Importantly, the mucous membrane is staged at each visit. We culture secretions whenever they’re present, because the underlying problem with a lot of these polyps and their recurrence is subsequent infection, he said.
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August 2008There are four stages used in a system Dr. Kuhn helped develop for this. Stage 0 is no evidence of disease; Stage 1 is beginning edema; Stage 2 is the development of polypoid edema; and Stage 3 is the recurrence of polyps.
Allergic Fungal Sinusitis
One type of eosinophilic inflammatory sinusitis is due to allergic fungal sinusitis (AFS). The major criteria for diagnosing AFS are Type 1 hypersensitivity, polyps, a characteristic CT scan, eosinophilic mucus, and a positive fungal smear.
However, patients who have previously undergone polyp surgery and present with AFS will not have a characteristic CT scan-and the diagnosis becomes more difficult, Dr. Kuhn said. These patients will meet the other criteria for AFS, though.
In general, AFS patients can be managed with a tapered regimen of oral prednisone until they reach Stage 0. After that they can be switched to other treatment modalities. Bursts and tapers of prednisone can be used for recurrence, and lesser disease may respond to only two or three cycles. Topical steroids can also be used, via irrigation or other modalities. Dr. Kuhn reported that in his experience, montelukast (Singulair) has not been very useful for this condition, but has had some minor success with nonsteroidal anti-inflammatory drugs
Eosinophilic inflammatory sinusitis is a chronic problem with no obvious cure, and it does not always have an obvious etiology. Consider, for instance, cases that appear to be AFS, but no fungus can be found. These patients generally meet three of the five criteria: Type-1 hypersensitivity, polyps, and eosinophilic mucus.
We believe the patients’ systems have become upregulated to the point that they have learned how to recruit eosinophils to the sinus wound, he said. There has been some suggestion that keeping infections under control may, over time, reduce eosinophil recruitment. I believe that if we can keep their infections under control for a lengthy period of time, perhaps their system downregulates in its willingness or ability to recruit eosinophils to the sinus lamina, he said.
What we’re dealing with is not really a disease in the true sense of the word. Nor is it an infection, Dr. Kuhn said. It is the result of eosinophilic-mediated inflammation. Possibly, it is infection-mediated (or maybe this is the case in some patients) by some sort of superantigen. In some cases, Type 1 hypersensitivity maybe involved in eosinophil recruitment. Patients may have a genetic predisposition to this problem, too.