Subject(s)
Dysplastic Nevus Syndrome/pathology , Early Detection of Cancer/statistics & numerical data , Melanoma/epidemiology , Skin Neoplasms/epidemiology , Adult , Biopsy , Case-Control Studies , Dermoscopy , Disease Progression , Early Detection of Cancer/standards , Female , Follow-Up Studies , Humans , Male , Melanoma/diagnosis , Melanoma/etiology , Melanoma/pathology , Middle Aged , Netherlands/epidemiology , Practice Guidelines as Topic , Risk Factors , Skin/diagnostic imaging , Skin/pathology , Skin/radiation effects , Skin Neoplasms/diagnosis , Skin Neoplasms/etiology , Skin Neoplasms/pathology , Skin Pigmentation , Ultraviolet Rays/adverse effects , Young AdultSubject(s)
Melanoma/diagnosis , Skin Neoplasms/diagnosis , Adolescent , Adult , Aged , Aged, 80 and over , Ambulatory Care , Diagnosis, Differential , Female , Humans , Male , Middle Aged , Pigmentation Disorders/diagnosis , Prospective Studies , Risk Factors , Young AdultABSTRACT
BACKGROUND: Previous analyses reported a higher risk of recurrent venous thrombosis in men than women. OBJECTIVES: We aimed to assess the risk of recurrence in men compared with women whilst taking female reproductive risk factors (oral contraception, postmenopausal hormone therapy and pregnancy) into account. In addition, we hypothesized that the sex difference in venous thrombosis was related to F9 Malmö, an X-linked prothrombotic factor. METHODS: In four pooled European cohorts (CARROT study, Glasgow, UK; CVTE study, Cambridge, UK; AUREC study, Vienna, Austria; and LETS follow-up study, Leiden, the Netherlands), the risk of recurrent venous thrombosis was calculated in men, women with reproductive risk factors and women without reproductive risk factors at the time of their first venous thrombosis. F9 Malmö was genotyped and carriers and non-carriers contrasted. RESULTS: In total, 2185 patients with a first venous thrombosis, 1043 men and 1142 women, were included. Overall, men had a 2.8-fold (95% confidence interval [CI], 2.2-3.4) higher risk of recurrent venous thrombosis than women. This risk was 5.2-fold (95% CI, 3.5-7.7) higher in men than in women with reproductive risk factors, and 2.3-fold (95% CI, 1.7-3.2) higher in men than in women without reproductive risk factors. No difference in risk of recurrence was found for carriers vs. non-carriers of F9 Malmö. CONCLUSION: Men experienced a recurrent venous thrombosis twice as often as women without reproductive risk factors. These findings indicate that men have a higher intrinsic risk of venous thrombosis than women, which is partly masked by female reproductive risk factors. The sex difference cannot be explained by F9 Malmö.
Subject(s)
Factor IX/genetics , Health Status Disparities , Venous Thrombosis/epidemiology , Adolescent , Adult , Aged , Aged, 80 and over , Blood Coagulation/genetics , Europe/epidemiology , Female , Genetic Predisposition to Disease , Humans , Male , Middle Aged , Mutation , Phenotype , Prospective Studies , Recurrence , Risk Assessment , Risk Factors , Sex Factors , Venous Thrombosis/diagnosis , Venous Thrombosis/genetics , Young AdultSubject(s)
Gene-Environment Interaction , Sex Factors , Venous Thrombosis/genetics , Venous Thrombosis/physiopathology , Female , Humans , MaleABSTRACT
Men have a higher risk of first and recurrent venous thrombosis than do women. However, the pathophysiology underlying this phenomenon is as yet unknown. In this review article, we assessed the prevalence and strength of genetic and acquired risk factors for venous thrombosis for men and women separately, because it is likely that either a difference in effect or distribution of a risk factor explains the risk difference between the sexes. We also summarized the sex-specific results of previous studies on the risk of first and recurrent venous thrombosis. Few explanations for the sex difference were found. The major factor, explaining about 20% difference in population-attributable fraction, was body height. No difference in prevalence or strength for other venous thrombosis risk factors was observed, such as plaster cast immobilization, hospitalization, surgery, trauma, malignancy, hyperhomocysteinemia, factor V Leiden, prothrombin G20210A, or blood group non-O. Alternative explanations for the sex difference are hypothesized in this review, including X- or Y-linked mutations or a mutation on a gene with a sex-specific effect. Future studies should focus on the sex-specific risk of venous thrombosis to unravel the pathophysiology and thereby improve sex-specific treatment and prevention strategies. Even so, male sex can be used as a tool through which individuals at increased risk of first or recurrent venous thrombosis may be identified.
Subject(s)
Gene-Environment Interaction , Sex Factors , Venous Thrombosis/diagnosis , Venous Thrombosis/genetics , ABO Blood-Group System , Adolescent , Adult , Aged , Anticoagulants/chemistry , Blood Coagulation , Body Height , Factor V/genetics , Female , Humans , Incidence , Male , Middle Aged , Mutation , Prevalence , Prothrombin/genetics , Recurrence , Research Design , Risk Factors , Young AdultABSTRACT
BACKGROUND: Oral contraception (OC) and postmenopausal hormone therapy (HT) can be used to alleviate menopausal symptoms. However, the risk of venous thrombosis (VT) associated with OC use in women over 50 years old has never been assessed and the two preparations have not been directly compared. OBJECTIVES: To determine and compare the risk of VT associated with OC and HT use. METHODS: From a large case-control study, 2550 women aged over 50 years old, 1082 patients with a first VT and 1468 controls, were included. Odds ratios (ORs) and 95% confidence intervals for VT were calculated for OC-users (164 patients and 54 controls) and HT-users (88 patients and 102 controls) compared with non-hormone users (823 patients and 1304 controls). RESULTS: OC-users had a 6.3-fold (4.6-9.8) increased risk of VT. This ranged from 5.4 (3.3-8.9) for preparations containing levonorgestrel to 10.2 (4.8-21.7) for desogestrel. The VT-risk associated with oral HT use was 4.0 (1.8-8.2) for conjugated equine estrogen combined with medroxyprogesterone acetate and 3.9 (1.5-10.7) for micronized estradiol combined with norethisterone acetate. Non-oral HT did not increase the risk of VT: OR 1.1 (0.6-1.8). Relative risk estimates were further increased in hormone users with factor V Leiden, prothrombin G20210A or blood group non-O and hormone users with a family history of VT. CONCLUSIONS: In this study, non-oral HT seemed to be the safest hormonal preparation in women over 50 years old. OC use increased the VT risk the most, especially in women with inherited thrombophilia or a family history of VT.
Subject(s)
Contraceptives, Oral, Hormonal/adverse effects , Estrogen Replacement Therapy/adverse effects , Estrogens/adverse effects , Progestins/adverse effects , Venous Thrombosis/chemically induced , Administration, Cutaneous , Age Factors , Aged , Case-Control Studies , Desogestrel/adverse effects , Estradiol/adverse effects , Estrogens/administration & dosage , Estrogens, Conjugated (USP)/adverse effects , Female , Humans , Levonorgestrel/adverse effects , Logistic Models , Medroxyprogesterone Acetate/adverse effects , Middle Aged , Netherlands/epidemiology , Norethindrone/adverse effects , Norethindrone/analogs & derivatives , Norethindrone Acetate , Odds Ratio , Postmenopause , Progestins/administration & dosage , Risk Assessment , Risk Factors , Sex Factors , Transdermal Patch , Venous Thrombosis/diagnosis , Venous Thrombosis/epidemiologyABSTRACT
BACKGROUND: Coffee consumption is associated with a lower risk of venous thrombosis, but the role of confounding and the pathophysiology behind these findings are unclear. OBJECTIVE: To assess the role of hemostatic factors in the relationship between coffee consumption and venous thrombosis. METHODS: From a large case-control study, 1803 patients with a first venous thrombosis and 1803 partner controls were included. With conditional logistic regression, odds ratios (ORs) and 95% confidence intervals (CIs) for venous thrombosis were calculated for coffee consumption vs. no coffee consumption. In addition, mean differences in hemostatic factor levels between these groups were calculated in the controls. RESULTS: Coffee consumption yielded a 30% lower risk of venous thrombosis than no coffee consumption (OR 0.7, 95% CI 0.5-0.9). Adjustment for several putative confounders (age, sex, body mass index, smoking, hormonal factors, statin, aspirin, alcohol, malignancy, and chronic disease) yielded an OR of 0.8 (95% CI 0.6-1.1). Results were similar for provoked and unprovoked events, and for deep vein thrombosis and pulmonary embolism. In controls, von Willebrand factor levels were 11 (3-19) IU dL(-1) lower and factor (F) VIII levels were 11 (1-21) IU dL(-1) lower in coffee consumers than in non-consumers. After adjustment of the risk estimates for these hemostatic factors, the inverse association between coffee consumption and venous thrombosis diminished (OR 1.0, 95% CI 0.7-1.4). There was no association between coffee consumption and anticoagulant proteins, fibrinogen levels, or fibrinolytic markers. CONCLUSIONS: Coffee consumption is associated with a lower risk of venous thrombosis, which seems to be mediated through von Willebrand factor and FVIII.
