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  • The mechanism by which OC use leads to

    2020-03-06

    The mechanism by which OC use leads to impaired glucose tolerance is yet to be fully clarified. Decreased insulin sensitivity appears to be mainly accounted for by estrogenic component and this effect may be modified by progestogenic component [14], [15]. Estrogenic effect on glucose tolerance has been suggested to be associated with decreased pancreatic β-cell response to rising glucose, thereby delaying the release of insulin. An increase in insulin clearance, with consequent decrease in glucose disposal by peripheral tissues, may also be involved [28], [40]. Others suggest that cantharidin increases hepatic insulin elimination, with no compensatory increase in the original pancreatic insulin response, resulting in a relative reduction in the initial plasma insulin level. This would result in a reduction in the glucose elimination and an overall rise in glucose concentrations [14], [41]. The unfavourable lipid profile associated with glucose intolerance or insulin resistance syndrome is characterized by elevated triglyceride, low HDL-cholesterol with normal or elevated LDL cholesterol levels [42]. Many studies have established the importance of low HDL cholesterol as well as high triglyceride as a strong independent predictor of the development of atherosclerotic cardiovascular diseases (CVD) [42], [43], [44]. Besides altering glucose tolerance in this animal model, estrogen–progestogen OC at high dose led to an increase in TG and a decrease in HDL-cholesterol, while combined estrogen–progestogen OC at low dose resulted in an increase in TG only. With exposure to estrogen, hepatic synthesis and secretion of TG-rich particles increase [45], [46], and Hokanson and Austin reported that especially in women, elevation in TG is associated with an increased risk of cardiovascular disease, even after adjusting for HDL-cholesterol levels. Hence, inducing an increase in TG level with or without a decrease HDL-cholesterol levels during estrogen–progestogen use may be deteriorating cardiovascular diseases associated with glucose intolerance. It is noteworthy that incidence of atherosclerotic CVD is a principal challenge in patients with impaired glucose tolerance, accounting for clinical complications leading to increased mortality [19], [42]. These results further suggest that OC-associated increased cardiovascular risk factors might be estrogen- but not progestogen-dependent in a dose-related manner. Hence, reduction in estrogen dose may help to minimise the OC impact on cardiovascular risk factors.
    Introduction Among the different methods of contraception, oral contraceptives are the most widely used, with 38.5% of women of reproductive age in Germany and over 60% of all women between the ages of 16 and 30 years utilizing them [1]. Oral contraceptives contain synthetic derivatives of natural female sex hormones. The majority of contraceptives contain ethinylestradiol as the estrogen component and one of the many synthetic progestogens, mostly derived from 17α-hydroxyprogesterone and 19-nortestosterone. Various side effects of oral contraceptives, including headache, nausea, edema, breast tenderness and pigmentary disorders, are due to the estrogen component, whereas tiredness, depression and loss of libido are attributed to the progestogens [2]. Melasma (synonym: chloasma) is a cosmetically undesirable side effect of the intake of contraceptives characterized by a hyperpigmentation of the skin due to an increase in the activity of melanogenic enzymes and in the number of melanocytes in the epidermis as demonstrated histologically [3], [4]. Clinically, melasma appears symmetrically as brownish patches at sun-exposed areas of the face (i.e., forehead, temples and cheeks). The development of melasma seems to be the consequence of increased levels of estrogen combined with exposure to sunlight and a genetic predisposition. Approximately 10–20% of all women taking oral contraceptives develop melasma (chloasma hormonale). Other commonly known trigger factors for melasma are pregnancy and certain ovarian tumors. Melasma in pregnancy (chloasma gravidarum) usually comes together with hyperpigmentation of the linea alba, areolae and genitals. It typically resolves spontaneously after birth [5]. Treatment for melasma is limited and includes discontinuing the intake of hormones, camouflage and using broad-spectrum sunscreens for prevention [6]. Topical skin bleaching with the help of hydrochinone, tretinoin or azelaic acid [7] can be tried — at present, the triple combination of hydrochinone, tretinoin and fluocinolone acetonide seems to be most promising [8], [9].