To compare the effects of oral and transdermal contraceptives containing similar hormone formulations on vascular risk markers.
We conducted a randomized, investigator-blinded, crossover, clinical trial with 24 healthy women, aged 18-35 years, who received 2 months of transdermal or oral contraceptive, 2 months washout, then 2 months of the alternative medication. The transdermal contraceptive contained 0.75 mg ethinyl estradiol and 6 mg norelgestromin. The oral contraceptive contained 35 mcg ethinyl estradiol and 250 mcg norgestimate. Blood samples taken before and after each treatment were analyzed in batch for D-dimer, von Willebrand factor, factor VIII, total and free protein S, antithrombin, fibrinogen, C-reactive protein, and normalized activated protein C sensitivity ratio (nAPCsr) determined with two thrombin generation-based assays, the alpha2macroglobulin-thrombin end point method (alpha2M-IIa) and calibrated automated thrombinography. Repeated measures analysis of variance was used for analysis.
For both contraceptives (transdermal, oral) there were significant declines in free (19%, 11%) and total protein S (19%, 13%) and antithrombin (13%, 10%); increases in fibrinogen (8%, 10%), C-reactive protein (220%, 292%), nAPCsr alpha2M-IIa (81%, 61%), and nAPCsr calibrated automated thrombinography (102%, 68%), all P<.05. Transdermal contraceptives had a greater effect than oral contraceptives on free protein S (P=.07), nAPCsr alpha2M-IIa (P=.06), and nAPCsr calibrated automated thrombinography (P=.03).
Oral and transdermal contraception with similar hormones had similar adverse effects on vascular risk markers. This suggests that this transdermal contraceptive has at least a similar thrombosis risk as its oral counterpart.
ClinicalTrials.gov, www.clinicaltrials.gov, NCT00554632
"Podczas przyjmowania antykoncepcji doustnej prawidłowy poziom niemal wszystkich białek układu krzepnięcia zostaje zaburzony. Nawet nieduże odstępstwo od normy jednego białka układu krzepnięcia zaburza delikatną równowagę i może powodować uruchomienie całej kaskady układu krzepnięcia i fibrynolizy     . Janczewski i wsp. "
[Show abstract][Hide abstract] ABSTRACT: IntroductionThe aim of the study was to evaluate the correlation between hormonal contraceptives and sex hormones levels as a possible cause of vertigo related to coagulation disorders and fibrinolyse.Material and methodsThe study was conducted on 25 female patients aged 23–39, who were treated at the Department of Otolaryngology and Laryngological Oncology, Medical University of Lodz, due to vertigo. The studied patients were divided into 3 groups: I – 7 women that used hormonal contraceptives; II – 9 women that no used hormonal contraceptives for the last 6 months; III – 9 women who never used contraceptives. The methodology included: an otoneurological and audiological examination, blood tests, levels of fibrinogen, D-dimers, APTT, PT, ALAT, ASPAT and BMI, estradiol and progesterone levels.ResultsIn 16 out of the 25 patients the obtained results diverged from normal sex hormones concentration in serum. In each studied group the relation between sex hormones concentration in serum and coagulation and fibrinolyse parameters was proved. The correlation between an increased concentration progesterone and D-dimers was found.Conclusions
An increased concentration of estrogens in serum may have an additional negative effect on a possibility of a thromboembolic episode. In the female patients interested in oral contraception, the prophylactic exclusion of risk factors for a thromboembolic disease seems to be vital.
Otolaryngologia polska. The Polish otolaryngology 02/2013; 67(1):25–29. DOI:10.1016/j.otpol.2012.09.008
"Despite intensive research, the underlying mechanisms of the OC-induced VT remained obscure for a long time. It appeared that OC use causes changes in plasma levels of almost all proteins involved in coagulation and fibrinolysis     . These changes are relatively modest and may have synergistic as well as opposing effects. "
[Show abstract][Hide abstract] ABSTRACT: The use of oral contraceptives (OC) is a well established risk factor for venous thrombosis. It has been known for many years that almost all haemostatic parameters i.e. plasma levels of coagulation factors, anticoagulant proteins and proteins involved in the fibrinolytic pathway change during OC use. The discovery of several risk factors of venous thrombosis in the 1990s shed new light on the association between the effects of OC on the haemostatic system and the increased risk of venous thrombosis. In this review, we summarize the current knowledge on the effects of different kinds of hormonal contraceptives (OC, transdermal contraceptives, vaginal ring and levonorgestrel-releasing intrauterine device) on haemostatic variables and the relationship between the changes of these variables and the risk of venous thrombosis.
Thrombosis Research 02/2010; 126(1):5-11. DOI:10.1016/j.thromres.2010.01.045 · 2.45 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The pathogenesis of atherosclerosis involves both hemostatic and inflammatory mechanisms. Fibrinogen is associated with both risk of thrombosis and inflammation. A recent meta-analysis showed that risk of coronary heart disease may increase 1.8 fold for 1 g/L of increased fibrinogen, independent of traditional risk factors. It is known that fibrinogen levels may be influenced by demographic, environmental and genetic factors. Epidemiologic and candidate gene studies are available; but few genome-wide linkage studies have been conducted, particularly in minority populations. The Strong Heart Study has demonstrated an increased incidence of cardiovascular disease in the American Indian population, and therefore represents an important source for genetic-epidemiological investigations.
The Strong Heart Family Study enrolled over 3,600 American Indian participants in large, multi-generational families, ascertained from an ongoing population-based study in the same communities. Fibrinogen was determined using standard technique in a central laboratory and extensive additional phenotypic measures were obtained. Participants were genotyped for 382 short tandem repeat markers distributed throughout the genome; and results were analyzed using a variance decomposition method, as implemented in the SOLAR 2.0 program.
Data from 3535 participants were included and after step-wise, linear regression analysis, two models were selected for investigation. Basic demographic adjustments constituted model 1, while model 2 considered waist circumference, diabetes mellitus and postmenopausal status as additional covariates. Five LOD scores between 1.82 and 3.02 were identified, with the maximally adjusted model showing the highest score on chromosome 7 at 28 cM. Genes for two key components of the inflammatory response, i.e. interleukin-6 and "signal transducer and activator of transcription 3" (STAT3), were identified within 2 and 8 Mb of this 1 LOD drop interval respectively. A LOD score of 1.82 on chromosome 17 between 68 and 93 cM is supported by reports from two other populations with LOD scores of 1.4 and 1.95.
In a minority population with a high prevalence of cardiovascular disease, strong evidence for a novel genetic determinant of fibrinogen levels is found on chromosome 7 at 28 cM. Four other loci, some of which have been suggested by previous studies, were also identified.
BMC Medical Genetics 02/2008; 9(1):77. DOI:10.1186/1471-2350-9-77 · 2.08 Impact Factor
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