Mortuaire, G., de Gabory, L., François, M., Massé, G., Bloch, F., Brion, N., ... Serrano, E. Rebound congestion and rhinitis medicamentosa: Nasal decongestants in clinical practice. (2013, June 1). Critical review of the literature by a medical panel. European Annals of Otorhinolaryngology, Head and Neck Diseases , 130(3), 137-144. Retrieved from https:///#!/content/playContent/1--S1879729612001378?returnurl=http:%2F%%2Fretrieve%2Fpii%2FS1879729612001378%3Fshowall%3Dtrue&referrer=https:%2F%2F .
There are no data with intranasal fluticasone furoate in patients with hepatic impairment. Data are available following inhaled administration of fluticasone furoate (as fluticasone furoate or fluticasone furoate/vilanterol) to subjects with hepatic impairment that are also applicable for intranasal dosing. A study of a single 400 microgram dose of orally inhaled fluticasone furoate in patients with moderate hepatic impairment (Child-Pugh B) resulted in increased C max (42 %) and AUC(0-∞) (172 %) and a modest (on average 23 %) decrease in cortisol levels in patients compared to healthy subjects. Following repeat dosing of orally inhaled fluticasone furoate/vilanterol for 7 days, there was an increase in fluticasone furoate systemic exposure (on average two-fold as measured by AUC (0–24) ) in subjects with moderate or severe hepatic impairment (Child-Pugh B or C) compared with healthy subjects. The increase in fluticasone furoate systemic exposure in subjects with moderate hepatic impairment (fluticasone furoate/vilanterol 200/25 micrograms) was associated with an average 34% reduction in serum cortisol compared with healthy subjects. There was no effect on serum cortisol in subjects with severe hepatic impairment (fluticasone furoate/vilanterol 100/ micrograms). Based on these findings the average predicted exposure of 110 micrograms of intranasal fluticasone furoate in this patient population would not be expected to result in suppression of cortisol.