Hyperandrogenism: Stroke Risk And Causes Explained

Hyperandrogenism is a medical condition characterised by high levels of androgens, which are a group of sex hormones. It is more common in women than men, and can cause acne, hair loss, increased body or facial hair, and irregular or absent menstruation.

The condition can lead to serious health issues, including high cholesterol, diabetes, and insulin resistance, which in turn can lead to type 2 diabetes. It can also cause virilisation, or the development of male characteristics, in women.

The most common cause of hyperandrogenism is polycystic ovary syndrome (PCOS), which accounts for about 70% of cases. Other causes include congenital adrenal hyperplasia, insulin resistance, hyperprolactinemia, Cushing's disease, certain types of cancers, and certain medications.

Given the range of potential health complications, it is important to understand the link between hyperandrogenism and stroke risk.

Hyperandrogenism and its symptoms

Hyperandrogenism is a medical condition characterised by high levels of androgens—a group of sex hormones—in the body. It is more common in women than men, affecting about 5–10% of women of reproductive age.

Symptoms of hyperandrogenism

• Excess body hair (hirsutism)
• Acne
• Abnormal menstruation (periods)
• Male-pattern balding (androgenic alopecia)
• Masculine appearance
• Skin inflammation (seborrhea)
• Increased sex drive (libido)
• Oily skin
• Male pattern balding
• Irregular menstruation
• Increased muscle mass and smaller breast size

Causes of hyperandrogenism

• Polycystic ovary syndrome (PCOS)
• Malfunction of the adrenal gland
• Diseases of the pituitary gland, such as Cushing syndrome or Acromegaly
• Obesity and metabolic syndrome
• Certain medications, including anabolic steroids

Diagnosis of hyperandrogenism

Diagnosis of hyperandrogenism often involves blood tests for testosterone, 17-hydroxyprogesterone, and prolactin, as well as a pelvic ultrasound.

Hyperandrogenism and polycystic ovary syndrome (PCOS)

Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder characterised by anovulation, hyperandrogenism, and polycystic ovarian morphology. It affects 6–20% of women in their reproductive years and is the most common cause of female infertility. The pathophysiology of PCOS is not entirely understood, but it is believed to be caused by a combination of genetic, environmental, and intrauterine factors, such as androgen exposure and prenatal nutrition.

Hyperandrogenism is a key feature of PCOS, with two-thirds of cases exhibiting hyperresponsiveness to gonadotropin stimulation and the remaining third exhibiting testosterone elevation after the suppression of adrenal androgen production. This results in a range of symptoms, including acne, hirsutism, and clitoromegaly. In males, hyperandrogenism during prepuberty leads to penile enlargement, excess hair growth, and a deepened voice.

The hormonal imbalances observed in PCOS can indirectly or directly cause hyperandrogenism. CYP genes involved in steroidogenesis play a crucial role in androgen production and are considered key players in hyperandrogenism in PCOS. Polymorphisms in these genes can upregulate or downregulate their expression, further increasing androgen levels.

Women with PCOS are at an increased risk of developing insulin resistance, type 2 diabetes, metabolic syndrome, and cardiovascular diseases. These comorbidities are believed to be linked to the degree of hyperandrogenism, which may also increase the risk of stroke. However, more research is needed to fully understand the relationship between PCOS, hyperandrogenism, and stroke risk.

Currently, treatments for PCOS are limited to regulating menses, inducing ovulation, and reducing androgen-induced hair growth with varying levels of success. A better understanding of hyperandrogenism and its role in PCOS may lead to improved treatments and a reduced risk of associated comorbidities, including stroke.

Hyperandrogenism and insulin resistance

Hyperandrogenism is a condition characterised by clinical signs of androgen excess, such as acne, hirsutism, or androgenic alopecia, or by the presence of elevated levels of circulating androgens in the body. It is the most common endocrinopathy of women of reproductive age and is associated with hyperandrogenism and chronic anovulation. Hyperandrogenism can be caused by polycystic ovary syndrome (PCOS), congenital adrenal hyperplasia, androgen-secreting tumours, and certain medications.

Insulin resistance and hyperandrogenism are both implicated in the pathogenesis of PCOS. In patients with PCOS, theca and granulosa cell functions are impaired, resulting in premature arrest of follicle growth and anovulation. Hyperinsulinemia has a role in amplifying LH-induced androgen production by theca cells.

In summary, hyperandrogenism and insulin resistance are closely linked, with hyperinsulinemia and insulin resistance being major causes of hyperandrogenism and PCOS.

Hyperandrogenism and Cushing's syndrome

Cushing's syndrome is an uncommon condition that occurs when the body has too much of the hormone cortisol. Cushing's disease, a benign tumour on the pituitary gland that releases too much adrenocorticotropic hormone (ACTH), is a type of Cushing's syndrome. Cushing's syndrome can cause hyperandrogenism, which is characterised by an excess of androgens (a group of sex hormones).

Hyperandrogenism is a condition that affects people assigned female at birth more commonly than those assigned male at birth. It is characterised by clinical signs of androgen excess, such as acne, hirsutism, and androgenic alopecia, or by elevated levels of circulating androgens in the body. It can be caused by polycystic ovary syndrome (PCOS), congenital adrenal hyperplasia, androgen-secreting tumours, or certain medications.

PCOS is a common cause of hyperandrogenism, affecting 5-10% of people assigned female at birth of reproductive age. It is characterised by chronic hyperandrogenism, oligo-anovulation, and polycystic ovaries. Insulin resistance and LH excess contribute to the pathogenesis of PCOS.

Congenital adrenal hyperplasia is a group of genetic conditions affecting the adrenal glands, causing them to overproduce hormones like testosterone. Non-classical congenital adrenal hyperplasia, involving a partial 21-hydroxylase deficiency, is the most common adrenal cause of hyperandrogenism.

Androgen-secreting tumours, such as ovarian or adrenal tumours, can also cause hyperandrogenism. These tumours can lead to a rapid onset of virilisation and are often severe. However, hyperandrogenism due to ovarian or adrenal tumours is rare, accounting for only 0.2% of cases.

Certain medications, such as anabolic-androgenic steroids, synthetic progestins, and antiepileptics, can also cause hyperandrogenism.

While Cushing's syndrome and hyperandrogenism are distinct conditions, there is some overlap between them. Cushing's syndrome can cause hyperandrogenism, and hyperandrogenism is a defining sign of PCOS, which can be a cause of Cushing's syndrome. Therefore, it is important to consider the possibility of Cushing's syndrome when screening for PCOS, especially if the patient presents with additional disturbances such as osteoporosis or bone fractures.

Hyperandrogenism and congenital adrenal hyperplasia

Hyperandrogenism is a condition characterised by an excess of androgens (a group of sex hormones) in the body. It is most common in people assigned female at birth and can cause symptoms such as hirsutism, acne, and irregular periods. One of the causes of hyperandrogenism is congenital adrenal hyperplasia (CAH), a group of genetic conditions affecting the adrenal glands. CAH involves a shortage of certain enzymes that help the body produce hormones, leading to an overproduction of other hormones such as testosterone.

Non-classical congenital adrenal hyperplasia (NC-CAH) is a mild form of CAH that affects 0.6 to 9% of women with androgen excess. It is characterised by androgen excess, including premature pubarche, acne, hirsutism, polycystic ovary syndrome (PCOS), and subfertility. NC-CAH is more frequently observed in females, with males being diagnosed less often due to less noticeable signs of androgen excess.

In CAH, the enzyme shortage often causes the adrenal glands to overproduce testosterone. This can lead to hyperandrogenism, which is associated with an increased risk of stroke. While the exact mechanism is not yet fully understood, it is believed that hyperandrogenism and the related metabolic disturbances caused by CAH contribute to the increased stroke risk.

The treatment for hyperandrogenism caused by CAH aims to lower adrenal androgen production and block the androgen action. Low-dose corticosteroids are typically used to slow down adrenal hyperandrogenism. In some cases, surgical removal of adrenal, ovarian, or testicular tumours may be necessary. Additionally, anti-androgen drugs are commonly used to block the effects of androgens such as testosterone.

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