| 1. |
- Lebwohl, Benjamin, et al.
(författare)
-
Mucosal Healing and Risk for Lymphoproliferative Malignancy in Celiac Disease A Population-Based Cohort Study
- 2013
-
Ingår i: Annals of Internal Medicine. - Columbia Univ, Coll Phys & Surg, New York, NY USA. Karolinska Univ Hosp, Stockholm, Sweden. Karolinska Inst, Stockholm, Sweden. Mayo Clin, Coll Med, Rochester, MN USA. Orebro Univ Hosp, SE-70185 Orebro, Sweden. : American College of Physicians. - 0003-4819 .- 1539-3704. ; 159:3, s. 169-
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Celiac disease (CD) is associated with an increased risk for lymphoproliferative malignancy (LPM). Whether this risk is affected by the results of follow-up intestinal biopsy, performed to document mucosal healing, is unknown. Objective: To examine the association between mucosal healing in CD and subsequent LPM. Design: Population-based cohort study. Setting: 28 pathology departments in Sweden. Patients: 7625 patients with CD who had follow-up biopsy after initial diagnosis. Measurements: The risk for LPM was compared with that of the general population by using expected rates. The rate of LPM in patients with persistent villous atrophy was compared with that of those with mucosal healing by using Cox regression. Results: Among 7625 patients with CD and follow-up biopsy, 3308 (43%) had persistent villous atrophy. The overall risk for LPM was higher than that in the general population (standardized incidence ratio [SIR], 2.81 [95% CI, 2.10 to 3.67]) and was greater among patients with persistent villous atrophy (SIR, 3.78 [CI, 2.71 to 5.12]) than among those with mucosal healing (SIR, 1.50 [CI, 0.77 to 2.62]). Persistent villous atrophy compared with mucosal healing was associated with an increased risk for LPM (hazard ratio [HR], 2.26 [CI, 1.18 to 4.34]). The risk for T-cell lymphoma was increased (HR, 3.51 [CI, 0.75 to 16.34]) but not for B-cell lymphoma (HR, 0.97 [CI, 0.21 to 4.49]). Limitation: No data on dietary adherence. Conclusion: Increased risk for LPM in CD is associated with the follow-up biopsy results, with a higher risk among patients with persistent villous atrophy. Follow-up biopsy may effectively stratify patients with CD by risk for subsequent LPM.
|
|
| 2. |
- Ludvigsson, Jonas F., 1969-, et al.
(författare)
-
Risk for Congenital Malformation With H1N1 Influenza Vaccine : A Cohort Study With Sibling Analysis
- 2016
-
Ingår i: Annals of Internal Medicine. - Philadelphia, USA : American College of Physicians. - 0003-4819 .- 1539-3704. ; 165:12, s. 848-855
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Earlier studies reporting varying risk estimates for congenital malformation in offspring of mothers undergoing vaccination against H1N1 influenza during pregnancy did not consider the potential role of confounding by familial (genetic and shared environmental) factors.Objective: To evaluate an association between maternal H1N1 vaccination during pregnancy and offspring malformation, with familial factors taken into account.Design: Population-based prospective study.Setting: Sweden.Participants: Liveborn offspring born between 1 October 2009 and 1 October 2011 to mothers receiving monovalent AS03-adjuvanted H1N1 influenza vaccine (Pandemrix [GlaxoSmithKline]) during pregnancy. A total of 40 983 offspring were prenatally exposed to the vaccine, 14 385 were exposed within the first trimester (14 weeks), and 7502 were exposed during the first 8 weeks of pregnancy. Exposed offspring were compared with 197 588 unexposed offspring. Corresponding risks in exposed versus unexposed siblings were also estimated.Measurements: Congenital malformation, with subanalyses for congenital heart disease, oral cleft, and limb deficiency.Results: Congenital malformation was observed in 2037 (4.97%) exposed offspring and 9443 (4.78%) unexposed offspring. Adjusted risk for congenital malformation was 4.98% in exposed offspring versus 4.96% in unexposed offspring (risk difference, 0.02% [95% CI, -0.26% to 0.30%]). The corresponding risk differences were 0.16% (CI, -0.23% to 0.56%) for vaccination during the first trimester and 0.10% (CI, -0.41% to 0.62%) for vaccination in the first 8 weeks. Using siblings as comparators yielded no statistically significant risk differences.Limitations: The study was based on live births, and the possibility that data on miscarriage or induced abortion could have influenced the findings cannot be ruled out. Study power was limited in analyses of specific malformations.Conclusion: When intrafamilial factors were taken into consideration, H1N1 vaccination during pregnancy did not seem to be linked to overall congenital malformation in offspring, although risk increases for specific malformations could not be ruled out completely.
|
|
