A comparison of effects of triamcinolone acetonide aqueous nasal spray, oral prednisone, and placebo on adrenocortical function in male patients with allergic rhinitis

Howland, William C.; Dockhorn, Robert J.; Gillman, Sherwin A.; Gross, Gary N.; Hille, Darcy A.; Simpson, Brandon; Furst, J.A.; Feiss, Gary; Smith, Joseph A.

doi:10.1016/s0091-6749(96)70223-3

Cited by 35 publications

(13 citation statements)

References 22 publications

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“…54,55 Studies that attempted to determine the effect of intranasal steroids on dynamic function (by evaluating adrenocorticotropic stimulation) similarly showed no significant effects with beclomethasone dipropionate 336 µg/day, fluticasone propionate 200 and 400 µg twice/day, or triamcinolone acetonide 220 and 400 µg/day. [57][58][59] These data suggest that the drugs have little or no effect on the HPA axis when administered at recommended dosages.…”

Section: Intranasal Corticosteroidsmentioning

confidence: 86%

Intranasal Corticosteroids for Allergic Rhinitis

2002

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Intranasal corticosteroids are accepted as safe and effective first-line therapy for allergic rhinitis. Several intranasal corticosteroids are available: beclomethasone dipropionate, budesonide, flunisolide, fluticasone propionate, mometasone furoate, and triamcinolone acetonide. All are efficacious in treating seasonal allergic rhinitis and as prophylaxis for perennial allergic rhinitis. In general, they relieve nasal congestion and itching, rhinorrhea, and sneezing that occur in the early and late phases of allergic response, with studies showing almost complete prevention of late-phase symptoms. The rationale for topical intranasal corticosteroids in the treatment of allergic rhinitis is that adequate drug concentrations can be achieved at receptor sites in the nasal mucosa. This leads to symptom control and reduces the risk of systemic adverse effects. Adverse reactions usually are limited to the nasal mucosa, such as dryness, burning and stinging, and sneezing, together with headache and epistaxis in 5-10% of patients regardless of formulation or compound. Differences among agents are limited to potency, patient preference, dosing regimens, and delivery, device and vehicle.

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Section: Intranasal Corticosteroidsmentioning

confidence: 86%

Intranasal Corticosteroids for Allergic Rhinitis

2002

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“…Triamcinolone Acetonide (TAA) No significant effect of 220-440 g/day TAA aqueous nasal spray for 6 weeks was observed on urinary free cortisol and in the response to cosyntropin (250 g) stimulation test in adult male subjects [46] . Furthermore, no major changes in morning cortisol levels have been reported in 93 patients with AR, treated with different dosages (110, 220, 440 g/day) for more than 1 year [47] .…”

Section: Budesonidementioning

confidence: 99%

Intranasal Corticosteroids and Adrenal Suppression

Bruni¹,

Luca²,

Venturoli³

et al. 2009

Neuroimmunomodulation

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Allergic rhinitis is a common condition that frequently coexists with asthma and atopic dermatitis. It is commonly treated with intranasal corticosteroids which may increase the potential inception of side effects of the same type of drugs used for the treatment of other allergic diseases. A method to assess the systemic effect of corticosteroids is the evaluation of their effect on the hypothalamic-pituitary-adrenal (HPA) axis. However, it is not clear which test is best for detection of clinically relevant HPA axis suppression in children Morning plasma cortisol levels are twice that of late afternoon and evening values and a delay in the time of onset in peak cortisol levels has been observed in children treated with inhaled corticosteroids. Single morning cortisol level has a low sensitivity for detecting adrenal insufficiency in children. 24-Hour plasma cortisol is a good test because it is a non-invasive measure of the biologically active free cortisol levels for the entire day. For research purposes, the 24-hour integrated concentration plasma cortisol test is preferred. Studies that have looked at HPA axis suppression with intranasal corticosteroids indicate that overall, intranasal corticosteroids have a minimal effect on the HPA axis. A review of the literature reveals one study in which there was a decreased output of urinary cortisol during treatment with either budesonide or fluticasone propionate in adults. Other studies with fluticasone propionate or budesonide have shown no effect on the HPA axis in children. Beclomethasone dipropionate was shown to affect urinary cortisol output in one study on healthy volunteers. However, in a long-term study in children, no effect on the HPA axis was found. Mometasone furoate has been extensively studied in more than 20 trials of adults and children. No effects on the HPA axis were detected in either children or adults. Fluticasone furoate nasal spray was not associated with HPA axis suppression. It is unlikely that children are more sensitive to corticosteroids than adults. There is no reason to perform routine monitoring of adrenal function in children who are treated with intranasal corticosteroid unless those drugs are used concomitantly with inhaled corticosteroids and/or steroid ointments for the possible concomitant presence of asthma and/or atopic dermatitis.

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“…Patients receiving only nasal corticosteroids appear to be at low risk of developing hypothalamic‐pituitary‐adrenal axis (HPAA) suppression because of the low drug availability and the low doses used ( 110). Studies have shown that intranasal corticosteroids have no effect on the HPAA, except for dexamethasone spray and betamethasone drops, which can rarely provoke systemic effects ( 86, 93, 111–113). The newer nasal steroids fluticasone propionate and budesonide usually show no effect on the HPAA ( 108, 114, 115).…”

Section: Topical Corticosteroidsmentioning

confidence: 99%