How common is increased ocular pressure in treatment with intranasal mometasone?

Fråga: How common is increased ocular pressure in treatment with intranasal mometasone?

Sammanfattning: Steroids have been shown to cause an elevation in IOP through all modes of administration but remain quite rare with intranasal use. Studies on the glaucomatous patients are controversial. In patients with preexisting glaucoma as in this current case, steroids with low systemic bioavailability such as mometasone nasal sprays could be used if the intraocular pressure is monitored closely to prevent any complications as irreversible optic nerve damage.

Svar: Increased intraocular pressure (IOP) and open-angle glaucoma are well-known adverse affects of steroid therapy. Physical and mechanical changes in the microstructure of the trabecular meshwork induced by steroids and consequently increased resistance to outflow are regarded as the main causes of IOP elevation (1).

Steroid-induced glaucoma is usually associated with topical steroid use (drops or ointments instilled in the eye), but it may develop with inhaled, oral, intravenous, periocular, or intravitreal steroid administration. The higher frequency of IOP elevation with topical steroids compared to systemic forms could be probably explained by the higher amount of steroid reaching the eye with topical application than systemic therapy (2).

Two mechanisms have been suggested for trabecular meshwork exposure to intranasal steroids, topically by a retrograde movement of nasal product from the nasal cavity to the eye via the nasolacrimal drainage system or systemically as steroids are expected to be absorbed by the hyper vascular nasal mucosa and to lesser extent by gastrointestinal tract. However, the first suggested mechanism is unlikely because of the one-way valve system found within the lacrimal drainage system. Likewise, systemic absorption and subsequent delivery to the eye is doubtful as intranasal steroids are absorbed systemically in small measurable amounts that have never been considered high enough to produce the same systemic side effects that oral or parenteral administration of steroids are known to produce (3). Currently, five nasal steroid formulations are available in the Sweden. Beclomethasone and budesonide nasal sprays have the higher bioavailability 44% and 33% respectively as opposed to 0.5% for the other fluticasone, triamcinolon and mometasone nasal sprays (4).

In the medical literature, we found two case reports of nasal steroid induced glaucoma. The first case showed an increase of IOP from 19 and 20 mmHg to 37 and 27 mmHg for right and left eyes respectively after five months nasal beclomethasone spray use in a diabetic, hypertensive non- glaucomatous patient (5). The second case was a patient with history of right primary open angle glaucoma and left ocular hypertension. IOP was 19 and 18 mmHg for right and left eyes, respectively. After being treated with nasal steroid spray, patient had an increase of IOP in both eyes (35 and 29 mmHg for the right and left eyes, respectively). In both patients, the IOP returned to pretreatment levels after discontinuing nasal corticosteroid spray (6). There is no case report where mometansone (Nasonex) has been suspected to cause increased IOP or glaucoma in the Swedish adverse drug reactions register, SWEDIS (7).

The literature evaluating the effect of nasal steroids in glaucoma patients is both scarce and contradictory.

In a retrospective study, the risk of IOP was increased with nasal steroids in patients with glaucoma. Ten of 12 patients experienced an increase in IOP after starting nasal steroids. Eleven of 12 patients experienced a decreased IOP 21-59 days after discontinuation of the nasal steroids. The average of all 12 patients´ mean IOP was 15.4 + 4.3mmHg in the pre-steroid use, 18.0 + 3.8 mmHg in steroid use and 14.5 + 3.3 mmHg in post-steroid use(8).

In contrast, the evidence of the lack of an IOP-rising effect from intranasal steroids in patients with ocular hypertension and primary open angle glaucoma was demonstrated in recently published (2013) prospective randomized double controlled study. The authors reported that 6 weeks of intranasal steroid use does not seem to increase IOP in this high risk group of patients. The study used beclomethasone nasal spray because of its high bioavailability; if a steroid response was not demonstrated with beclomethasone, then it is unlikely to occur with alternate nasal steroids of lower bioavailability. However, the study has some limitations; small sample size of 19 and limited follow-up time to 6 weeks (9).

On the other hand, studies in patients without ocular pathology namely ocular hypertension or glaucoma have shown no substantial risk of intranasal steroids.

In a large Canadian register based case-control study (cases n=9793, controls n=38325) current use of inhaled and nasal glucocorticoids was not associated with an increased risk of ocular hypertension or open-angle glaucoma. However, the risk was increased in patients who had used high doses of inhaled glucocorticoids continuously for more than 3 months. (10). Another smaller prospective study of 26 non-glaucomatous patients received either budesonide or beclomethasone after endoscopic sinus surgery revealed similar outcome; no evidence of ocular hypertension after prolonged use of intranasal steroids (11).

Again, 54 non-glaucomatous patients being treated with nasal steroids for allergic rhinitis have been followed up for one month regarding IOP. The authors found no significant elevation in IOP after nasal steroid administration (12). Furthermore, a prospective double-blind study in 360 non- glaucomatous patients showed that the use of fluticasone, mometasone and beclomethasone for the conventional treatment of rhinitis did not cause a statistically significant raise in the intraocular pressure after the completion of treatment, with a 1-year follow up(13).