How does polycystic ovary syndrome (PCOS) cause hirsutism in female patients?

How PCOS Causes Hirsutism

PCOS causes hirsutism through a hormonal cascade where accelerated GnRH pulsatility drives excessive LH secretion, which stimulates ovarian theca cells to overproduce androgens (particularly testosterone), while simultaneously the FSH-granulosa cell axis becomes dysfunctional—this hyperandrogenism then acts directly on hair follicles to convert vellus hair to terminal hair in male-pattern distribution. 1, 2

The Hormonal Cascade

The pathophysiology begins at the hypothalamic level:

• Accelerated GnRH pulsatility is the upstream driver that initiates the entire cascade, leading to disordered gonadotropin secretion 1, 2
• LH hypersecretion results from this accelerated GnRH pulsing, with the LH/FSH ratio typically exceeding 2:1, which is both diagnostically significant and mechanistically critical 2
• Ovarian theca stromal cell hyperactivity occurs in direct response to elevated LH, causing these cells to massively overproduce androgens, particularly testosterone 1, 2
• FSH-granulosa cell axis hypofunction develops simultaneously, with FSH levels remaining relatively low or normal, preventing proper follicular maturation 1, 2

The Metabolic Amplification Loop

Insulin resistance and hyperinsulinemia actively amplify androgen production through two independent mechanisms:

• Direct ovarian stimulation: Hyperinsulinemia directly stimulates ovarian theca cells to produce even more androgens, independent of LH stimulation 2
• SHBG suppression: Insulin suppresses hepatic production of sex hormone-binding globulin (SHBG), which increases the fraction of free (biologically active) testosterone circulating in the blood 2
• This creates a vicious cycle where obesity and insulin resistance worsen hyperandrogenism, which in turn promotes further metabolic dysfunction 2

From Androgens to Terminal Hair Growth

The final step occurs at the pilosebaceous unit level:

• Individual follicular sensitivity to androgens varies significantly between women, explaining why some women with PCOS develop severe hirsutism while others with similar androgen levels do not 3
• Androgens convert vellus hair to terminal hair in androgen-sensitive areas (face, chest, abdomen, back, inner thighs) through direct action on hair follicles 3
• Local androgen generation can occur de novo within the hair follicle itself via 5α-reductase activity, meaning circulating androgen levels don't fully quantify the hair follicle's true androgen exposure 4
• Hirsutism prevalence in PCOS ranges from 70-80%, compared to only 4-11% in the general female population 3

Critical Clinical Context

Hyperandrogenism is present in 75% of PCOS cases and serves as both a diagnostic criterion and a central pathogenic driver 1

The diagnosis of biochemical hyperandrogenism should prioritize:

• Total testosterone (TT) and free testosterone (FT) as first-line laboratory tests 1
• Calculated free testosterone (cFT) should be assessed by equilibrium dialysis, ammonium sulfate precipitation, or calculated using free androgen index (FAI) 1
• LC-MS/MS methodology is superior to immunoassay for androgen measurement given its higher accuracy 1
• If TT or cFT are not elevated, androstenedione (A4) and DHEAS can be considered, though they have poorer specificity 1

Important Caveats

Weight gain is a major trigger for PCOS development and worsening hirsutism in genetically susceptible women, making lifestyle intervention essential 2

Certain medications can exacerbate PCOS, particularly valproate (an antiepileptic drug), which can trigger or worsen PCOS-like symptoms including hirsutism 5, 2

Rapid-onset or severe hirsutism with virilization (clitoromegaly, voice deepening, male-pattern baldness) suggests androgen-secreting tumor rather than PCOS and demands immediate aggressive workup 5