scholarly journals Venous Thrombosis Risk after Cast Immobilization of the Lower Extremity: Derivation and Validation of a Clinical Prediction Score, L-TRiP(cast), in Three Population-Based Case–Control Studies

PLoS Medicine ◽  
2015 ◽  
Vol 12 (11) ◽  
pp. e1001899 ◽  
Author(s):  
Banne Nemeth ◽  
Raymond A. van Adrichem ◽  
Astrid van Hylckama Vlieg ◽  
Paolo Bucciarelli ◽  
Ida Martinelli ◽  
...  
2014 ◽  
Vol 12 (9) ◽  
pp. 1461-1469 ◽  
Author(s):  
R. A. van Adrichem ◽  
J. Debeij ◽  
R. G. H. H. Nelissen ◽  
I. B. Schipper ◽  
F. R. Rosendaal ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1378
Author(s):  
Tú Nguyen-Dumont ◽  
James G. Dowty ◽  
Jason A. Steen ◽  
Anne-Laure Renault ◽  
Fleur Hammet ◽  
...  

Case-control studies of breast cancer have consistently shown that pathogenic variants in CHEK2 are associated with about a 3-fold increased risk of breast cancer. Information about the recurrent protein-truncating variant CHEK2 c.1100delC dominates this estimate. There have been no formal estimates of age-specific cumulative risk of breast cancer for all CHEK2 pathogenic (including likely pathogenic) variants combined. We conducted a population-based case-control-family study of pathogenic CHEK2 variants (26 families, 1071 relatives) and estimated the age-specific cumulative risk of breast cancer using segregation analysis. The estimated hazard ratio for carriers of pathogenic CHEK2 variants (combined) was 4.9 (95% CI 2.5–9.5) relative to non-carriers. The HR for carriers of the CHEK2 c.1100delC variant was estimated to be 3.5 (95% CI 1.02–11.6) and the HR for carriers of all other CHEK2 variants combined was estimated to be 5.7 (95% CI 2.5–12.9). The age-specific cumulative risk of breast cancer was estimated to be 18% (95% CI 11–30%) and 33% (95% CI 21–48%) to age 60 and 80 years, respectively. These findings provide important information for the clinical management of breast cancer risk for women carrying pathogenic variants in CHEK2.


2017 ◽  
Vol 17 (9) ◽  
pp. 965-973 ◽  
Author(s):  
Grant A Mackenzie ◽  
Philip C Hill ◽  
Shah M Sahito ◽  
David J Jeffries ◽  
Ilias Hossain ◽  
...  

Author(s):  
Jane Pirkis ◽  
Angela Nicholas ◽  
David Gunnell

Abstract Much of our knowledge about the risk factors for suicide comes from case–control studies that either use a psychological autopsy approach or are nested within large register-based cohort studies. We would argue that case–control studies are appropriate in the context of a rare outcome like suicide, but there are issues with using this design. Some of these issues are common in psychological autopsy studies and relate to the selection of controls (e.g. selection bias caused by the use of controls who have died by other causes, rather than live controls) and the reliance on interviewing informants (e.g. recall bias caused by the loved ones of cases having thought about the events leading up to the suicide in considerable detail). Register-based studies can overcome some of these problems because they draw upon contain information that is routinely collected for administrative purposes and gathered in the same way for cases and controls. However, they face issues that mean that psychological autopsy studies will still sometimes be the study design of choice for investigating risk factors for suicide. Some countries, particularly low and middle income countries, don't have sophisticated population-based registers. Even where they do exist, there will be variable of interest that are not captured by them (e.g. acute stressful life events that may immediately precede a suicide death), or not captured in a comprehensive way (e.g. suicide attempts and mental illness that do not result in hospital admissions). Future studies of risk factors should be designed to progress knowledge in the field and overcome the problems with the existing studies, particularly those using a case–control design. The priority should be pinning down the risk factors that are amenable to modification or mitigation through interventions that can successfully be rolled out at scale.


Blood ◽  
1995 ◽  
Vol 85 (10) ◽  
pp. 2756-2761 ◽  
Author(s):  
T Koster ◽  
FR Rosendaal ◽  
E Briet ◽  
FJ van der Meer ◽  
LP Colly ◽  
...  

A deficiency of protein C (PC), antithrombin, or protein S is strongly associated with deep-vein thrombosis in selected patients and their families. However, the strength of the association with venous thrombosis in the general population is unknown. This study was a population-based, patient-control study of 474 consecutive outpatients, aged less than 70 years, with a first, objectively diagnosed, episode of venous thrombosis and without an underlying malignant disease, and 474 healthy controls who matched for age and sex. Relative risks were estimated as matched odds ratios. Based on a single measurement, there were 22 (4.6%) patients with a PC deficiency (PC activity, less than 0.67 U/mL or PC antigen, less than 0.33 U/mL when using coumarins). Among the controls, the frequency was 1.5% (seven subjects). Thus, there is a threefold increase in risk of thrombosis in subjects with PC levels below 0.67 or 0.33 U/mL [matched odds ratio, 3.1; 95% confidence interval (CI), 1.4 to 7.0]. When a PC deficiency was based on two repeated measurements, the relative risk for thrombosis increased to 3.8 (95% CI, 1.3 to 10); when it was based on DNA-confirmation, the relative risk increased further to 6.5 (95% CI, 1.8 to 24). In addition, there was a gradient in thrombosis risk, according to PC levels. The results for antithrombin are similar to those for PC, although less pronounced (relative risk, 2.2; 95% CI, 1.0 to 4.7). We could not find an association between reduced total protein S (relative risk, 0.7; 95% CI, 0.3 to 1.8) or free protein S levels (relative risk, 1.6; 95% CI, 0.6 to 4.0) and thrombosis risk. Although not very frequent, PC and antithrombin deficiency are clearly associated with an increase in thrombosis risk.


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