Fluticasone chemical structure
Find information on thousands of medical conditions and prescription drugs.


Fluticasone proprionate is a glucocorticoid often prescribed as treatment for asthma and allergic rhinitis. It is marketed with the brand name Flixotide® and Flixonase® by Allen & Hanburys and Flovent® and Flonase® by GlaxoSmithKline. more...

Folic acid
Fusidic acid

How it works

The precise mechanisms of glucocorticoid action in asthma are unknown. Inflammation is recognized as an important component in the pathogenesis of asthma. Glucocorticoids have been shown to inhibit multiple cell types (e.g., mast cells, eosinophils, basophils, lymphocytes, macrophages, and neutrophils) and mediator production or secretion (e.g., histamine, eicosanoids, leukotrienes, and cytokines) involved in the asthmatic response. These anti-inflammatory actions of glucocorticoids may contribute to their efficacy in asthma. Typically, however, the action on the cells affected requires several days. Therefore, inhaled steroids are not used for immediate relief of asthma, but instead as preventive and maintenance therapy.

Clinical trials

This listing is NOT complete and should NOT be construed as support for treatment decisions. See also PubMed clinical manuscripts referring to fluticasone

  • Burge, P.S.; Calverley, P.M.; Jones, P.W.; Spencer, S.; Anderson, J.A.; and Maslen T.K. (2000). Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. British Medical Journal 320 (7245), 1297-1303. PMID 10807619.
  • Paggiaro, P.L.; Dahle, R.; Bakran, I.; Frith, L.; Hollingworth, K.; and Efthimiou, J. (1998). Multicentre randomised placebo-controlled trial of inhaled fluticasone propionate in patients with chronic obstructive pulmonary disease. The Lancet 351 (9105), 773-780. PMID 9519948.
both support a positive outcome for use of fluticasone in patients with chronic obstructive pulmonary disease, also referred to as COPD

Read more at Wikipedia.org

[List your site here Free!]

The effect of topical fluticasone on nasal nitric oxide levels in a patient with allergic rhinitis - Original Article
From Ear, Nose & Throat Journal, 8/1/03 by Cetin Vural


Nitric oxide (NO) in exhaled breath is produced primarily by the upper respiratory airway mucosa. The nasal output of this gas is increased in patients with allergic rhinitis. We performed a study on a 41-year-old nonsmoking male volunteer with allergic rhinitis to investigate the effect fluticasone nasal spray on nasal NO output ([V.sub.NO]). A total of 28 nasal NO measurements from both nostrils we taken during the 2-month period of June and July 2002 During the second half of the study period (treatment phase), the patient took fluticasone in doses of 100 [micro]g per nostril once a day. During the treatment phase, nasal NO measurements were taken 10 days after the initiation treatment. In addition, we also recorded the patient's nasal symptom scores and tile grass pollen counts in the greater Pittsburgh area, The patient's mean [V.sub.NO] was 989.9 nl/min prior to treatment and 787. 7 nl/min following treatment--a statistically significant 20.4% decrease (p<0.01) The findings of our study support the observation that topical nasal steroid treatment decreases A production in sinonasal mucosa.


Nitric oxide (NO), a gas that was once believed to present only in the atmosphere, is produced in human tissues by the enzyme nitric oxide synthase (NOS), with L-arginine as the substrate. (1) Thus far, two forms of this enzyme have been identified: constitutive NOS (cNOS which is expressed constantly regardless of environmental conditions, and inducible (type 2) NOS (iNOS), which is expressed only as a reaction to endotoxins and inflammatory mediators.

Constitutive NOS can be classified according to its site of origin as either neuronal (type 1) NOS (nNOS) or endothelial (type 3) NOS (eNOS). (2) In the constitutive form, which is calcium-calmodulin-dependent, only small amounts of NO arc produced.

In the inducible form, which is calcium-calmodulin-independent, activation by proinflammatory cytokines and endotoxins results in up to a 1,000-fold increase in NO production compared with the eNOS form. Inducible NOS is the result of stimulation by gent transcription, probably via nuclear factor-kappa B; this process can be inhibited by glucocorticoids. (3) After induction, the increase in NO production lasts for hours and sometimes continues for days. (2) Lundberg et al first reported that the dominant NOS activity in nasal mucosa is calcium-dependent cNOS and the dominant activity in sinus mucosa is calcium-independent iNOS. (4) However, others have found iNOS expression in nasal biopsy and scraping specimens obtained from patients with allergic rhinitis, viral rhinitis, and chronic rhinitis. (5-7)

The presence of endogenous NO in the exhaled breath of animals and humans was first described by Gustafsson et al in 1991. (8) Five years later, Lundberg reported that the primary production site of exhaled NO is the upper airways. (9) In 2000, Silkoff et al reported that NO is a marker of airway inflammation. (10) Indeed, during the past decade, several studies have found that patients with allergic rhinitis or asthma have increased amounts of exhaled and nasal NO. (11-18) In patients with allergic rhinitis, increased iNOS expression caused by the release of proinflammatory cytokines in the upper and lower respiratory tract mucosae has emerged as a possible cause of increased NO levels. Studies of human (6,19) and murine (20) lung epithelial cells have demonstrated that cytokines can induce lung epithelialiNOS expression. Robbins et al also demonstrated that iNOS expression in both human and murine lung epithelial cells can be attenuated by dexamethasone. (19,20) They wrote that this effect is probably the result of a reduction in iNOS mRNA at the transcriptional level. (20)

In this article, we describe our investigation of the effect that topical nasal steroid treatment has on [V.sub.NO] in a patient with symptomatic allergic rhinitis.

Materials and methods

One of the authors (C.V.), a nonsmoking 4 l-year old man, volunteered to serve as the subject for this study. Nasal examination revealed that he had a mild nasal septal deviation that obstructed less than 25% of the left nasal passage. Skin-prick testing was positive for dust mites (Dermatophagoides pteronyssinus) and certain grasses (Kentucky blue, orchard, and redtop). During the study, the patient did not use avoidance measures to reduce his exposure to dust mites and pollen.

On the morning of June 25, 2002, when the patient's allergic symptoms were at peak levels, he began to administer fluticasone nasal spray, at 100 [micro]g per nostril once a day immediately following his NO measurement. He continued taking fluticasone for 4 weeks. In the greater Pittsburgh area that year, the seasonal increase in grass pollen levels began in the middle of May and continued through the end of July.

The patient's NO levels were measured with a rapid-response chemiluminescent Sievers 280 NOA analyzer (Sievers Instruments; Boulder, Colo.). The analyzer pump's sampling flow was 0.2 L/min. A two-point calibration was performed daily, first with air passed through an NO scrubber tube that contained KMn[O.sub.4] and activated charcoal to zero and then with certified NO gas (45 parts per million) for the span (Datex-Ohmeda; Madison, Wis.). Ambient NO was recorded before each measurement. The NO analyzer signal output was fed into a computer data acquisition program (NO analysis software for the NOA 280, version 3.00 PNE; Sievers Instruments). The program featured a real-time display of NO vs time that was written directly into the computer's hard disk as a data file, and results were displayed as a graphic output. The components of the sampling device were a latex nasal olive (ENTsol Adapter; KenwoodTherapeutics; Fairfield, N.J.), a filter (Resp-Bac; Medicomp; Princeton, Minn.), a respirator tube (Airlife; Allegiance Healthcare; McGaw Park, Ill.), and a gas-sampling connector with a midstream sampling port (Respiratory Support Products; Irvine, Calif.) (figure 1).


After the olive was gently inserted into the patient's naris, he closed his velum by holding his breath. Room air entered through the left nostril and was aspirated from the right nostril at a constant rate of 5 L/min. The flow through the nasal cavities was created by suction and continuously monitored with a highly accurate flow meter (Aalborg Instruments; Monsey, N.Y.). NO was sampled through a side port just distal to the tube. After an interval of 1 to 2 minutes, the procedure was repeated on the other side.

On each measurement day, on-line nasal NO measurements were taken between 9 a.m. and 10 a.m. from both sides of the nose following a 1-hour period of adjustment to the environment. After 10 to 20 seconds of breath-holding, a plateau of NO level was reached. Extrapolation of the mean by the software from this plateau was accepted as the on-line measurement value. To calculate the [V.sub.NO], the ambient NO values were subtracted from the mean values of both sides of the nose, and the resulting values were multiplied by the aspiration flow rate (5 L/ min).

The patient filled out a symptom questionnaire once every measurement day to rate the degree of nasal itching, sneezing, nasal discharge, congestion, and facial pain or pressure. Symptoms were scored as 0 (no symptoms), 1 (mild), 2 (moderate), and 3 (severe). Total and specific symptom scores were calculated and recorded for each day. Each day's grass pollen counts were obtained from the Children's Hospital of Pittsburgh's pollen count station as often as possible (the station was closed on weekends and holidays).

In all, 14 nasal NO measurements were obtained before steroid treatment and 14 afterward; post-treatment measurements began 10 days following the initiation of treatment. The Student's t test was used for statistical analysis.


During the pretreatment phase, the patient's nasal symptoms related to allergic rhinitis were prominent and his [V.sub.NO] levels were substantial (mean [V.sub.NO]: 989.9 nl/min). At the post-treatment evaluations, nasal symptom scores and [V.sub.NO] levels (mean [V.sub.NO]: 787.7 nl/min) were reduced (figures 2 and 3). The 20.4% difference between the pre- and post-treatment [V.sub.NO] levels was statistically significant (p<0.01).



Topical nasal steroids are one of the most effective treatments for allergic rhinitis. As expected, our patient experienced a marked decrease in nasal symptoms and a significant decrease in his mean [V.sub.NO] level following steroid therapy.

Although Lundberg et al (4) found that topical nasal steroids had no effect on nasal NO levels, others reported the opposite. Baraldi et al found that nasal steroids reduced elevated nasal NO levels in patients with allergic rhinitis. (18) Dillon et al (21) and Kharitonov et al (22) also reported a reduction in nasal NO levels after steroid treatment. However, a common limitation of these studies was their suboptimal NO sampling techniques.

Springall et al found an increased expression of iNOS in the pulmonary epithelium of asthma patients, and they reported that this expression was reduced by corticosteroid treatment. (23) They concluded that this reduction might be the result of a resolution of inflammation and the subsequent reduction in the release of cytokines that stimulate iNOS expression. The same group of researchers also found that the expression of iNOS in nasal mucosa was increased in patients with allergic rhinitis. (24) This increased expression is possibly a result of an increase in the release of cytokines in sinonasal mucosa, which might explain the high [V.sub.NO] levels seen in allergic rhinitis patients.

The decline in [V.sub.NO] in our patient supports the observation that iNOS, which can be inhibited by steroids, contributes to nasal NO production. (21) Even so, the fact that the decrease was only 20.4% indicates that a significant amount of nasal NO production appears to be resistant to steroid treatment. This resistance might be attributable to the production of NO by cNOS or the production of NO in sinus mucosa, neither of which should be affected by nasal steroid sprays. Still, we cannot rule out the possibility that an incomplete suppression of iNOS is attributable to an inadequate corticosteroid dosage.

To minimize the probable topical effects that steroid-spray vehicles have on nasal [V.sub.NO] levels, our patient used the spray immediately after nasal NO measurements were obtained. As a result, the interval of almost 24 hours was likely to have mitigated any effects of the vehicle. One might argue that the decrease in our patient's [V.sub.NO] levels was related to the decrease in grass pollen concentration during the treatment period, but his [V.sub.NO] levels were just as high before the onset of the grass pollen season as they were during the pollen season.

In conclusion, [V.sub.NO] measurement is a simple, noninvasive procedure. Changes in [V.sub.NO] can serve as a marker of sinonasal inflammation and can be used to monitor therapeutic efficacy. We believe that our preliminary study had one advantage over other studies (18,21,22) in that we used an optimal sampling technique and standardized measuring and reporting methods. (25) We hope our findings and methods will be put to the test in larger groups of patients.


(1.) Moncada S, Higgs A. The L-arginine-nitric oxide pathway. N Engl J Med 1993;329:2002-12.

(2.) Djupesland PG, Chatkin JM, Qian W, Haight JS. Nitric oxide in the nasal airway: A new dimension in otorhinolaryngology. Am J Otolaryngol 2001;22:19-32.

(3.) Singh S, Evans TW. Nitric oxide, the biological mediator of the decade: Fact or fiction? Eur Respir J 1997;10:699-707.

(4.) Lundberg JO, Weitzberg E, Rinder J, et al. Calcium-independent and steroid resistant nitric oxide synthase activity in human paranasal sinus mueosa. Eur Respir J 1996;9:1344-7.

(5.) Kang BH, Chert SS, Jou LS, et al. Immunolocalization of inducible nitric oxide synthase and 3-nitrotyrosine in the nagal mucosa of patients with rhinitis. Eur Arch Otorhinolaryngol 2000;257: 242-6.

(6.) Sanders SP, Siekierski ES, Richards SM, ct al. Rhinovirus infection induces expression of type 2 nitric oxide synthase in human respiratory epithelial cells in vitro and in vivo. J Allergy Clin Immunol 2001;107:235-43.

(7.) Furukawa K, Harrison DG, Saleh D, et al. Expression of nitric oxide synthase ia the human nasal mucosa. Am J Respir Crit Care Med 1996;153:847-50.

(8.) Gustafsson LE, Leone AM, Persson MG, et al. Endogenous nitric oxide is present in the exhaled air of rabbits, guinea pigs and humans. Biochem Biophys Res Commun 1991;181:852-7.

(9.) Lundberg JO. Airborne nitric oxide: Inflammatory marker and aerocrine messenger in man. Acta Physiol Scand Suppl 1996; 633:1-27.

(10.) Silkoff PE, Robbins RA, Gaston B, et al. Endogenous nitric oxide in allergic airway disease. J Allergy Clin Immunol 2000:105: 438-48.

(11.) Martin U, Bryden K, Devoy M, Howarth P. Increased levels of exhaled nitric oxide during nasal and oral breathing in subjects with seasonal rhinitis. J Allergy Clin Immunol 1996;97:768-72.

(12.) Arnal JF, Didier A, Rami J, et al. Nasal nitric oxide is increased in allergic rhinitis. Clin Exp Allergy 1997;27:358-62.

(13.) Djupesland PG, Chatkiu JM. Qian W, et al. Aerodynamic influences on nasal nitric oxide output measurements. Acta Otolaryngol 1999:119:479-85.

(14.) Alving K, Weitzberg E, Lundberg JM. Increased amount of nitric oxide in exhaled air nf asthmatics. Eur Respir J 1993:6:1368-70

(15.) Kharitonov SA, Yates D, Robbins RA, et al. Increased nitric oxide in exhaled air of asthmatic patients. Lancet 1994;343:133-5.

(16.) Lundberg JO, Nordvall SL, Weitzberg E, et al. Exhaled nitric oxide in paediatric asthma and cystic fibrosis. Arch Dis Chile 1996;75:323-6.

(17.) Baraldi E, Azzolin NM, Zancouato S, et al. Corticosteroid decrease exhaled nitric oxide in children with acute asthma. Pediatr 1997; 131:381-5.

(18.) Baraldi E. Azzoliu NM, Carra S, el al. Effect of topical steroids or nasal nitric oxide production in children with perennial allergic rhinitis: A pilot study. Respir Med 1998;92:558-61.

(19.) Robbins RA. Barnes PJ, Springall DR, el al. Expression o inducible nitric oxide in human lung epithelial cells. Biochem Biophys Res Commun 1994;203:209 18.

(20.) Robbins RA, Springall DR. Warren JB, et al. Inducible nitric oxide synthase is increased in routine lung epithelial cells by cytokine stimulmion. Biocbem Biophys Res Commun 1994;198 835-43.

(21.) Dillon WC. Hampl V, Shultz PJ, et al. Origins of breath nitric oxide in humans. Chest 1996;110:930-8.

(22.) Kharitonov SA, Rajakulasingam K, O'Connor B. et al. Nasal nitric oxide is increased in patients with asthma and allergic rhinitis and may be modulated by nasal glucocorticoids. J Allergy Clin Immunol 1997;99(Pt 1):58-64.

(23.) Springall DR, Meng Oil, Redington A, el al. Inducible nitric oxide synthase in asthmatic airway epithelium is reduced by corticosteroid therapy [abstract]. Am I Respir Crit Care Med 1995:151:A833.

(24.) Springall DR, Mason NA, Redington A, et al. Inducible nitric oxide synthasc is upregulated in nasal epithelium in perennial allergic rhinitis ]abstract]. Am J Respir Cril Care Med 1996; 153:A800.

(25.) AmericanThoracic Society. Recommendations for standardized procedures for the on-line and off-line measurement of exhaled lower respiratory nitric oxide and nasal nitric oxide in adults and children--1999. AmJ Respir Crit Care Med 1999;160:2104-17.

From the Sisli Etfal Training and Research Hospital, Istanbul, Turkey (Dr. Vural), and the Department of Pediatric Otolaryngology, Children's Hospital of Pittsburgh (Dr. Gungor).

Reprint requests: Anil Gungor, MD, Department of Pediatric Otolaryngology, Children's Hospital of Pittsburgh, 3705 Fifth Ave., Pittsburgh, PA 15213-2583. Phone: (412) 692-5460; fax: (412) 692-6074; e-mail: anil.gungor@chp.edu

COPYRIGHT 2003 Medquest Communications, LLC
COPYRIGHT 2003 Gale Group

Return to Fluticasone
Home Contact Resources Exchange Links ebay