Q:

5/10/2013
I have a 62 year-old African-American patient with nasal polyposis who was thoroughly tested for aeroallergen hypersensitivity and was negative to all allergens tested with good positive and negative controls. He does not have asthma and he takes a 325 mg ASA regularly as he has suffered a mild CVA. He cannot take Plavix because it caused him to hive. On his CT he had extensive polyposis but no hyperechoic areas to suggest AFS and on exam (per the ENT) there was no thick mucin to suggest the diagnosis.

He's undergone a polypectomy, just 2 months ago, and his repeat CT (done because he decompensated just a month after his surgery) demonstrated extensive polyposis that was just as severe as before the surgery.

His ENT wants him to have a work up for immunodeficiency disease, which I am sure the patient does not have, and is questioning the ASA as the cause of his recurrence.

I do not at all believe that his ASA is an issue as he has no evidence of hypersensitivity and there is absolutely no asthma. I strongly believe that this patient is just one of the 50% or so of polyp patients who have recurrences, and that we are simply unable to determine a cause.

By the way, Singulair did not help him.

A:

Thank you for your inquiry.

I do agree with your perspective of this patient’s problem. Recurrent nasal polyps can exist in the absence of asthma, aspirin-exacerbated respiratory tract disease, atopy, and immunodeficiency. Your patient could well fit into this category of individuals who have chronic sinusitis and nasal polyps without any of the aforementioned conditions. However, I think it is wise to keep in mind that aspirin-exacerbated respiratory tract disease can evolve, beginning with nasal polyps and later manifesting the other components of this syndrome. So, he should be observed for the development of the other components of this syndrome and educated about the symptoms of asthma since he is at risk of developing lower respiratory tract disease. Nonetheless, I do agree that aspirin is not “driving” his present condition, and I would not discontinue it. What might be helpful to you in this regard is to look for the presence of nasal eosinophilia as well as peripheral blood eosinophilia. It would not alter the care of the patient at the present time (which should be intranasal steroids), but the presence of peripheral eosinophilia might indicate a greater risk for the development of asthma in the future. I also believe that it is unlikely for him to have immunodeficiency, but there would certainly be no harm in at least ordering immunoglobulin levels.

In summary, as noted, I agree with the analysis of your patient’s problem at this time, but I think it is important to keep in mind that his condition could evolve over time and therefore he should be kept under observation for the development of lower respiratory tract symptoms.

Thank you again for your inquiry and we hope this response is helpful to you.

Sincerely,
Phil Lieberman, M.D.



AAAAI - American Academy of Allergy Asthma & Immunology