| 1. |
|
|
| 2. |
|
|
| 3. |
- Chong, K. Y., et al.
(författare)
-
A core outcome set for future research in ectopic pregnancy: an international consensus development study
- 2023
-
Ingår i: Fertility and Sterility. - : Elsevier BV. - 0015-0282. ; 119:5, s. 804-812
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: To address methodological deficiencies in published randomized controlled trials and systematic reviews, this study has developed a core outcome set to guide future research in ectopic pregnancy (EP).Design: To identify potential outcomes, we performed a comprehensive literature review and interviews with individuals with lived experience in EP. Potential core outcomes were then entered into a 3-round Delphi survey. A total of 154 participants from 6 continents, comprising health care professionals, researchers, and individuals with lived experience in EP, completed all 3 rounds of the Delphi survey. Outcomes were prioritized at 3 consensus development meetings, and recommendations were developed on how to report these outcomes where possible.Setting: Not applicable.Patient(s): Health care professionals, researchers, and individuals with lived experience in EP.Intervention(s): Not applicable.Main Outcome Measure(s): Consensus for inclusion in core outcome set.Result(s): Six outcomes reached full consensus, including treatment success, resolution time, the number of additional interventions, adverse events, mortality and severe morbidity, and treatment satisfaction.Conclusion(s): The core outcome set with 6 outcomes for EP will help standardize reporting of clinical trials, facilitate implementation of findings into clinical practice, and enhance patient-centered care. (Fertil Sterile 2023;119:804-12. (c) 2023 by American Society for Reproductive Medicine.) El resumen esta disponible en Espanol al final del articulo.
|
|
| 4. |
- Chong, K. Y., et al.
(författare)
-
A protocol for developing a core outcome set for ectopic pregnancy
- 2021
-
Ingår i: Trials. - : Springer Science and Business Media LLC. - 1745-6215. ; 22:1
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Randomised controlled trials (RCTs) evaluating ectopic pregnancy have reported many different outcomes, which are themselves often defined and measured in distinct ways. This level of variation results in an inability to compare results of individual RCTs. The development of a core outcome set to ensure outcomes important to key stakeholders are collected consistently will guide future research in ectopic pregnancy. Study aim: To develop and implement a core outcome set to guide future research in ectopic pregnancy. Methods and analysis: We have established an international steering group of key stakeholders, including healthcare professionals, researchers, and individuals with lived experience of ectopic pregnancy. We will identify potential outcomes from ectopic pregnancy from a comprehensive literature review of published randomised controlled trials. We will then utilise a modified Delphi method to prioritise outcomes. Subsequently, key stakeholders will be invited to score potential core outcomes on a nine-point Likert scale, ranging from 1 (not important) to 9 (critical). Repeated reflection and rescoring should promote whole and individual stakeholder group convergence towards consensus 'core' outcomes. We will also establish standardised definitions and recommend high-quality measurements for individual core outcomes.
|
|
| 5. |
|
|
| 6. |
- Nicoletti, Paola, et al.
(författare)
-
Association of Liver Injury From Specific Drugs, or Groups of Drugs, With Polymorphisms in HLA and Other Genes in a Genome-Wide Association Study
- 2017
-
Ingår i: Gastroenterology. - : W B SAUNDERS CO-ELSEVIER INC. - 0016-5085 .- 1528-0012. ; 152:5, s. 1078-1089
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS: We performed a genome-wide association study (GWAS) to identify genetic risk factors for druginduced liver injury (DILI) from licensed drugs without previously reported genetic risk factors. METHODS: We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs. RESULTS: We associated DILI with rs114577328 (a proxy for A* 33: 01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9 - 3.8; P = 2.4 x 10(-8)) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6 - 2.5; P = 9.7 x 10(-9)). The association with A* 33: 01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A* 33: 01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6 - 2.7; P = 4.8 x 10(-9)). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0 - 9.5; P = 7.1 x 10(-9)). We validated the association between A* 33: 01 terbinafine-and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224. CONCLUSIONS: In a GWAS of persons of European descent with DILI, we associated HLA-A* 33: 01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors.
|
|
