In fact, in the veins progestins may increase the capacitance resulting in a decrease blood flow[48,49]. Modification in hemostasis parameters seems to depend to type and dose of progestogen, the presence of estrogen compound and the duration of use[57,85,86].
The risk of combined formulation could be a consequence of vascular action of progestins. In fact, it seems that some progestins may up-regulate thrombin receptor expression while, other progestins did not..
Definitive conclusions about the significance of these findings have not yet achieved. In this light, the prudent choice of hormonal regimen could be recommended.
Adverse Effects of Hormonal contraception
- Cardiovascular Effects
- - Myocardial Infarction
- - Stroke
- - Arterial Accidents
- - Venous Thromboembolism
- - Blood Hypertension
- Other Effects
- - Angioedema
- - Peliosis Hepatis
- - Severe Adverse Ocular Reactions
- - Vasculitis
- Moderate adverse effects
- Cancer Risks
- - Breast cancer risk
- - Ovarian cancer risk
- - Endometrial cancer risk
- - Cervical cancer risk
- - Colorectal cancer risk
- - Skin cancer risk
- - Liver cancer risk
- - Pancreatic cancer risk
- - Neurofibromas growth
- - Unclear cancer risks
- Hazardous prescription
- Hormonal contraception in female transplant recipients
- - Hormonal contraception in female kidney recipients
- - Hormonal contraception in female liver transplant recipients
- - Hormonal contraception in female heart transplant recipients
- - Contraception in women HIV infected
- Mild Adverse effects
- New Perspectives immunocontraception
- Contraceptive counseling
Using progestins with minimal vascular toxicity may lead to relative safety of estrogen-progestin preparations for pre-menopausal women, also HHT-affected.
Desogestrel is less androgenic than previous generations of synthetic progestins. Consequently, when the dose of EE in HC was reduced, the potency of progestagens was increased.
Moreover, progestagens with no or reduced androgenic activity were preferred for use in HC with respect to lipid and carbohydrate metabolism (87).
A beneficial effect of these progestins on the coagulation factors is less apparent. It has been suggested that with a reduced androgenic effect of the progestins, the activity of ethinylestradiol is more sensible, since the estrogens are the source of disturbance in coagulation factors.
The third generation of progestins does not appear to represent an advance in reducing arterial accidents, whereas the reduction from 50 to 30 mcg of ethinylestradiol did in reducing venous pathology.
Moreover, the crude rate of VTE per 10.000 woman years was 4.10 in current users : 3.10 in users of second-generation HCs,and 4.96 in users of third- generation HCs. Among users of third generation progestagens, the risk of VTE was higher in users of desogestrel (DSG) with 20 mcg EE than in users of gestodene or desogestrel with 30 mcg EE. The odds-ratio for VTE was estimated 3.49 in the first case and 1.18 for the others. (86,87).
The risk of VTE in users of desogestrel-containing HCs is significantly elevated compared to that of LNG –containing HCs. While, the risk of VTE in users of norgestimate-containing HCs was similar to that of users of LNG-containing HCs. (88,89).
Unexpected idiopathic cardiovascular death rates among 303.470 women who were current HCs, users were 4.3/100.000 for LNG,1.5/100.000 for desogestrel (DSG) and 4.8/100.000 for gestodene. When compared with LNG the relative risk adjusted for age and calendar period was 0.4 for DSG and 1.4 for gestodene HCs (86,87).
The studies carried out on women with and without family history of thrombosis and /or carrier of the factor V Leiden mutation treated with DSG-containing HCs reported the same risk of deep–vein-thrombosis (DVT).
This risk resulted higher of 2.2-fold when compared with LNG-containing HCs with the same amount of EE and it was highest in the youngest age categories (82,90,91,92).