All patients were not allergic and show as at objective exam as at citologic observation an inflammatory distress with widespread epithelial pain, with prevalence of mucipar cells and eosinophils, classifiable as not allergic eosinophilic rhinitis (9). The last ones are the expression of eterogeneous pathologies, whose cause it is not well defined. However, Armone Caruso et coll. Associates them with colon adenocarcinoma (10) and Younis, associates them with squamous carcinoma of mouth (11).
Clinical cases of eosinophilia of respiratory system and RA are rare in literature, but the possibility of this associations and rheumatological desease it was discuss by most authors (12-15). But cases of eosinophilia and RA are never been describes. At the first time we report this correlation.
The relation between nose and pulmons is given obviously from their streight embryological derivation and from the same immunological behavior of both anatomical structures. The first description of Eosinophilia of respiratory system associated at RA was maden by Payne et al , which tried to demonstrate the same origin not related with immunity. Yousem et al. in the 1985 analized 40 casual patients with RA and pulmonary pathologies and one of them present eosinophilia of respiratory system. Van Esch et al.  in the 2001 described as iperactivation of T-cells, through the reticulation of B-cells mediated by CD40, it is at the same time responsible of the sistemyc chemotaxis of eosinophils and production of RF. Most recently, it is demonstrated that the role of some interleukines (IL6,IL1,IL10; IL5,IL4 and IL12 in mouse model CIA)( 24) and Chemokines (eotaxin 1 and 2) induce the recruitment of eosinophils by macrophages and limphocites T and inhibit apopthosis of eosinophilic infiltrates in tissues.
As we put in evidence in studies about animals (18), the mechanisms that induce the eosinophilic recruitment are mainly lead from a TH2-limphocitary way.
However the RA is a desease mainly lead by TH1/TH17, the switch purpose by a regulation of the flogistic way (use of drugs like Tocilizumab, prednisone, methotrexate), suggest an improvement of the desease towards an allergic inflammatory stimulation. Sandhya et al.  suggest that the switch from Th1/Th17 way to Th2 could be a mecchanism that causes remission by RA, with a massive release of eosinophils in blood with conseguent infiltration in target organs. [20-22].
In Our study we demonstrate that simptoms of RA are inactivated in the moment of the nasal withdrawal . Actually there aren’t studies that make a correlation between nasal cytology and RA; However even if the number of the patients it is slender, we can hipothize that the presence of eosinophils is a prognostic indicator of the evolution of the desease or could have a predictive role, in conseguence of the sthreight relations between RA and respiratory system.