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  • Liu, Po-Hong, et al. (författare)
  • Dietary Gluten Intake and Risk of Microscopic Colitis Among US Women without Celiac Disease : A Prospective Cohort Study
  • 2019
  • Ingår i: American Journal of Gastroenterology. - Blackwell Publishing. - 0002-9270 .- 1572-0241. ; 114:1, s. 127-134
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>OBJECTIVE:</strong> Microscopic colitis is a common cause of chronic watery diarrhea among the elderly. Although the prevalence of celiac disease appears to be higher in patients with microscopic colitis, the relationship between dietary gluten intake and risk of microscopic colitis among individuals without celiac disease has not been explored.</p><p><strong>METHODS:</strong> We conducted a prospective study of 160,744 US women without celiac disease enrolled in the Nurses' Health Study (NHS) and the NHSII. Dietary gluten intake was estimated using validated food frequency questionnaires every 4 years. Microscopic colitis was confirmed through medical records review. We used Cox proportional hazard modeling to estimate the multivariable-adjusted hazard ratio (HR) and 95% confidence interval (CI).</p><p><strong>RESULTS:</strong> We documented 219 incident cases of microscopic colitis over more than 20 years of follow-up encompassing 3,716,718 person-years (crude incidence rate: 5.9/100,000 person-years) in NHS and NHSII. Dietary gluten intake was not associated with risk of microscopic colitis (P<sub>trend</sub> = 0.88). Compared to individuals in the lowest quintile of energy-adjusted gluten intake, the adjusted HR of microscopic colitis was 1.18 (95% CI: 0.77-1.78) for the middle quintile and 1.03 (95% CI: 0.67-1.58) for the highest quintile. Additional adjustment for primary dietary sources of gluten including refined and whole grains did not materially alter the effect estimates (All P<sub>trend</sub> ≥ 0.69). The null association did not differ according to lymphocytic or collagenous subtypes (P<sub>heterogeneity</sub> = 0.72) and was not modified by age, smoking status, or body mass index (All P<sub>interaction</sub> ≥ 0.17).</p><p><strong>CONCLUSION:</strong> Dietary gluten intake during adulthood was not associated with risk of microscopic colitis among women without celiac disease.</p>
  • Ludvigsson, Jonas, et al. (författare)
  • Elemental versus polymeric enteral nutrtion in paediatric Crohn´s disease : a multicentre randomized controlled trial.
  • 2004
  • Ingår i: Acta Paediatrica. - 0803-5253 .- 1651-2227. ; 93, s. 327-335
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Aim: To compare the efficacy and safety of an elemental and a polymeric diet as the primary therapy for active Crohn's disease in children. Methods: In a randomized, non-blind, multicentre, controlled trial in Sweden, 16 children with Crohn's disease received Elemental 028 Extra (E028E) and 17 Nutrison Standard (NuS). Remission rates (Paediatric Crohn's Disease Activity Index (PCDAI) &lt; 10 or a PCDAI decrease of 40% or 15 points of initial level) were compared at 6 wk. Results: There was no significant difference between the two groups in remission rate at 6 wk (intent-to-treat analysis): E028E 11/16 (69%) and NuS 14/17 (82%) (p = 0.438). There was no difference in the decrease in PCDAI and CDAI between patients treated with E028E and those treated with NuS from 0 to 6 wk. Patients treated with NuS gained significantly more weight than patients treated with E028E (+2.5 kg, 95% CI 0.9, 4.1, p = 0.004), this difference remained when adjusting for maximum caloric intake per kilogram bodyweight (+2.9 kg, 95% CI 1.4, 4.5, p = 0.001). Concomitant disease, complications and side effects were seen in 5/33 patients (pyelonephritis, pneumonia, intraabdominal abscess, perianal abscess and borborygmi). Conclusion: E028E and NuS did not differ in terms of remission rate. Patients treated with NuS gained more weight than patients with E028E. Polymeric diet may be superior to elemental diet in the treatment of paediatric Crohn's disease where the primary aim is to increase the patient's weight.</p>
  • Ludvigsson, Jonas F., 1969-, et al. (författare)
  • IgA Deficiency &amp; Mortality : A Population-Based Cohort Study
  • 2013
  • Ingår i: Journal of Clinical Immunology. - 0271-9142 .- 1573-2592. ; 33:8, s. 1317-1324
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>IgA deficiency has been linked to increased morbidity but data on mortality is lacking. In this population-based prospective cohort study we examined mortality in patients with IgA deficiency compared with the general population. Through six university hospitals in Sweden we identified 2,495 individuals with IgA deficiency (IgA deficiencya parts per thousand currency sign0.07 mg/L) diagnosed between 1980 and 2012. Each patient with IgA deficiency was matched on age, sex, place of residence, and year of diagnosis with up to 10 general population controls (n = 24,509). Data on education level and emigration status were obtained from Statistics Sweden. Our main outcome measure was all-cause mortality retrieved from the nationwide Causes of Death Register, which includes &gt; 99 % of all deaths in Sweden. We used Cox regression to estimate mortality hazard ratios conditioned on the matching factors and adjusted for education level. During 25,367 person-years of follow-up (median 8.3), there were 260 deaths in the IgA deficiency group versus 1,599 deaths during 257,219 person-years (median 8.6) in the general population controls (102 versus 62 deaths per 10,000 person-years; incidence rate difference, 40, 95%CI 28-53, P &lt; .001). This corresponded to a conditional mortality hazard ratio of 1.8 (95%CI 1.6-2.1, P &lt; .001). Relative mortality varied by follow-up time (P &lt; .001) from a hazard ratio of 3.6 (95%CI 2.5-5.3; P &lt; .001) during the first year to 1.9 (95%CI 1.5-2.4; P &lt; .001) year 1-4; 1.9 (95%CI 1.4-2.4; P &lt; .001) year 5-9; 1.5 (1.0-2.2; P = .054) year 10-14.9; and 1.1 (0.7-1.6; P = .66) year 15-25. Effect modification was also seen by age in each stratum of follow-up time, with higher relative mortality in younger than older patients (P &lt; .001). In conclusion, patients with IgA deficiency are at increased risk of death in the first 10 to 15 years after diagnosis.</p>
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