammatory effects in bronchi.
Side effects: Oral thrush, hoarseness (rinse mouth). (For asthma control; ABPA flares still need systemic therapy.) PMCICS/LABA combination (e.g., budesonide-formoterol, fluticasone-vilanterol)
Dose & time: Daily controller, sometimes maintenance-and-reliever with formoterol per guidelines.
Purpose: Improve airflow and symptoms.
Mechanism: Anti-inflammatory + bronchodilation.
Side effects: Palpitations, tremor, thrush. PMCLong-acting muscarinic antagonist (LAMA: tiotropium)
Dose & time: Inhaled once daily as add-on.
Purpose: Extra bronchodilation when symptoms persist.
Mechanism: Blocks vagal-mediated bronchoconstriction.
Side effects: Dry mouth.Short-acting β2 agonist (SABA: albuterol/salbutamol)
Dose & time: 2 puffs as needed for relief.
Purpose: Quick symptom relief.
Mechanism: Smooth muscle relaxation.
Side effects: Jitteriness, fast pulse.Leukotriene receptor antagonist (montelukast)
Dose & time: 10 mg nightly (adult).
Purpose: Helpful in allergic asthma with nocturnal symptoms; modest effect.
Mechanism: Blocks leukotriene pathway.
Side effects: Rare mood changes; discuss risks/benefits.Azithromycin (long-term, specialist-directed in bronchiectasis)
Dose & time: e.g., 250–500 mg 3x/week for months if recurrent infections.
Purpose: Anti-inflammatory and anti-biofilm effects; reduce exacerbations.
Mechanism: Immunomodulatory macrolide action.
Side effects: QT prolongation, GI upset, resistance—requires ECG/drug review.Omalizumab (anti-IgE biologic)
Dose & time: Subcutaneous every 2–4 weeks based on body weight and baseline IgE (upper dosing ranges often used in ABPA; specialists may individualize).
Purpose: Steroid-sparing in recurrent or steroid-dependent ABPA.
Mechanism: Binds free IgE, dampening allergic cascade.
Side effects: Injection reactions, rare anaphylaxis; observation after dosing. Meta-analyses show fewer exacerbations and less oral steroid use. PubMed+1Mepolizumab (anti-IL-5)
Dose & time: 100 mg SC every 4 weeks.
Purpose: For eosinophilic allergic disease with frequent flares or poor steroid tolerance.
Mechanism: Lowers eosinophils to reduce airway inflammation.
Side effects: Headache, injection site pain; herpes zoster risk small. Emerging supportive data. PubMed+1Benralizumab (anti-IL-5 receptor)
Dose & time: 30 mg SC every 4 weeks for 3 doses, then every 8 weeks.
Purpose: Similar to mepolizumab, with near-complete eosinophil depletion.
Mechanism: Antibody-dependent cell-mediated cytotoxicity against eosinophils.
Side effects: Injection reactions; real-world evidence suggests benefit. PubMedReslizumab (anti-IL-5, IV)
Dose & time: 3 mg/kg IV every 4 weeks.
Purpose: Option in severe eosinophilic phenotype.
Mechanism: Neutralizes IL-5.
Side effects: Myalgias, rare anaphylaxis; ABPA data limited but mechanistically plausible. AAAAIDupilumab (anti-IL-4Rα; blocks IL-4/IL-13)**
Dose & time: Loading dose (e.g., 600 mg) then 300 mg SC every 2 weeks.
Purpose: For type-2 high disease when other biologics fail or are unsuitable.
Mechanism: Down-regulates type-2 inflammation and mucus pathways.
Side effects: Conjunctivitis, injection reactions; case reports/series show benefit in ABPA including after other biologic failure. PMC+1Tezepelumab (anti-TSLP)
Dose & time: 210 mg SC every 4 weeks.
Purpose: Broad upstream blocker of airway inflammation; used off-label in select ABPA with severe asthma.
Mechanism: Inhibits epithelial “alarmin” TSLP.
Side effects: Arthralgia, injection reactions; ABPA-specific evidence is evolving. AAAAICombination therapy: Prednisolone + Itraconazole (acute stage)
Dose & time: Standard prednisolone taper plus itraconazole 200 mg bid for ~16 weeks.
Purpose: Reduce fungal load and inflammation together; may reduce 1-year exacerbations versus steroid alone.
Mechanism: Dual hit on allergy and fungal burden.
Side effects: Adds liver/interaction monitoring. RCT showed trend favoring the combo. ERS Publications+1Nebulized amphotericin B (specialist, selected cases)
Dose & time: Intermittent inhaled dosing in centers with experience.
Purpose: Local antifungal effect if azoles fail.
Mechanism: Binds fungal membranes.
Side effects: Cough, bronchospasm; evidence limited; specialist only. PMCBone-health protection during steroids (e.g., calcium/vitamin D ± bisphosphonate when indicated)
Dose & time: As per bone-health guidelines.
Purpose: Prevent steroid-induced osteoporosis.
Mechanism: Supports bone remodeling and density.
Side effects: GI upset (oral bisphosphonates), hypocalcemia if vitamin D low; clinician-guided.
Dietary molecular supplements
Supplements are adjuncts, not primary therapy. Discuss interactions (especially with azoles and biologics) before use.
Vitamin D3: 1000–2000 IU/day (or as prescribed to correct deficiency).
Function: Immune balance; bone protection on steroids.
Mechanism: Modulates T-cell responses; supports calcium metabolism.Omega-3 fatty acids (EPA/DHA): 1–2 g/day combined.
Function: Anti-inflammatory support.
Mechanism: Competes with omega-6 arachidonic acid to reduce pro-inflammatory mediators.N-acetylcysteine (NAC): 600 mg once or twice daily.
Function: Mucus thinning; antioxidant.
Mechanism: Breaks disulfide bonds in mucus; glutathione precursor.Magnesium: 200–400 mg/day (watch kidneys).
Function: Smooth-muscle relaxation, may support bronchodilation.
Mechanism: Calcium antagonism in airway muscle.Probiotics (e.g., Lactobacillus/Bifidobacterium blends): per label.
Function: Gut-lung axis support; may reduce infection risk.
Mechanism: Modulates mucosal immunity.Vitamin C: 250–500 mg/day.
Function: Antioxidant; supports epithelial repair.
Mechanism: Scavenges reactive oxygen species.Zinc: 10–20 mg/day (short courses).
Function: Immune enzyme cofactor.
Mechanism: Supports innate and adaptive immunity.Selenium: 50–100 mcg/day.
Function: Antioxidant enzymes (glutathione peroxidase).
Mechanism: Reduces oxidative stress in inflamed airways.Quercetin: 250–500 mg/day.
Function: Flavonoid with mast-cell stabilizing potential.
Mechanism: Inhibits histamine release and inflammatory signaling (preclinical/limited clinical data).Curcumin (with piperine for absorption): 500–1000 mg/day.
Function: Anti-inflammatory adjunct.
Mechanism: Down-regulates NF-κB pathways (limited respiratory data; adjunctive only).
Immunity-modulating / regenerative” drug options
There are no approved stem-cell drugs or “hard immunity boosters” for ABPA. What we do have are targeted immune biologics used by specialists in selected patients to cut steroid use and flares:
Omalizumab (anti-IgE) — see details above.
Dose: Weight/IgE-based every 2–4 weeks.
Function: Steroid-sparing; reduces exacerbations.
Mechanism: Binds free IgE, blunting allergic cascade. PubMed+1Mepolizumab (anti-IL-5)
Dose: 100 mg SC every 4 weeks.
Function: Cuts eosinophilic inflammation; fewer flares.
Mechanism: Neutralizes IL-5 to lower eosinophils. PubMedBenralizumab (anti-IL-5R)
Dose: 30 mg SC q4wk ×3, then q8wk.
Function: Deep eosinophil depletion; symptom relief.
Mechanism: ADCC against eosinophils. PubMedReslizumab (anti-IL-5, IV)
Dose: 3 mg/kg IV q4wk.
Function: Alternative IL-5 blockade when SC agents unsuitable.
Mechanism: Neutralizes IL-5 (evidence in ABPA smaller). AAAAIDupilumab (anti-IL-4Rα)
Dose: 600 mg load, then 300 mg SC q2wk.
Function: Useful after failure of other biologics in some ABPA cases.
Mechanism: Blocks IL-4/IL-13 signaling. PMCTezepelumab (anti-TSLP)
Dose: 210 mg SC q4wk.
Function: Broad upstream control of type-2 inflammation (off-label in ABPA).
Mechanism: Inhibits epithelial alarmin TSLP; evidence emerging. AAAAI
Specialists choose among these based on your asthma/CF phenotype, eosinophils, IgE, prior responses, cost, and safety.
Procedures / surgeries
Bronchoscopy with airway toilet
What: A camera is passed into the lungs to suction thick mucus plugs during severe obstruction.
Why: Rapidly relieve blockage when clearance fails and oxygen is low.Bronchial artery embolization
What: Interventional radiology blocks bleeding bronchial arteries.
Why: Control life-threatening hemoptysis from damaged airways.Lobectomy (surgical removal of a severely destroyed lobe)
What: Thoracic surgery removes a localized, non-functioning, infection-prone lobe.
Why: Reduce repeated infections and bleeding in end-stage, localized bronchiectasis (rare, last resort).Functional endoscopic sinus surgery (FESS)
What: ENT opens blocked sinus pathways.
Why: In patients with coexisting allergic fungal rhinosinusitis causing constant lower-airway triggers.Lung transplantation
What: Replaces end-stage lungs.
Why: Extremely rare in ABPA alone; considered in end-stage CF with multiple complications despite maximal therapy.
Prevention strategies
Keep humidity 40–50%; fix leaks quickly.
Use HEPA filtration in key rooms.
Avoid high-mold exposures (compost, damp barns, flood cleanup).
Adhere to controller inhalers and antifungals as prescribed.
Follow a written action plan; step up promptly at first signs.
Vaccinate (influenza yearly; pneumococcal as advised).
Do airway clearance every day; more often during colds.
Check drug interactions (especially azoles) before adding new meds/supplements.
Monitor total IgE and symptoms with your team; rising IgE can signal relapse.
Maintain fitness, sleep, and nutrition to support immune balance.
When to see a doctor
You cough up blood, have blue lips/fingertips, or oxygen levels fall.
Wheeze or breathlessness does not improve after quick-relief inhaler.
You cough out brown plugs or have fever and chest pain.
Your peak flow drops >20% from personal best for more than a few hours.
You start new medicines and feel severe side effects (jaundice, severe rash, vision change, palpitations, high sugar on steroids).
Your total IgE shoots up or symptoms return after a quiet period. PMC
What to eat and what to avoid
What to eat:
A whole-food pattern: vegetables, fruits, legumes, whole grains, lean proteins (fish, poultry, soy), and omega-3 sources (fatty fish, flax, walnuts) to support anti-inflammatory balance.
Adequate protein to protect muscles during steroid courses.
Calcium + vitamin D foods (dairy, fortified plant milks, small bony fish, leafy greens) to protect bones.
Plenty of fluids unless you must restrict them. Hydration helps mucus clearance.
What to limit/avoid:
Grapefruit and Seville orange when on triazole antifungals (itraconazole, voriconazole, posaconazole). They raise drug levels and side-effects risk.
Alcohol with azoles or steroids (adds liver stress, worsens glucose).
Very salty foods during steroid courses (fluid retention, blood pressure).
Foods visibly moldy or spoiled; and if you notice personal symptom triggers with fermented/mold-ripened foods (e.g., certain cheeses), limit them.
Frequently Asked Questions (FAQs)
1) Is ABPA an infection or an allergy?
It is mainly an allergic reaction to a fungus, not an invasive lung infection. We treat the inflammation and also reduce the airway fungus burden. PMC
2) Can I be “cured”?
Many people achieve long quiet periods. Because you keep being exposed to spores, relapses can happen. The goal is control, protection of lung function, and quick treatment of flares. PMC
3) Why are steroids used first?
They work fast to shut down the allergic surge and protect your airways. We taper to the lowest effective dose to limit side effects. PMC
4) Do antifungals replace steroids?
In some patients, itraconazole or other azoles can control the acute stage or reduce steroid needs, but steroids remain the classic first-line for strong flares. Trials show prednisolone is more effective than itraconazole alone for initial response, though itraconazole helps and can be an alternative when steroids are risky. PubMed
5) Is combination therapy better?
Adding itraconazole to prednisolone may reduce 1-year exacerbations versus steroid alone, but results vary and risks/interactions increase; your doctor will individualize. ERS Publications+1
6) What does total IgE mean?
It is a blood marker of allergic activity. A high IgE (often ≥500 IU/mL with modern assays) supports ABPA diagnosis; a big drop with treatment suggests response; later rises can signal relapse. PMC
7) Are biologics (like omalizumab) proven?
Growing evidence (systematic reviews and expert guidance) shows biologics can cut exacerbations and steroid use in selected patients, but they are add-ons, not replacements for core therapy. PubMed+2JACI In Practice+2
8) If I have cystic fibrosis, is ABPA care different?
Principles are similar, but CF care is specialized. CF guidelines emphasize preventing decline in lung function, strong airway clearance, and careful use of steroids/antifungals within CF programs. Cystic Fibrosis Foundation+1
9) Will I need surgery?
Rarely. Surgery is for complications like massive bleeding or a destroyed, infected lobe that does not respond to other care.
10) Do I need to avoid all fungi in foods?
Not routinely. Focus on avoiding visible mold and any foods you notice personally trigger symptoms. Main prevention is environmental control at home.
11) Can ABPA cause permanent damage?
Yes, repeated flares can cause bronchiectasis. That is why early diagnosis, airway clearance, and steady control are vital. PMC
12) How often should I be followed?
During a flare, visits and labs may be frequent (e.g., monthly). In stable periods, your team may space visits but will still track symptoms, IgE, and sometimes imaging.
13) Are there drug interactions I should know about?
Triazole antifungals interact with many medicines (and grapefruit). Bring a full medication list to every visit. Liver tests and drug-level checks may be done. PMC
14) Can I exercise?
Yes—gradually and with your inhalers as prescribed. Exercise helps mucus clearance, endurance, and mood. Pause during acute flares if your team advises.
15) What is the long-term outlook?
With a personalized plan, good adherence, environmental control, and early treatment of flares, many people live active lives and protect their lungs for the long term. PMC
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: September 12, 2025.
