Hyperandrogenism and Insulin Resistance in Pcos

Hyperandrogenism and Insulin Resistance in Polycystic Ovary Syndrome

Ilmary Jimenez

Florida International University

Hyperandrogenism and Insulin Resistance in Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) was originally described in medical literature in 1935 by Stein and Leventhal, their study presented seven patients who suffered from amenorrhea, obesity, hirsutism, engorged ovaries with multiple cysts and infertility. (Stein and Leventhal, 1935) Today research suggests PCOS is a common disease all around the globe with an incidence fluctuating from 5% to 10%. It is detected in females of childbearing age through all cultures, and ethnical backgrounds. (Azziz et al., 2004). Regardless of being multifactorial in its origin, the hallmark characteristics of the disease are hyperandrogenism and chronic anovulation. (Sheehan, 2004)

Pathophysiology

The two main hormonal abnormalities found in patients with PCOS include elevation of circulating levels of luteinizing hormone (LH) and insulin. The most acceptable hypothesis suggests a synergism between the two, which ends up causing in the ovary, follicular atresia and inability to Estrogen formation. In this context, the ovarian hyperstimulation due to insulin, would cause hyperandrogenism.

It is now known that apart from FSH and LH secreted by the pituitary gland, insulin and some other hormones are involved in regulating the ovarian function. Also, they have identified in the human ovary receptors for insulin and the growth factors similar to insulin type 1 (IGF-1), which are homologues of the receptors of insulin by 40% and, although with lower affinity, they join it in the presence of certain pathologies that occur with states of insulin resistance and compensatory hyperinsulinemia. As a vicious cycle, hyperinsulinemia increases training of IGF-1 receptors. the pituitary gland also contains receptors for insulin and under its stimulus the secretion of LH increases.

The paradoxical fact that in patients with insulin resistance, the ovary remains with a normal sensitivity and even increased insulin and manifest this hyperstimulation with an increase in the formation of androgens exclusively, it has been reason for numerous experimental studies. It is important to emphasize that the term resistance to Insulin refers to a decrease in your power biological in terms of glycemic control. Do not necessarily its efficiency is diminished in all tissues and in some places the compensatory hyperinsulinemia would lead to a hyperstimulation.

The hypothalamic-pituitary-adrenal axis also seems to be involved in the syndrome, since approximately in 40-70% of the cases. The circulating levels of some adrenal androgens with answers inappropriately high during the tests of stimulation with adrenocorticotropin (ACTH). This could be related to high levels of the cytochrome P450c17alpha ovarian enzyme, which is related to androgen biosynthesis and increases the levels of 17 alpha-hydroxyprogesterone. (McCance and Huether, 2014)

Diagnostic

PCOS can have clinical, endocrinological and metabolic manifestations, constituting a broad spectrum throughout life. In general, the diagnosis of PCOS is based mainly on the clinical history, but currently it is enough to have two of the following three criteria proposed in 2003 at the Rotterdam meeting: 1. Oligo-ovulation or anovulation. 2. Elevated levels of circulating androgens or clinical manifestations of excess ovarian androgens.3. Morphology of polycystic ovaries determined by ultrasound. (Sirmans and Pate, 2013)

Differential diagnosis and laboratory testing

Laboratory evaluation comprises the determination of the blood levels of total testosterone, fasting glucose, DHEAS, prolactin and FSH/LH ratio. The preferred and less expensive method to visually recognize the characteristics of enlarged polycystic ovaries is a transvaginal ultrasound or a transabdominal ultrasound for non-sexually active patients. Many disorders can manifest with symptoms and signs that are common to PCOS. We must rule out the presence of some pathologies, which although they are not frequent, they require management and specific treatments. In this group we include benign and malignant tumors of the adrenal glands and ovaries and congenital adrenal hyperplasia.