Second Chapter
Dr. Álvaro Monterrosa Castro, MD
Hormonal synthetic steroids
Hormonal synthetic steroids are related to the risk of developing impaired glucose tolerance by inducing insulin resistance (83).
Glucose intolerance is characterized by normal fasting blood glucose values plus postprandial hyperglycemia, but the risk of developing diabetes appears to be negligible.
Glucose intolerance has been associated with coronary heart disease, high blood pressure, dyslipoproteinemia, and obesity.
Combined oral contraceptives, mainly old macrodose ones, can cause glucose intolerance, hyperinsulinemia, increased LDL-cholesterol, hypertriglyceridemia, decreased HDL-cholesterol, hypertension and increased fatty tissue.
Progestin is mainly responsible for alterations in carbohydrate metabolism, but the estrogenic component can modulate this adverse influence, the impact being different. The hormonal dose provided and the steroids used are important.
The third generation progestins: Gestodene, Norgestimate and Desogestrel, induce mild changes in the first three cycles, which have no clinical significance (83) and tend to disappear with continued use and, therefore, should not increase the risk of atherogenesis. (13.33).
Burkman et al (128) in users of norgestimate plus triphasic ethinyl estradiol studied glycemia, insulin and the A-10 subunit of glycosylated hemoglobin, before starting the contraceptive and at the end of the third, sixth, twelfth and second cycles. twenty fourth.
Alteration in carbohydrate metabolism
The glycemic and insulin data indicate some evidence of alteration in carbohydrate metabolism in the first 12 cycles, but thereafter there appears to be a very minimal effect.
No changes were observed in glycosylated hemoglobin, which suggests that norgestimate has very little effect on carbohydrate metabolism (13,128).
Dueñas Díez (86) also asserts when noting that oral contraceptives with doses of less than 50 Ug/day of ethinyl estradiol, combined with small amounts of progestins and especially third generation ones (gestodene, desogestrel), slightly modify glucose tolerance and the response to insulin, without modifying the concentrations of glycosylated hemoglobin.
These variations have no clinical significance in a normal woman without prior risk.
Oral contraceptives should not be administered to patients with established diabetes and precautions should be taken in patients with a history of gestational diabetes, obesity, and first-degree relatives with a diagnosis of diabetes mellitus. However, Petersen et al (133) consider that opinions on the use of oral contraceptives in patients with insulin-dependent diabetes mellitus (IDDM) are found.
They compared patients with well-controlled IDDM who received desogestrel/ethinyl estradiol with other patients with the same pathology who used non-hormonal methods.
Evaluated at the first, third, sixth and twelfth cycle of use of the combined oral contraceptive, no changes were found in blood pressure, bone mass index and glycemic controls. They suggest (133) that since no adverse alterations related to cardiovascular risks have been observed, well-controlled diabetic patients could receive microdose, very low dose or ultra low dose oral contraceptives.
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Patients with a recent history of gestational diabetes
With respect to patients with a recent history of gestational diabetes, who do not breastfeed, Kjos et al (134), based on a study carried out in Latin women, stated that in the long term the use of very low-dose combined oral contraceptives does not increase the risk of type 2 diabetes, compared to women who use non-hormonal contraception, also asserts Dueñas Díez (86).
After six cycles of use of 30 ug/day of ethinyl estradiol plus 2 mg/day of dienogest, studies indicate that there are no significant changes in blood glucose, insulin, and glycosylated hemoglobin. The oral glucose tolerance test is also not usually modified.
All of this is explained by the lack of affinity of dienogest to the androgen receptor. The androgenic capacity of progestin is what usually induces insulin resistance through a decrease in insulin or a reduction in the sensitivity of the receptors (56,135).
Dr. Álvaro Monterrosa Castro, MD
