Nasal nitric oxide, the guardian of paranasal sinuses, is paradoxically increased by high doses of intravenous glucocorticoids.

Abstract

High concentrations of nitric oxide (NO) originating from a type-2 nitric oxide synthase (NOS2) located within the paranasal sinuses are measured in nasal air in man. NO is believed to play a central role in nonspecific defense of paranasal sinuses. Glucocorticoids (GCs), a therapeutic often used for a wide range of diseases, is known to strongly downregulate NOS2. To investigate the effect of very high intravenous doses of GCs on nasal NO in man. Nasal NO was measured in 15 patients without any history of allergy or chronic airway disorder who were treated for 3 days with a daily dose of 1000 mg methylprednisolone for an exacerbation of multiple sclerosis. Nasal NO was also measured in 30 matched control subjects. In control subjects, the maximal value of nasal NO [mean (SE)] was 233 (8) part per billion (ppb), and did not differ from patients with multiple sclerosis [maximum value: 219 (13) ppb; left nostril: 214 (12) ppb; right nostril: 215 (12) ppb]. After GCs treatment, nasal NO increased in patients [maximum value: 250 (13) ppb (P < 0.0001); left nostril: 249 (12) ppb (P < 0.0001); right nostril: 244 (13) ppb (P < 0.0001)]. We conclude that GCs do not decrease but even increase nasal NO.