Background: Recent guidelines recommend establishing a local reference interval (RI) for thyroid function. We aimed to establish trimester-specific RIs for thyrotropin (TSH) and free thyroxine (FT4) in a cohort of healthy pregnant women in Catalonia (Spain). Methods: A prospective observational study was conducted with 332 healthy pregnant women, from the first trimester (1T) to delivery. TSH was measured using an Architect^® immunoassay (Abbott) and FT4 by two immunoassays, Architect^® (Abbott) and Cobas^® (Roche), in the three trimesters. FT4 was also measured by liquid chromatography mass spectrometry (LC/MS/MS) in the 1T. Results: TSH (µUI/mL) increased throughout pregnancy (1T: 0.03–3.78; 2T: 0.51–3.53; 3T: 0.50–4.32; p < 0.0001) and FT4 (pmol/L) progressively decreased (Architect^® 1T: 10.42–15.96; 2T: 8.37–12.74; 3T: 8.24–12.49; p < 0.0001; and Cobas^®: 1T: 11.46–19.05; 2T: 9.65–14.67; 3T: 8.88–14.54; p < 0.0067). The FT4 RI during 1T determined LC/MS/MS was 8.75–18.27. Despite the 1T FT4 results measured by LC/MS/MS and with the two immunoassays being significantly correlated, the results obtained by the three methods were found to be non-interchangeable. Conclusions: We established trimester-specific RIs for TSH and for FT4 with immunoassays in our population. We also validated the 1T FT4 using LC/MS/MS to confirm the results of FT4 lower than the 2.5th percentile or higher than the 97.5th percentile.

Background: Previous studies suggested that Interleukin‐10 (IL‐10) depletion in Crohn's disease (CD) could predict outcome. Aim: To determine IL‐10 in blood and at different intestinal locations in patients with active CD and to assess its potential prognostic capacity to identify aggressive CD.Methods: Twenty‐three patients with CD were included. Ulcerative colitis (UC), infectious colitis and healthy individuals acted as controls. Serum and mucosal samples were taken at baseline and 1 month after steroid initiation in CD patients. Patients were classified according to steroid response. Control samples were obtained from different intestinal locations. IL‐10 expression was measured with real‐time polymerase chain reaction, immunofluorescence (intestine) and ELISA (serum, biopsy cultures' supernatants and tissue homogenates).Results: CD and UC showed an increase in IL‐10 messenger RNA (mRNA) versus controls (p < .0001) in mucosa, whereas IL‐10 protein secretion was increased in all types of intestinal inflammation (p < .001). No differences in IL‐10 mRNA were found in CD at baseline regarding steroid response, but levels decreased in non‐responders versus responders (p = .027) and were restored with rescue therapy. Serum IL‐10 was increased in steroid‐refractory CD at baseline and after treatment.Conclusions: Abnormal IL‐10 levels in refractory patients in both mucosa and blood have physiopathological relevance and may have potential clinical applications.