CHAPTER ONE
1.0 INTRODUCTION
Oral contraceptives are among the most widely used prescription medications all over the world. The goal of oral contraceptive therapy is to use a preparation that will minimize complications and side effects yet still prevent pregnancy (Dosseter, 1995).
In general, the estrogen component of oral contraceptives blocks ovulation by inhibiting the release of follicle-stimulating hormone (FSH) and leutinizing hormone (LH) via negative feedback on the pituitary gland and hypothalamus (Bacon and Shenfield, 1990). The progestin component of oral contraceptives increases the viscosity of the cervical fluid, changes the endometrial lining to make it unsuitable for egg implantation, and provides some anti-ovulatory action. To be effective, oral contraceptives must have adequate circulating concentrations of active hormone to prevent ovulation (DeSano and Hurley, 1990). In general, estrogens are present in very low concentrations (pg/ml) and sensitive and specific assays have only recently become available. Through these assays, it has become evident that even without any significant drug interactions; there is tremendous variation in plasma concentrations of active hormone among women (Bainton, 1996).
It is likely that women who have the lowest concentrations of estrogen are most likely to suffer interactions with other drugs. Though it is the most effective form of reversible contraception, oral contraceptives, like any medication, are not 100% effective, and many women conceive while taking these preparations (Back et al., 1998). When taken correctly, they reduce the chance of pregnancy to less than 1%. The reported failure rate among United States women is approximately3%. In the teenage population, the failure rate can be as high as 8%, often attributed to missed doses (Back et al., 1998).
The most common causes of the pregnancies are thought to be missed pills, mal-absorption, and drug interactions. Oral contraceptives are not without side effects. The most critical side effect of the estrogen component is an increased risk of venous throboembolytic disease (Bacon and Shenfield, 1990). The progestin component has been associated with increases in blood pressure, serum glucose, and serum lipid levels. An increased risk of myocardial infarction and stroke has been reported in oral contraceptive users who smoke and are greater than 35 years of age. These significant adverse effects have led to the development of pills with reduced dosages of both estrogen and progestin components (Bacon and Shenfield, 1990; Dosseter, 1995).
Ethinyl estradiol (EE)is aderivative of 17β-estradiol (E2), the major endogenous estrogen inhumans. EE is an orally bioactive estrogen used in manyformulations of combined oral contraceptive pills. It is one of themost commonly used medications for this purpose (Maisel and Albert, 1995). Transdermal ethinyl estradiol carries a greater risk of clotformation and venous thrombo–embolism than 17 beta estradiol,which some have theorized to be related to different amounts ofhepatic metabolism after absorption. The same contraindicationsand precautions apply for EE as with other estrogen medications.Estinyl was a preparation of EE alone that was used for themanagement of menopausal symptoms and female hypogonadism (Djerassi and Carl, 2006). EE is released into the environment as a xenoestrogen from theurine and feces of people who take it as a medication.The major concern with unopposed estrogen is of endometrialcancer. As such, the medication is generally prescribed withprogesterone in the setting of birth control (Inhoffen and Hohlweg, 1998).
1.1 AIM OF STUDY
The aim of this study is to investigate the modulating effects ethanoic extract of mistletoe and ethinyl estradiol on serum lipid profile, aromatase and uterine morphological changes in female albino rats.