© 2005 American Thoracic Society
Acute Purulent Sinusitis Triggered by Topical Nasal Nitric Oxide Synthase InhibitionTo the Editor:The gas nitric oxide (NO) is continuously being generated by NO synthase in the epithelium of the nose and the paranasal sinuses (1, 2). A role for nasal NO in host defense has been suggested since this gas has both antibacterial and cilia-stimulating effects and since nasal NO levels are greatly reduced in patients susceptible to sinus infections (1, 2). The case presented here involves the author and lends further support to an important role for NO in airway host defense.
I (the subject) am a nonsmoking 40-year-old male with no history of chronic nasal disorders. I have never experienced any episode suggestive of acute sinusitis. Some weeks ago I was doing some basic experiments in my lab that involved topical application of an NO synthase inhibitor to one side of the nose to study the acute effect on nasal NO release. The study was approved by the local ethics committee. NG-monomethyl-L-arginine (L-NMMA) (50 mg) was sprayed in the right nostril and then nasal NO was measured by exhaling at 0.05 L/second through one nostril via a tight-fitting nasal olive into a chemiluminescence NO analyzer (NIOX; Aerocrine AB, Stockholm, Sweden). Exhalation procedures followed the guidelines for exhaled NO measurements (3). During nasal exhalation the contralateral nostril was blocked with the thumb. Nasal NO levels (left and right side) were calculated by subtracting the levels obtained during an oral exhalation (0.05 L/second) from the nasal value. Nasal NO decreased markedly (
There is reason to believe that this episode of acute purulent sinusitis was triggered by the pharmacologically induced inhibition of nasal NO production. Indeed, the sinusitis developed on the side where L-NMMA was administered, and it was coupled with a marked decrease in nasal NO on that side. In addition, the subject had no history of sinus problems whatsoever. At the time of the study I was experiencing typical signs of a common cold with rhinorrhea. The mechanism by which a low nasal NO increases the susceptibility to sinusitis probably involves impaired mucociliary clearance as well as less direct antibacterial effects of NO gas. The acute drop in nasal NO was most likely caused by inhibition of NO synthase in the epithelium. The even more marked right-sided decrease in nasal NO present many days later at the onset of the sinusitis is more likely a result of the infection with decreased sinus NO generation and a blocked passage of NO into the nasal cavity (2, 4, 5). In conclusion, the presented case supports the notion that NO plays an important role in primary unspecific host defense in the upper airways. The observation also calls for some caution when using NO synthase inhibitors in respiratory research.
Karolinska Institutet, Stockholm, Sweden FOOTNOTES Conflict of Interest Statement: J.O.L. owns shares in Aerocrine AB, Stockholm, Sweden. REFERENCES
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50% after 30 minutes) on the right (L-NMMA) side but remained unaffected on the left untreated side. Four days after the experiment I developed a gradually increasing pain over the right side of the face coupled with right-sided purulent nasal secretions. On Day 6 the pain increased further and a CT scan was done. This showed extensive opacification of the right maxillary sinus while the left sinus was air filled and clear (
