| 1. |
- Dahlqvist, Johanna, 1979-, et al.
(författare)
-
Identification and functional characterization of a novel susceptibility locus for small vessel vasculitis with MPO-ANCA
- 2022
-
Ingår i: Rheumatology. - Oxford, United Kingdom : Oxford University Press (OUP). - 1462-0324 .- 1462-0332. ; 61:8
-
Tidskriftsartikel (refereegranskat)abstract
- Objective To identify and characterize genetic loci associated with the risk of developing ANCA-associated vasculitides (AAV). Methods Genetic association analyses were performed after Illumina sequencing of 1853 genes and subsequent replication with genotyping of selected single nucleotide polymorphisms in a total cohort of 1110 Scandinavian cases with granulomatosis with polyangiitis or microscopic polyangiitis, and 1589 controls. A novel AAV-associated single nucleotide polymorphism was analysed for allele-specific effects on gene expression using luciferase reporter assay. Results PR3-ANCA(+) AAV was significantly associated with two independent loci in the HLA-DPB1/HLA-DPA1 region [rs1042335, P = 6.3 x 10(-61), odds ratio (OR) 0.10; rs9277341, P = 1.5 x 10(-44), OR 0.22] and with rs28929474 in the SERPINA1 gene (P = 2.7 x 10(-10), OR 2.9). MPO-ANCA(+) AAV was significantly associated with the HLA-DQB1/HLA-DQA2 locus (rs9274619, P = 5.4 x 10(-25), OR 3.7) and with a rare variant in the BACH2 gene (rs78275221, P = 7.9 x 10(-7), OR 3.0), the latter a novel susceptibility locus for MPO-ANCA(+) granulomatosis with polyangiitis/microscopic polyangiitis. The rs78275221-A risk allele reduced luciferase gene expression in endothelial cells, specifically, as compared with the non-risk allele. Conclusion We identified a novel susceptibility locus for MPO-ANCA(+) AAV and propose that the associated variant is of mechanistic importance, exerting a regulatory function on gene expression in specific cell types.
|
|
| 2. |
- Djarv, T., et al.
(författare)
-
Traumatic cardiac arrest in Sweden 1990-2016 : a population-based national cohort study
- 2018
-
Ingår i: Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. - : BioMed Central (BMC). - 1757-7241. ; 26
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Trauma is a main cause of death among young adults worldwide. Patients experiencing a traumatic cardiac arrest (TCA) certainly have a poor prognosis but population-based studies are sparse. Primarily to describe characteristics and 30-day survival following a TCA as compared with a medical out-of-hospital cardiac arrest (medical CA). Methods: A cohort study based on data from the nationwide, prospective population-based Swedish Registry for Cardiopulmonary Resuscitation (SRCR), a medical cardiac arrest registry, between 1990 and 2016. The definition of a TCA in the SRCR is a patient who is unresponsive with apnoea where cardiopulmonary resuscitation and/or defibrillation have been initiated and in whom the Emergency Medical Services (EMS, mainly a nurse-based system) reported trauma as the aetiology. Outcome was overall 30-day survival. Descriptive statistics as well as multivariable logistic regression models were used. Results: In all, between 1990 and 2016, 1774 (2.4%) cases had a TCA and 72,547 had a medical CA. Overall 30-day survival gradually increased over the years, and was 3.7% for TCAs compared to 8.2% following a medical CA (p < 0.01). Among TCAs, factors associated with a higher 30-day survival were bystander witnessed and having a shockable initial rhythm (adjusted OR 2.67, 95% C.I. 1.15-6.22 and OR 8.94 95% C.I. 4.27-18.69, respectively). Discussion: Association in registry-based studies do not imply causality but TCA had short time intervals in the chain of survival as well as high rates of bystander-CPR. C onclusion: In a medical CA registry like ours, prevalence of TCAs is low and survival is poor. Registries like ours might not capture the true incidence. However, many individuals do survive and resuscitation in TCAs should not be seen futile.
|
|
| 3. |
- Hofmann, Robin, et al.
(författare)
-
Oxygen therapy in suspected acute myocardial infarction
- 2017
-
Ingår i: New England Journal of Medicine. - : MASSACHUSETTS MEDICAL SOC. - 0028-4793 .- 1533-4406. ; 377:13, s. 1240-1249
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The clinical effect of routine oxygen therapy in patients with suspected acute myocardial infarction who do not have hypoxemia at baseline is uncertain. METHODS: In this registry-based randomized clinical trial, we used nationwide Swedish registries for patient enrollment and data collection. Patients with suspected myocardial infarction and an oxygen saturation of 90% or higher were randomly assigned to receive either supplemental oxygen (6 liters per minute for 6 to 12 hours, delivered through an open face mask) or ambient air. RESULTS: A total of 6629 patients were enrolled. The median duration of oxygen therapy was 11.6 hours, and the median oxygen saturation at the end of the treatment period was 99% among patients assigned to oxygen and 97% among patients assigned to ambient air. Hypoxemia developed in 62 patients (1.9%) in the oxygen group, as compared with 254 patients (7.7%) in the ambient-air group. The median of the highest troponin level during hospitalization was 946.5 ng per liter in the oxygen group and 983.0 ng per liter in the ambient-air group. The primary end point of death from any cause within 1 year after randomization occurred in 5.0% of patients (166 of 3311) assigned to oxygen and in 5.1% of patients (168 of 3318) assigned to ambient air (hazard ratio, 0.97; 95% confidence interval [CI], 0.79 to 1.21; P=0.80). Rehospitalization with myocardial infarction within 1 year occurred in 126 patients (3.8%) assigned to oxygen and in 111 patients (3.3%) assigned to ambient air (hazard ratio, 1.13; 95% CI, 0.88 to 1.46; P=0.33). The results were consistent across all predefined subgroups. CONCLUSIONS: Routine use of supplemental oxygen in patients with suspected myocardial infarction who did not have hypoxemia was not found to reduce 1-year all-cause mortality. (Funded by the Swedish Heart–Lung Foundation and others; DETO2X-AMI ClinicalTrials.gov number, NCT01787110.)
|
|
| 4. |
|
|
| 5. |
|
|
