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Editor: Shashikanth Ambati Updated: 8/28/2023 9:45:13 PM


Budesonide is a potent anti-inflammatory agent with a broad spectrum of clinically significant activity, and its FDA-approved indications are as below.

The nasal spray is available for allergic rhinitis and other upper respiratory allergies; one spray contains 32 mcg of budesonide: for adults and children 12 years of age and older, two sprays are administered into each nostril while sniffing gently once per day, and once allergy symptoms improve, the dose is decreased to one spray into each nostril once per day. Use in patients from 6 years to under 12 years of age is recommended only under the supervision of adults; instill one spray into each nostril daily. If symptoms do not improve, the dose can be increased to two sprays into each nostril daily. If symptoms do not improve after two weeks, consultation with a physician is required. If budesonide spray is necessary for more than two months in a year, then monitoring the growth of the children is needed.

Budesonide inhalation suspension solution is used for asthma treatment in pediatric patients of 1 to 8 years old.[1] The recommended starting and highest doses depend on the history of prior asthma therapy. If previously treated with either inhaled corticosteroids or bronchodilators, a total dose of 0.5 mg per day of budesonide is administered either as a single dose or in two divided doses. If the patient used oral corticosteroid therapy for asthma in the past, 1 mg total per day of budesonide is administered either as a single dose or in two divided doses. The maximum recommended dose of the budesonide is 1mg/day if prior asthma treatment included inhaled or oral corticosteroids and 0.5mg/day for children that previously received therapy with bronchodilators alone.

As budesonide acts synergistically with the long-acting sympathetic beta-2 agonist, a combination of budesonide and formoterol in aerosol form in the metered-dose inhaler is indicated for the maintenance treatment of asthma. Pediatric patients under 12 years of age are prescribed two inhalations of budesonide 80/formoterol 4.5 mcg two times daily. Patients 12 years old and older should use 2 inhalations of budesonide 80/formoterol 4.5 mcg twice daily; starting dosage depends on the severity of the condition. Two inhalations of budesonide 160/formoterol 4.5 mcg from a metered-dose inhaler are used in the maintenance treatment of airway obstruction and reducing exacerbations in patients with chronic bronchitis and/or emphysema (COPD-chronic obstructive pulmonary disease). Nebulized budesonide treatment facilitates the weaning from mechanical ventilation in patients with very severe COPD.[2]

Budesonide inhalation powder is useful to treat both pediatric and adult patients with asthma, and it is for oral inhalation only. For pediatric patients aged 6 to 17 years, the recommended starting dosage is 180 mcg two times per day. A starting dose of 360 mcg (maximum dose) two times a day may be appropriate for some pediatric patients. For adults (>18 years of age), the recommended starting dose is 360 mcg two times per day. For some adult patients, a starting dose of 180 mcg two times a day may be adequate. The maximum dose of 720 mcg two times per day should not be exceeded.

Treatment of mild to moderate Crohn disease: Budesonide is used to induce remission in the active phase of mild to moderate Crohn disease and maintenance of remission following the treatment of active Crohn disease.[3] To induce remission, adult patients are prescribed 9 mg of budesonide orally once daily for eight weeks. For recurring episodes of active disease, another eight weeks of 9 mg budesonide course can be repeated. Pediatric patients aged 8 to 17 years and weighing more than 25 kg can be prescribed 9 mg of budesonide, taken by mouth once a day for eight weeks, followed by 6 mg one time a day for two weeks. For the maintenance of clinical remission: the recommended dosage in adult patients, following an 8-week course(s) of budesonide treatment for active phase and once the patient's symptoms are controlled (Chrohn's Disease Activity Index [CDAI] less than 150), is budesonide 6 mg taken by mouth once a day for up to 3 months. If symptoms are still well controlled at three months, the clinician should attempt to taper to complete cessation. Continued treatment with budesonide 6 mg for more than three months has not demonstrated any substantial clinical benefits. 

Budesonide is used for ulcerative colitis as a second-line therapeutic agent and promotes the mucosal healing of the distal lesions.[4] Budesonide rectal foam formulation is for rectal administration only, and it contains 2 mg of budesonide per one metered dose. Budesonide's indications include the induction of remission in patients suffering from active mild to moderate distal ulcerative colitis affecting the rectum and sigmoid colon, precisely not extending beyond 40 cm from the anal verge. The recommended dosage of budesonide is one metered dose rectally administered twice a day for 14 days, followed by one metered dose rectally administered once a day for 28 days. Rectal foam is inflammable, and therefore, the patient must avoid flame, fire, and smoking during and immediately after administration. The newer budesonide capsule designed to release the drug throughout the entire colon is also useful to induce remission in active mild to moderate ulcerative colitis refractory to oral mesalamine.[5] Budesonide suppositories are indicated for the treatment of acute ulcerative proctitis.[6]

Non-FDA Approved Uses

Acute Sinusitis

Chronic rhinosinusitis (CRS) with or without polyposis: Off-label high-volume sinonasal budesonide irrigations are commonly used to manage chronic rhinosinusitis and will not cause hypothalamic pituitary adrenal axis suppression despite extended use for more than two years.[7] In patients with chronic rhinosinusitis with nasal polyps after endoscopic surgery, nasal budesonide is an important aspect of the therapy. It is beneficial in relieving mucosal inflammation, shortening the stage of epithelization, and accelerating the recovery of the mucosa.[8]

Oral viscous budesonide is useful in treating eosinophilic esophagitis, and it improves not only symptomatic parameters but also reverses endoscopic and histological changes.[9]

  • Lymphocytic esophagitis
  • Refractory celiac disease(RCD)[10] 
  • Microscopic colitis (collagenous colitis, eosinophilic colitis)
  • Autoimmune hepatitis without cirrhosis
  • Primary biliary cholangitis[11] 


2 mg of nebulized budesonide is effective for mild to moderate croup.[12][13] If patients on oral dexamethasone concomitantly receive nebulized budesonide, added benefits are obtainable.[14] Budesonide treatment also decreases the rate of hospitalization.[15]

In the early stages of sarcoidosis, inhaled budesonide may be an effective and safe alternative to oral corticosteroids for maintenance treatment.[16]

In very low birth weight infants, intratracheal administration of budesonide-surfactant combination results in reduced incidence of bronchopulmonary dysplasia (BPD) or composite outcome of BPD or death.[17] Besides, early initiation of treatment with 1 mg of budesonide inhalation suspension appears to reduce overall corticosteroid usage and the need for mechanical ventilation in premature, very low birth weight babies at risk for chronic pulmonary disease.[18]

Mechanism of Action

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Mechanism of Action

Budesonide is a potent topical anti-inflammatory agent.[19] It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP (HAT). This budesonide-CBP (HAT) receptor complex prevents the production of inflammatory genes (inhibition of gene transcription) that might cause bronchoconstriction. Also, the budesonide-receptor complex activates the HDCA2 increasing the gene expression, which reduces the formation of cytokines such as ILs and TNF.

It also inhibits the activation of the eosinophils by increasing apoptosis and suppresses the activation of the inflammatory cells such as mast cells, neutrophils, T-lymphocytes, macrophages, and dendritic cells. The overall inhibition of ILs and TNF leads to reduced airway inflammation and hyperreactivity, causing inhibition of the bronchospasm, wheezing, and coughing. 


Budesonide exerts a powerful topical anti-inflammatory effect on the respiratory and gastrointestinal systems. Budesonide administration can be via different routes such as oral, rectal, nasal, and inhalation. Each of these routes has gotten specific purposes, advantages, and disadvantages. The various budesonide formulations available in the market, depending on the indicated use, are administered as follows: the dosing of extended (delayed) release tablets and capsules is by mouth, suspension solution and powder are used for oral inhalation, over the counter spray for nasal application, and foam, enema, and suppositories for rectal administration. Patients should not chew, crush, or open the extended-release formulations. The inhaled formulation is available as a standalone inhaler or often combined with a long-acting beta-2 adrenergic agent.

Adverse Effects

Budesonide can cause the following adverse reactions.[20]

Paradoxical bronchospasm. If asthma symptoms worsen immediately after using the inhalation formulation of budesonide, discontinuation of budesonide is indicated. When paradoxical bronchospasm occurs, acute symptoms should receive treatment with a rescue short-acting beta-2 agonist inhaler.

Localized infections of the oral cavity and pharynx: Patients on inhalation formula are prone to develop a localized infection of the oral cavity and pharynx with candida (fungus). Patients are counseled to rinse the mouth with water and spit it out immediately after oral inhalation to prevent systemic absorption that can lead to these infections. The use of the spacer also decreases the rate of occurrence of thrush. When oral thrush (oral candidiasis) develops, treatment with an antifungal agent is required while treatment with a budesonide inhaler continues, or sometimes, therapy must be temporarily interrupted. Patients on budesonide inhalation treatment require monitoring for symptoms and signs of oropharyngeal fungal infections.

Glucocorticoids, including budesonide, are immunosuppressant drugs. Patients who are immunocompromised are at a higher risk of developing infections than healthy individuals. Candida albicans, an opportunistic fungus, can overgrow in the genitalia of females with immunosuppression leading to vulvovaginal candidiasis; this is not a sexually transmitted disease. Infections like chickenpox and measles can run to a more serious and even fatal course in persons with suppressed immunity. If patients suffer exposure to chickenpox or measles infection, preventative treatment is indicated as appropriate, and if chickenpox occurs, treatment with antiviral medications may merit consideration. The long term inhalation budesonide users are at high risk for acquiring tuberculosis infection.[21] Budesonide treatment is prescribed with high precaution, only if necessary, to patients with latent tuberculosis, ocular herpes simplex, active bacterial, viral, fungal, and parasitic infections with effective and appropriate antimicrobial or antifungal treatment.

All types of budesonide formulations can give rise to hypersensitivity reactions. During budesonide treatment, if patients develop allergic reactions such as anaphylaxis, angioedema, bronchospasm (cough, wheezing, shortness of breath), rash, urticaria, contact dermatitis, delayed typed sensitization, etc., then treatment should be discontinued.[22][23] Anaphylaxis is a life-threatening reaction and requires immediate treatment with an intramuscular injection of epinephrine in the thigh. 

Other common adverse reactions from budesonide are nasopharyngitis, nasal congestion, pharyngitis, rhinitis allergic, viral upper respiratory tract infection, nausea, viral gastroenteritis, otitis media, conjunctivitis., toothache, oropharyngeal pain, cough, dysphonia, backpain, procedural pain, throat irritation, back pain, and headache.[24]

Budesonide is a potent topical anti-inflammatory glucocorticoid that controls the symptoms of diseases with less dysfunction of the hypothalamic-pituitary-adrenal axis than therapeutically equivalent doses of oral prednisone. Budesonide gets absorbed into the systemic circulation and can become active at higher doses. Therefore, the beneficial effects of budesonide in minimizing the suppression of the HPA axis may be preserved only when prescribed doses are within the recommended dose range and each patient is titrated for the minimum effective dose. At high systemic levels, the budesonide can cause negative feedback effects on the brain and suppresses the secretion of corticotropin-releasing hormone (ACTH-RH) from the hypothalamus.

ACTH-RH acts as the secretory signal for the pituitary gland. In the absence of ACTH-RH, the anterior pituitary will not release ACTH, and ultimately, ACTH-dependent adrenal cortical function also becomes inhibited, leading to central adrenal insufficiency (AI). The suppression of the HPA axis is more likely to occur in patients who have received budesonide for prolonged periods and/or in higher doses. HPA axis suppression can occur even at normal doses in sensitive individuals. Moreover, patients with cushingoid features are more likely to have a suppressed HPA axis. Complete recovery of HPA axis normal function occurs in a few months and, in some cases, may take up to one year or more after discontinuation of the steroid therapy. Patients with adrenal insufficiency present with a wide variety of symptoms, including nausea, vomiting, loss of appetite, weakness, and fatigue. The diagnosis of central adrenal insufficiency starts with measuring morning plasma cortisol (low level) and ACTH (low level). The aldosterone level will be normal, along with only mild hyponatremia. 

The physician needs to exercise care while transferring the patient from systemically active corticosteroids to inhaled budesonide. The suppression of the HPA axis is more likely to happen in the patients who have received corticosteroids for more than three weeks or 20mg/day of prednisone or more or therapeutically equivalent doses of other steroids. HPA axis suppression can occur even at normal doses in sensitive individuals. Adrenal insufficiency can cause patient death during and after the transition from systemic glucocorticoids to inhalation formulation of budesonide. Therefore, patients on oral glucocorticoids must slowly taper from the systemic glucocorticoids use after transitioning to the inhalational budesonide formulations. There is a proposed protocol for discontinuing long-term glucocorticoid treatment. For prednisone reduction, there can be a dose reduction of 2.5 mg weekly. Patients need monitoring for asthma symptoms (cough, wheezing, and shortness of breath), rescue inhaler (beta-2 agonists bronchodilator) use, and pulmonary function test (FEV1 forced expiratory volume in one second).  

During this glucocorticoid withdrawal, patients need monitoring for manifestations of adrenal insufficiency such as nausea, vomiting, loss of appetite, weakness, fatigue, unstable vitals such as hypotension. During the period of HPA axis suppression, exposure of the patients to stress such as infections, particularly gastroenteritis, surgery, trauma, or other conditions where electrolyte imbalance coexists can precipitate the adrenal crisis, which is the worst form of adrenal insufficiency. This life-threatening condition manifests as pyrexia, nausea, emesis, abdominal pain, altered sensorium, and cardiovascular collapse. Immediate treatment with hydrocortisone and fluids is lifesaving.

During this episode, recommended doses of inhalation formulation of budesonide can control asthma but cannot provide normal physiological systemic glucocorticoid levels and lack enough mineralocorticoid activity that is essential to deal with this emergency. Patients who have withdrawn from systemic steroid therapy should also carry a medical identification card to indicate that these patients may need replacement of the systemic corticosteroids during stressful medical situations, including severe asthma attacks. In some cases, patients experience withdrawal symptoms, despite the stable or improved function of the respiratory system. Switching the treatment from systemic glucocorticoids to inhalation formulation of budesonide may unmask or flare up the medical conditions suppressed by systemic glucocorticoid treatment such as eosinophilic conditions such as eczema, allergic rhinitis, conjunctivitis, etc.

Patients with mild to moderately active Crohn disease affecting the ileum and/or ascending colon have been transitioned from oral prednisolone to oral budesonide without reported episodes of adrenal insufficiency. Tapering should start concomitantly while initiating oral budesonide treatment since prednisolone cannot be discontinued suddenly.

Budesonide, like other glucocorticoids, if administered in high doses for a prolonged duration, causes hypercortisolism. Patients develop characteristic features of Cushing syndrome, such as fat deposition at specific sites such as round(moon) and plethoric face, buffalo hump, truncal obesity, mesenteric fat bed. Other clinical findings may include fatigue, muscular weakness (myopathy, may involve respiratory muscles), hypertension, cutaneous striae, easy bruising, osteoporosis due to increased catabolism of the bones. Females may have acne vulgaris, hirsutism, and menstrual irregularities such as oligomenorrhea and even amenorrhea from adrenal androgen excess. Insomnia and emotional changes range from mood lability or irritation to confusion, major depression, confusion, and even overt psychosis can happen. Besides, delayed wound healing, renal stones, glaucoma, cataract, polyuria from hyperglycemia can occur.

Metabolic abnormalities, such as abnormal glucose intolerance and hypokalemia, are common. A white blood count will be high, although impaired neutrophil migration leads to increased susceptibility to infections. Initial testing to confirm hypercortisolism can include a measurement of free cortisol in a 24-hour urine sample, a late-night cortisol level in saliva, or a suppression test by a low dose of dexamethasone. After establishing the presence of hypercortisolism, the level of ACTH will decide whether it is ACTH dependent or ACTH-independent (exogenous glucocorticoid administration). Patients who have high levels of ACTH will receive a high-dose dexamethasone suppression test to determine whether the source of ACTH is pituitary or ectopic.

The patients on any formulations of budesonide need careful monitoring for signs and symptoms of hypercortisolism and adrenal suppression. If hypercortisolism or adrenal suppression occurs, the dose of the budesonide is reduced slowly, strictly following the protocol for decreasing systemic glucocorticoids and asthma symptoms management.

The main route of budesonide metabolism is via hepatocytic cytochrome P450 isoenzyme 3A4 (CYP3A4). Therefore, any drug that changes the activity of CYP3A4 can increase or decrease the budesonide level in the body. If budesonide and ketoconazole, a potent CYP3A4 inhibitor, is coadministered by mouth, the mean plasma concentration of the budesonide increases because of the inhibition of its metabolism. Grapefruit is also a potent inhibitor of CYP3A4, and its consumption is not recommended while on budesonide treatment. This increased budesonide level predisposes to systemic toxicity such as hypercortisolism and Cushing syndrome. When considering the concomitant administration of budesonide and other CYP3A4 inhibitors, for example, macrolide compounds such as erythromycin, clarithromycin, and telithromycin, azole group of medicines itraconazole, antiretroviral medicines ritonavir, atazanavir, indinavir, nelfinavir, saquinavir, the antidepressant nefazodone, caution is necessary. There is an enteric-coated budesonide ER tablet on the market. Since the dissolution of its coating is dependent on pH, the release properties and uptake of the budesonide may require alteration when administering this dosage form after treatment with antacids, H2 blockers, and proton pump inhibitors (gastric acid-reducing agents).

Osteoporosis is a serious and frequent complication of budesonide therapy. It affects patients of all ages and both genders and depends on the amount of dose and duration of treatment. Approximately 30% to 50% of all patients who receive chronic budesonide treatment ultimately will suffer from osteoporotic fractures. Budesonide preferentially affects the cortical rim of the vertebral body and trabecular bone; the most frequent sites of fracture are the ribs and vertebrae. Multiple mechanisms by which budesonide reduces bone density include diminished calcium absorption from the gastrointestinal tract, inhibition of gonadal steroid hormones, and suppression of bone formation due to inhibitory effects on osteoblasts and stimulation of osteoclastic resorption via changes in RANK ligand and osteoprotegerin production. Moreover, budesonide's negative influence on calcium uptake from the intestines may lead to secondary hyperparathyroidism, further accelerating bone resorption.

The initiation of budesonide therapy at doses equivalent to prednisone 5 mg/day or more for three months or longer is an indication for patient monitoring by bone densitometry that detects trabecular bony abnormalities. Because bone loss from budesonide therapy predominantly occurs within the first six months of the administration, initiation of hip and lumbar spine densitometric assessment along with prophylactic measures are recommended. Most authorities suggest maintaining a high intake of calcium, a total of 1500 mg/day by diet plus supplementation and 800 IU/day of vitamin D intake, and assuming that these measures do not cause an abnormal elevation in urinary calcium excretion. Bisphosphonates such as zoledronic acid and risedronate are important advancements in the preventive treatment of budesonide induce osteoporosis. These medications have proven the benefits of reducing the rate of bone resorption and osteoporotic fracture.

Osteonecrosis is also known as aseptic or avascular necrosis. It is a complication of budesonide therapy. The head of the femur is affected most often, but this process can affect other bones, such as the head of the humerus and distal femur. The earliest manifestations of the condition are joint pain and stiffness. If the patient on budesonide therapy presents with acute onset pain of the hip, shoulder, or knee joint, the clinician should consider this diagnosis. Although the risk of osteonecrosis depends on the dose and duration of budesonide treatment, it can occur when using high doses of budesonide for short periods. Generally, osteoporosis is progressive, and most patients finally require joint replacement. When the X-ray of the affected joint is normal in the early stage of the necrosis, MRI can confirm the clinical diagnosis.

Controlled drug trials have shown that budesonide, including orally inhaled formulation, can reduce the linear growth velocity in pediatric patients.[25] This effect depends on the dose of budesonide and the duration of the treatment. On average, there is a 1 cm decrease in growth rate per year. This effect can be found even in the absence of HPA axis dysfunction. Therefore, it seems that growth velocity is a more sensitive indicator of the systemic toxicity of budesonide. There are no detailed studies regarding the impact on the final height and catch-up growth after discontinuation of the therapy. To minimize the growth retardation, each patient’s dose requires titration to the minimum effective dose. The patient’s linear growth is monitored periodically by the stadiometer.

A cataract is a well-established complication of budesonide treatment and is related to the dose and duration of the treatment. Pediatric patients are at high risk. Complete cessation of therapy may not reverse the changes in the lenses. Cataracts can even progress sometimes despite the reduction in the dose or cessation of treatment. The patients should undergo a periodic slit-lamp examination to detect budesonide-induced posterior subscapular cataract lesions. The patient also requires close monitoring for the signs and symptoms of glaucoma.

Rarely, patients on inhalation formulation of budesonide present to the clinic with eosinophilic conditions. Some of them have clinical manifestations of Churg-Strauss disease, a type of vasculitis. Clinicians should look for warning signs of eosinophilia, vasculitis rash, neuropathy, aggravation of respiratory symptoms, and/or cardiac complications to diagnose early and initiate systemic steroid treatment. These events usually, but not always, follow during and after transitioning the patients from systemic steroid therapy to inhalation formulation of the budesonide, and there is no evidence to prove a causal relationship.

Peptic Ulcers: The glucocorticoid increases the risk for the development of gastritis and peptic ulcer. Because of the insidious onset hemorrhage and perforation of ulcers, they are therapeutic challenges, especially during the post-operative period in joint replacement surgeries where patients require therapy with anticoagulants. High vigilance for ulcer formation in patients receiving budesonide is necessary when administered with NSAIDs.

Budesonide administration can cause proximal myopathy of the limbs and is an indication to discontinue the treatment. It may affect the respiratory muscles and reduce respiratory function, which is a significant concern in patients with asthma and chronic obstructive pulmonary disease. Recovery is slow and incomplete in cases of steroid-induced myopathy.

Sometimes the reduction in budesonide dose or withdrawal can cause pseudotumor cerebri.


Budesonide is not a bronchodilator, and therefore, it is contraindicated for the rapid bronchospasm relief in status asthmaticus or other episodes of acute asthma where intensive therapeutic measures are required. Budesonide is for maintenance treatment and prophylactic therapy for patients with asthma. 

Budesonide is contraindicated in any patients with a history of hypersensitivity to budesonide or any of the ingredients of the budesonide formulation. The orally inhaled powder formulation of budesonide is contraindicated in patients with severe milk protein allergies. This formulation contains micronized lactose monohydrate, which contains traces of milk protein particles and may cause hypersensitivity reactions.[26] The allergenic cross-sensitivity of corticosteroid compounds does not have much documentation. However, due to their structural and functional similarities, potential cross-reactivity cannot be excluded with certainty.

Per Canadian labeling, additional contraindications are untreated bacterial, fungal, or viral respiratory infection, moderate-to-severe bronchiectasis, and active or quiescent pulmonary tuberculosis.


Patients on budesonide therapy must be monitored by symptoms and signs and PFTs (pulmonary function tests) to evaluate the effectiveness of treatment and titrate the dose. As the liver mainly metabolizes budesonide, impairment of hepatocyte function may cause accumulation of the budesonide in the blood. Therefore, patients with diseases of the liver need close monitoring.

Patients taking loop diuretics, thiazide, and thiazide-like diuretics while on budesonide may have an increased risk of developing hypokalemia beyond what is typical of using these medications. Patients require close monitoring and follow-up to detect other adverse events, as described in budesonide adverse reactions.


The potential for acute toxicity is rare, but overdosing of budesonide for a prolonged period may result in systemic toxicity such as hypercortisolism.

There are not well controlled and adequate clinical trials in pregnant females on budesonide to determine the teratogenic effects on the fetuses. It falls in Pregnancy Category C, and extended-release budesonide should only be used if potential benefits outweigh the harmful effects to the fetus. Both inhaled and intranasal budesonide formulations are rated Pregnancy Category B, which means the drug is safe for use in pregnancy.

No data from controlled clinical studies on the use of extended-release budesonide by lactating mothers or their infants at this point, but the potential for serious adverse events in breastfeeding infants is still a consideration. Licensed practitioners and mothers should make a wise decision on whether to discontinue breastfeeding or budesonide ER.

The selection of extended-release budesonide treatment requires extreme caution in the geriatric patient population due to reduced hepatic, kidney, or cardiac function, comorbidities, or other concomitant drug therapy.

Patients with moderate to severe hepatic disorders require monitoring for manifestations of hypercorticism. Clinical research trials revealed that systemic availability increased 2.5 folds among subjects with cirrhosis compared with healthy subjects, whereas researchers noted no difference in absorption or clearance in either group.

Enhancing Healthcare Team Outcomes

Budesonide is used for various conditions affecting patients of all ages. It is prescribed by interprofessional team members such as physicians of different specialties, physician assistants, and nurse practitioners. The licensed providers must monitor the patients closely for treatment efficacy and systemic toxicity. Besides, they should counsel the patients at each visit, particularly the importance of treatment compliance, and clinicians should emphasize not to stop treatment abruptly.

If the patient is using budesonide for asthma, the importance of a rescue inhaler requires explanation. Nurses are the health professionals who see the patients immediately before discharge from the emergency room and floors. Therefore, this presents an excellent opportunity for them to educate the patients and family about budesonide treatment. This counseling must include a strict dietary restriction for grapefruit and abstinence of alcohol, as well as avoiding smoking, flame, and fire during and after administration of rectal foam as it is flammable. As most patients on budesonide treatment are under outpatient management, pharmacists also play a crucial role in the patient treatment management prescribed by the providers.

The pharmacists can provide education regarding techniques using new and old inhalers as well as rectal foam administration. Pharmacists should check for symptoms that may reflect potential adverse drug reactions, a drug to drug interactions, or even worsening of the underlying condition due to poor compliance. As the nasal spray is available over the counter also, pharmacists should ensure the patients use it properly. If pharmacists have any concerns, they should immediately communicate with the physicians. The collaboration and cooperation among the interprofessional team members improve the patient’s adherence to treatment regimen and outcome, patient satisfaction, and cost of community health care.



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