Inhaled corticosteroids (ICS)
ATC code: R03BA02 (Budesonide)
Brand names
Pulmicort, Rhinocort, Pulmicort Flexhaler
A glucocorticoid with high topical anti-inflammatory activity and low systemic bioavailability. Suppresses pro-inflammatory gene transcription via genomic and non-genomic mechanisms. Reduces the number and activity of mast cells, eosinophils, and lymphocytes in airway mucosa. In inhaled form, effect begins within hours and peaks after 1-2 weeks of regular use. Addresses the underlying airway inflammation in asthma, unlike bronchodilators, which only relieve bronchospasm.
First line
First-line controller for asthma in adults and children per 2024. At GINA steps 1–2 in adults, GINA recommends as-needed low-dose budesonide/formoterol (anti-inflammatory reliever). At step 3, regular low- or medium-dose ICS combined with LABA (formoterol, salmeterol). ICS reduce asthma mortality per large meta-analyses. Starting dose 200 mcg twice daily.
Individual decision
Per 2024, ICS in COPD is not for everyone. Triple therapy (ICS + LABA + LAMA) is indicated with frequent exacerbations or eosinophilia. In patients without these criteria, ICS confer no benefit and increase pneumonia risk — dual bronchodilation (LABA + LAMA) is preferred.
ICS in COPD only with frequent exacerbations (≥ 2/year or 1 with hospitalization) or blood eosinophils ≥ 300/μL.
The drug is promoted for these uses outside international guidelines. Each entry below is analyzed against AEMPS, FDA, EMA, Cochrane and major RCTs.
Not recommended
Inhaled corticosteroids are not a rescue medication for acute bronchospasm. The effect develops over hours to days, not minutes. During an attack, short-acting beta-2 agonists (salbutamol) are used and systemic corticosteroids added if needed. Nebulised budesonide in severe paediatric exacerbations can be considered as an adjunct but not a replacement for systemic corticosteroids.
Not recommended
Inhaled budesonide for viral URI in patients without underlying asthma or COPD is not supported by international guidelines. , CDC, BMJ Best Practice, and do not include ICS in cold treatment standards. Self-prescribing Pulmicort «for cough» in adults and children is common in Russia and the CIS and frequently delays correct diagnosis and adds unjustified glucocorticoid exposure.
Not recommended
In 2020-2021, after the STOIC and PRINCIPLE trials, inhaled budesonide received attention as an outpatient COVID-19 treatment. Subsequent meta-analyses and , NIH, guidelines did not include it as standard therapy. Effects on recovery time were modest, effects on serious outcomes were not significant. Routine use of budesonide for COVID-19 is currently not recommended.
19 pairs found. Sorted from critical to minor.
Mechanism
Clarithromycin blocks CYP3A4 – the main hepatic metabolic route for budesonide. Systemic budesonide exposure (oral or inhaled) rises 4- to 8-fold. Cushing's syndrome and adrenal insufficiency have been reported.
Symptoms
Moon face, central obesity, abdominal striae, hypertension, hyperglycaemia (Cushing's syndrome). With prolonged combination and abrupt withdrawal: risk of adrenal insufficiency with hypotension and weakness.
Management
For short clarithromycin courses (5–7 days), halve budesonide temporarily. For prolonged therapy, switch antibiotics (azithromycin, doxycycline) or replace budesonide with fluticasone/mometasone (less CYP3A4-dependent).
Mechanism
Ketoconazole strongly blocks CYP3A4 – the main budesonide metabolic route. Systemic budesonide exposure (oral or inhaled) rises 6- to 12-fold. High Cushing's syndrome risk with prolonged combination.
Symptoms
Moon face, central obesity, abdominal striae, hypertension, hyperglycaemia. With prolonged combination and abrupt withdrawal: adrenal insufficiency risk.
Management
The combination is not prescribed. Alternative antifungals: terbinafine for dermatophytosis or echinocandins for systemic mycoses. Alternative inhaled corticosteroid: fluticasone/mometasone (less CYP3A4-dependent).
Sources
Mechanism
Ritonavir is the most potent CYP3A4 inhibitor available. Systemic budesonide exposure (inhaled or oral) rises 8- to 10-fold. High risk of iatrogenic Cushing's syndrome, especially during long-term inhaled therapy for asthma or COPD.
Symptoms
Moon face, central obesity, abdominal striae, hypertension, hyperglycaemia. With prolonged combination and abrupt withdrawal: adrenal insufficiency risk.
Management
Avoid the combination. Alternative inhaled corticosteroid: beclomethasone (less CYP3A4-dependent) or short-acting β2-agonists with inhaled anticholinergics. If replacement is impossible: minimum effective budesonide dose with glucose and blood pressure monitoring.
Mechanism
Additive ulcerogenic effect with oral budesonide (used in inflammatory bowel disease). Inhaled forms have minimal systemic effect.
Symptoms
Epigastric pain, nausea, heartburn. With prolonged therapy: peptic ulcer and GI bleeding risk (black stools, vomiting blood or coffee-ground material). Older patients and prior peptic ulcer disease: higher risk.
Management
Inhaled budesonide for asthma or COPD requires no special measures. For oral therapy (Crohn's disease, ulcerative colitis): PPI cover with pantoprazole, cardioprotective aspirin no more than 100 mg/day.
Mechanism
Amiodarone inhibits CYP3A4 — the enzyme responsible for budesonide metabolism. Oral budesonide levels may rise, increasing iatrogenic hypercortisolism risk in long-term therapy. Inhaled budesonide is minimally absorbed — the effect is weaker.
Symptoms
On long-term therapy: moon face, weight gain with fat redistribution, skin thinning, acne, muscle weakness, mood disturbance, hyperglycaemia.
Management
For inhaled budesonide (Symbicort, Pulmicort) plus amiodarone, no adjustment needed. On oral budesonide (Cortiment, Entocort) over 8 weeks, assess for hypercortisolism and consider dose reduction or switching to mesalazine (in Crohn's disease). Amiodarone alternative in atrial fibrillation: dronedarone (no CYP3A4 effect).
Mechanism
Systemic (oral) budesonide causes sodium retention and weakens the antihypertensive effect of the beta-blocker. With inhaled use, systemic effect is minimal, so no clinical impact.
Symptoms
Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.
Management
Inhaled budesonide for asthma or COPD does not require bisoprolol adjustment. For oral therapy in inflammatory bowel disease, check blood pressure every 2–4 weeks.
Mechanism
Systemic budesonide retains sodium and water via mineralocorticoid effect (weaker than prednisolone), antagonising the ACE inhibitor's antihypertensive effect. Inhaled budesonide does not clinically affect BP.
Symptoms
On long-term therapy: return or rise of blood pressure, leg oedema. Hyperkalaemia possible with reduced renal function.
Management
For short systemic budesonide courses (3–7 days), no specific adjustment needed. For long-term therapy, check BP weekly in the first month. If BP rises, intensify antihypertensives or switch to an oral corticosteroid with less mineralocorticoid activity (methylprednisolone). Inhaled budesonide with captopril is unproblematic.
Mechanism
Systemic budesonide retains sodium and water, blunting the beta-blocker's antihypertensive effect. Inhaled budesonide does not clinically affect BP.
Symptoms
On long-term systemic therapy: return or rise of blood pressure, leg oedema.
Management
For short systemic budesonide courses, no specific adjustment needed. For long-term therapy, check BP weekly in the first month. If BP rises, increase carvedilol or add an ACE inhibitor. Inhaled budesonide with carvedilol is unproblematic.
Mechanism
Glucocorticoid plus NSAID — additive GI ulcer risk with systemic budesonide. Celecoxib (selective COX-2 inhibitor) gives lower gastric risk than non-selective NSAIDs, but the effect persists.
Symptoms
Epigastric pain, heartburn, black or tarry stools, blood in vomit, bruising. Higher risk in older patients, prior peptic ulcer, and concurrent anticoagulants.
Management
On systemic budesonide and celecoxib, in older patients, prior peptic ulcer, or long-term therapy: pantoprazole 20 mg/day. Alternatives in osteoarthritis: topical NSAIDs, paracetamol up to 2 g/day. Inhaled budesonide with celecoxib is safe.
Mechanism
Fluoroquinolone plus systemic glucocorticoid — tendinitis and tendon rupture risk (mainly Achilles tendon). The effect is amplified at age over 60, chronic kidney disease, and organ transplantation. Inhaled budesonide does not clinically affect risk.
Symptoms
Pain in the Achilles or other tendons, swelling, impaired function. Symptoms appear in the first weeks after starting ciprofloxacin and may persist for months after stopping.
Management
On systemic budesonide, choose a non-fluoroquinolone antibiotic: cephalosporin, amoxicillin-clavulanate, doxycycline. If a fluoroquinolone is unavoidable, advise the patient to limit physical activity during and for a month after the course. If tendon pain appears, stop ciprofloxacin. Inhaled budesonide with ciprofloxacin is safe.
Mechanism
Systemic budesonide retains sodium and water via mineralocorticoid effect, blunting clonidine's antihypertensive effect. Inhaled budesonide does not clinically affect BP.
Symptoms
On long-term systemic therapy: return or rise of blood pressure, leg oedema.
Management
For short systemic budesonide courses, no specific adjustment needed. For long-term therapy, check BP weekly in the first month. If BP rises, increase clonidine or add a diuretic. Inhaled budesonide with clonidine is unproblematic.
Mechanism
Glucocorticoid plus NSAID — additive GI ulcer and bleeding risk with systemic budesonide. Inhaled budesonide does not clinically affect risk.
Symptoms
Epigastric pain, heartburn, black or tarry stools, blood in vomit, bruising. Higher risk in older patients, prior peptic ulcer, and concurrent anticoagulants.
Management
On systemic budesonide, limit diclofenac to short courses (no more than 5–7 days) with pantoprazole 20 mg/day. For long-term analgesia: paracetamol up to 2 g/day or topical NSAIDs. Inhaled budesonide with diclofenac is safe. In older patients and prior peptic ulcer, risk outweighs benefit.
Mechanism
Oestradiol raises corticosteroid-binding globulin, increasing the bound budesonide fraction. The free fraction changes minimally. The interaction is clinically minor.
Symptoms
No specific clinical manifestations. On long-term systemic therapy, both drugs' side effects may appear.
Management
No dose adjustment needed. In women on menopausal hormone therapy and oral budesonide, check BP, weight, and lipid profile every 6 months. With systemic budesonide over 3 months, consider switching to inhaled glucocorticoids.
Mechanism
Oestrogens raise corticosteroid-binding globulin, increasing the bound budesonide fraction, but the effective free fraction changes minimally. The interaction is clinically minor.
Symptoms
No specific clinical manifestations. On systemic long-term therapy, both drugs' side effects may appear.
Management
No dose adjustment needed. In women on combined oral contraceptives and oral budesonide, check BP and weight every 3 months. With significant systemic budesonide side effects, consider switching to inhaled glucocorticoids or mesalazine.
Mechanism
Fluvoxamine is a CYP3A4 inhibitor; budesonide is a CYP3A4 substrate. Oral budesonide AUC may rise, increasing hypercortisolism risk in long-term therapy. Inhaled budesonide is minimally absorbed — the effect is weaker.
Symptoms
On long-term therapy: moon face, weight gain with fat redistribution, skin thinning, acne, muscle weakness, mood disturbance, hyperglycaemia.
Management
For inhaled budesonide and fluvoxamine, no adjustment needed. On oral budesonide over 8 weeks, assess for hypercortisolism and consider antidepressant alternatives — sertraline or escitalopram (minimal CYP3A4 effect).
Sources
Mechanism
Additive GI ulcer and bleeding risk with systemic budesonide. Inhaled budesonide does not clinically affect risk.
Symptoms
Epigastric pain, heartburn, black or tarry stools, blood in vomit, bruising. Higher risk in older patients, prior peptic ulcer, and concurrent anticoagulants.
Management
On systemic budesonide, limit ibuprofen to short courses (no more than 5–7 days) with pantoprazole 20 mg/day. For long-term analgesia: paracetamol up to 2 g/day. Inhaled budesonide with ibuprofen is safe. In older patients and prior peptic ulcer, risk outweighs benefit — consider paracetamol or topical NSAIDs.
Mechanism
Dual immunomodulation. Isotretinoin is teratogenic and affects liver function and skin barrier. Systemic budesonide suppresses immunity and raises infection risk. No direct pharmacokinetic interaction.
Symptoms
On long-term combination: increased infection susceptibility (bacterial sinusitis, pneumonia, candidiasis). Skin and mucosal dryness intensifies. Cases of intestinal mucosal ulceration on the combination have been reported.
Management
Systemic budesonide and isotretinoin are not co-prescribed without strong indication. In inflammatory bowel disease (Crohn's) with severe acne, options: treat acne topically and with adapalene, or start isotretinoin after inflammation remits and glucocorticoids are stopped. Inhaled budesonide with isotretinoin is safe.
Mechanism
Glucocorticoid plus NSAID — additive risk of GI ulcers and bleeding. Systemic budesonide (Cortiment, Entocort) raises risk; inhaled budesonide does not.
Symptoms
Epigastric pain, heartburn, black or tarry stools, blood in vomit, bruising. Higher risk in older patients, prior peptic ulcer, and concurrent anticoagulants.
Management
Ketorolac is not prescribed with systemic budesonide — risk outweighs benefit. For acute pain: paracetamol up to 3 g/day or metamizole. If NSAIDs are necessary (short course in cancer or postoperative pain), add pantoprazole 20 mg/day and cap ketorolac at 5 days. Inhaled budesonide with NSAIDs is safe.
Mechanism
No clinically significant direct interaction. With long-term oral budesonide, mild additive sodium retention may slightly reduce amlodipine's antihypertensive effect. Inhaled budesonide does not clinically affect BP.
Symptoms
The combination usually causes no specific symptoms. Each drug's individual side effects remain.
Management
For short systemic budesonide courses, no adjustment needed. For long-term therapy, check BP monthly. If BP rises, increase amlodipine or add a diuretic.
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FDA categories were retired in 2015. Inhaled budesonide has the largest pregnancy safety dataset among ICS. The Swedish Medical Birth Registry on thousands of pregnancies showed no increased malformation risk. ICS are not withdrawn in pregnant asthma patients — the risk of uncontrolled asthma exceeds the drug risk.
Compatible with breastfeeding. Systemic exposure after inhalation is low and milk concentrations are minimal.
Reference information, not a clinical decision. Discuss feeding pauses or changes with your physician or an IBCLC.
Budesonide is evaluated for the following indications with varying evidence strength: Asthma (evidence tier A), Chronic obstructive pulmonary disease (evidence tier B), Acute bronchospasm (evidence tier C). See the full indication matrix with dosing and citations above on this page.
Common side effects of Budesonide (≥ 1 in 100): Oral candidiasis (up to 5 % when mouth rinsing is omitted), Dysphonia, hoarseness, Throat irritation, Post-inhalation cough. See the Safety section for uncommon and serious reactions.
FDA category B. FDA categories were retired in 2015. Inhaled budesonide has the largest pregnancy safety dataset among ICS. The Swedish Medical Birth Registry on thousands of pregnancies showed no increased malformation risk. ICS are not withdrawn in pregnant asthma patients — the risk of uncontrolled asthma exceeds the drug risk.
Compatible with breastfeeding. Systemic exposure after inhalation is low and milk concentrations are minimal.
Budesonide is contraindicated in: Hypersensitivity; Active pulmonary tuberculosis; Systemic fungal infections; Age under 6 months (most formulations). Full list in the Safety section.
with inhalation delivery, systemic bioavailability of budesonide is less than 10%. Most of the drug deposits in the airways. Proven adverse effects are local (candidiasis, hoarseness); systemic effects at standard doses are clinically insignificant. Fear of ICS leads to refusal of maintenance therapy and SABA overuse, which genuinely increases the risk of severe exacerbation and asthma death.