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Background and study aims The wide use of PET-CT for the staging of neoplasms has extended to enlarged lymph nodes of unknown origin. Nevertheless, upper abdominal and mediastinal nodes are accessible to endoscopic ultrasonography-fine needle aspiration (EUS-FNA), providing a cytological diagnosis, with a high diagnostic yield in previous reports. In this paper, we have compared the accuracy of both procedures in this particular setting. Patients and methods After the finding of a lymphadenopathy in a conventional CT, both PET-CT and EUS-FNA were performed. The endoscopist had no information about PET-CT results. FNA was performed after a systematic EUS exam, with a 25 G needle and no suction. We considered the pathologic results as the gold standard or, if not available, the patients' outcome as a surrogate marker. Results A total of 54 patients were included. Common locations of nodes included subcarinal space (33.3%), porta hepatis (31.5%), upper mediastinum (15%), peripancreatic (7.4%), and other locations (12.8%). Adequate specimens were obtained in 48/54 patients (89%). The most common diagnoses based on cytology were benign/reactive (42%), epidermoid carcinoma (8.4%), lymphoma (8.4%), and ductal adenocarcinoma of pancreatic origin (6.3%). PET was positive in 67% of patients. The sensitivity, specificity, positive predictive value, negative predictive value, and overall accuracy of EUS-FNA were 91.3, 100, 100, 92.5, and 95.8%, respectively. The same values for PET-CT were 75, 25, 50, 50, and 50%, respectively. Conclusion In our series, EUS-FNA has proven to be the best diagnostic procedure to accurately establish the etiology of isolated adenopathies, showing a much better diagnostic yield than PET-CT, the role of which should be re-evaluated in this setting.

Substantial proportion of Crohn’s disease (CD) patients shows no response or a limited response to treatment with infliximab (IFX) and to identify biomarkers of response would be of great clinical and economic benefit. The expression profile of five genes (S100A8-S100A9, G0S2, TNFAIP6, andIL11) reportedly predicted response to IFX and we aimed at investigating their etiologic role through genetic association analysis. Patients with active CD (350) who received at least three induction doses of IFX were included and classified according to IFX response. A tagging strategy was used to select genetic polymorphisms that cover the variability present in the chromosomal regions encoding the identified genes with altered expression. Following genotyping, differences between responders and nonresponders to IFX were observed in haplotypes of the studied regions:S100A8-S100A9(rs11205276*G/rs3014866*C/rs724781*C/rs3006488*A;P=0.05);G0S2(rs4844486*A/rs1473683*T;P=0.15);TNFAIP6(rs11677200*C/rs2342910*A/rs3755480*G/rs10432475*A;P=0.10); andIL11(rs1126760*C/rs1042506*G;P=0.07). These differences were amplified in patients with colonic and ileocolonic location for all but theTNFAIP6haplotype, which evidenced significant difference in ileal CD patients. Our results support the role of the reported expression signature as predictive of anti-TNF outcome in CD patients and suggest an etiological role of those top-five genes in the IFX response pathway.