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Genomics and Pharmacogenomics of Rhinosinusitis



Polymorphisms of selected inflammatory and metabolic genes
have been described in the etiology of chronic rhinosinusitis, and these effects can be explained
on a pharmacogenetic basis.



The purpose of this study was to examine whether there is an association between
inflammatory factors and some of these alleles, by associating these genetic variables
with each other.



CYP1A2, CYP2D6, CYP2C19, CYP2C9, CYP3A4, CYP3A5, G6PD, NAT2,
UGT1A1, VKORC1, ABCB1, SLCO1B1, APOE, TNF, IL1B, IL6 and IL6R gene polymorphisms
were analyzed by PCR. Drug-metabolizing enzymes were classified according to
their phenotype. Blood cell counts and biochemical parameters were also considered.



Significant differences were found in the CYP1A2 phenotype, with fewer
CYP1A2 normal metabolizers (NMs) expressing sinusitis (14.3% vs 30%) and a greater
number of CYP1A2 ultra-rapid-metabolizers (UMs)(85% vs 69%); and in TNF, affecting
TNF-A/A (4% vs 2%) and TNF-G/G (78% vs 66%) compared with TNF-G/A (19% vs
32%) carriers. 96% of patients with CRS had at least one G allele. When trigenic variables
involved in sinusitis were analyzed, statistical differences were found in SLCO1B1-TNFCYP1A2,
with a higher proportion of subjects with 1/1-GG-UM (44.3%); and IL1B-TNFCYP1A2
with CC-GG-UM (26%), CT-GG-UM (19.8%) and CC-GG-NM (13.7%) genophenotypes,
respectively. Subjects with sinusitis had a higher eosinophil count (308.80
cel/mcL vs 263.14 cel/mcL) and lower HDL levels (265.34 vs 297.85 mg/dL).



SLCO1B1-TNF-CYP1A2 and IL1B-TNF-CYP1A2 trigenic clusters may condition
the chronicity of sinusitis. Eosinophilia and HDL are factors involved in inflammation,
and thus in the development of CRS.
