Hyperandronism in female
"hyperandrogenism" AND "female" AND "diagnosis"
hyperandrogenism female hirsutism PCOS clinical features

A composite clinical photograph illustrating dermatological manifestations of hyperandrogenism, specifically in the context of Polycystic Ovary Syndrome (PCOS). The left image provides a lateral view of the lower face and neck of a female patient, showing inflammatory acne vulgaris characterized by a dense distribution of erythematous papules and pustules along the jawline, mandibular area, and upper neck. Significant hirsutism is also visible, with terminal hair growth in androgen-dependent areas such as the preauricular region and chin. The right image is a frontal view of a female patient exhibiting androgenetic alopecia. Notable features include a receding frontal hairline with temporal sparing, resulting in an 'M' shaped pattern, along with diffuse thinning of the hair on the vertex and mid-scalp. Together, these images demonstrate the cutaneous 'SAHA' syndrome (seborrhea, acne, hirsutism, and alopecia) associated with systemic androgen excess, providing a key educational example for endocrine-related skin disorders.

Clinical photograph of the lower face, neck, and upper chest of a female patient exhibiting signs of hyperandrogenism. The primary clinical finding is hirsutism, characterized by coarse, dark, androgenic terminal hair growth in a male-pattern distribution, specifically along the chin, jawline, and submandibular region of the neck. Accompanying dermatological features include inflammatory acne vulgaris, presenting as erythematous papules and pustules scattered across the neck and upper chest. Additionally, there are multiple pigmented macules and small nevi visible on the neck. The skin on the chin demonstrates a slightly thickened and irregular texture, consistent with follicular stimulation. This visual presentation is a key clinical indicator of endocrine dysfunction, such as that seen in polycystic ovary syndrome (PCOS), Cushing syndrome, or androgen-secreting tumors (e.g., adrenocortical carcinoma), where excess androgens stimulate the conversion of vellus hair to terminal hair in androgen-sensitive areas.

A clinical photograph of a female patient's face and neck in a lateral profile view, demonstrating clinical signs of hyperandrogenism and virilization. The image reveals prominent hirsutism, characterized by coarse, dark hair growth in an androgen-dependent distribution, specifically involving the preauricular (sideburn) area, cheeks, and along the mandibular jawline. Accompanying these findings is an inflammatory acneiform eruption, presenting as erythematous papules and pustules clustered around the jaw and upper neck. This combination of acne and hirsutism is highly suggestive of an underlying hyperandrogenic state. The educational focus of this image is the recognition of physical manifestations of excessive androgen levels in female patients, which may be associated with conditions such as polycystic ovary syndrome (PCOS) or, in this clinical context, pregnancy-related luteoma.

This clinical photograph displays significant dermatological and endocrine-related signs on a female patient, illustrating virilization. The primary finding is androgenic alopecia, characterized by a receding hairline and marked thinning of the hair at the frontal and temporal scalp, following a male-pattern distribution. Additionally, the patient exhibits severe hirsutism, with coarse terminal hair growth visible on the upper lip, chin, and mandibular regions. Notable stubble in these areas suggests recent hair removal efforts. The facial skin appears slightly oily with scattered blemishes on the cheeks, possibly related to hyperandrogenism. These visual features—male-pattern baldness combined with excess facial hair in a female—are classic indicators of hyperandrogenic states, such as those caused by androgen-secreting tumors or severe polycystic ovary syndrome (PCOS).
| Feature | Details |
|---|---|
| Hirsutism | Excess coarse terminal hair - chin, lip, chest, inner thigh, lower back, abdomen (midline) |
| Acne | Particularly severe, jawline-distributed, sudden-onset acne |
| Androgenic alopecia | Male-pattern scalp thinning/recession |
| Menstrual irregularity | Oligomenorrhea or amenorrhea from anovulation |
| Virilization | Voice deepening, clitoromegaly, breast atrophy, increased muscle bulk - suggests tumor |
| Acanthosis nigricans | Indicates associated insulin resistance |


50% of PCOS patients have obesity (central/android distribution); metabolic risk is significant
| Hormone | Interpretation |
|---|---|
| Total / free testosterone | First-line; >200 ng/dL strongly suggests androgen-secreting tumor |
| DHEA-S | Elevated in adrenal source (>700 μg/dL → adrenal tumor) |
| 17-OHP (fasting, follicular phase) | Elevated in non-classic CAH (21-hydroxylase deficiency); confirm with ACTH stimulation if 17-OHP >2 ng/mL |
| LH:FSH ratio | Often >2:1 in PCOS |
| Fasting insulin / glucose | Assess insulin resistance |
| Prolactin | Exclude hyperprolactinemia |
| TSH | Exclude hypothyroidism |
| SHBG | Low in PCOS/hyperinsulinemia → high free testosterone |
| Drug | Mechanism | Notes |
|---|---|---|
| Spironolactone | Androgen receptor blocker + reduces androgen synthesis | 50-200 mg/day; first choice anti-androgen; use with OCP (teratogenic in male fetus) |
| Cyproterone acetate | Potent androgen receptor blocker | Combined with ethinyl estradiol (Diane-35); widely used outside USA |
| Flutamide | Androgen receptor blocker | Risk of hepatotoxicity; less preferred |
| Finasteride | 5α-reductase inhibitor (type II) | 5 mg may benefit post-menopausal; teratogenic |
Evaluate
Ferriman Gallwey score hirsutism grading scale diagram

<table><thead><tr><th>No. Living*</th><th>Type</th><th>Recommendation</th><th>Grade/ Quality</th></tr></thead><tbody><tr><td>1.3.5</td><td>CR</td><td>A modified Ferriman Gallwey score (mFG) of 4–6 should be used to detect hirsutism, depending on ethnicity, acknowledging that self-treatment is common and can limit clinical assessment.</td><td>◊◊◊◊</td></tr><tr><td>1.3.6</td><td>CR</td><td>Healthcare professionals should consider that the severity of hirsutism may vary by ethnicity but the prevalence of hirsutism appears similar across ethnicities.</td><td>◊◊◊</td></tr><tr><td>1.3.7</td><td>PP</td><td>Healthcare professionals should: • be aware that standardised visual scales are preferred when assessing hirsutism, such as the mFG scale in combination with a photographic atlas • consider the Ludwig or Olsen visual scales for assessing female pattern hair loss • note that there are no universally accepted visual instruments for assessing the presence of acne • recognise that women commonly treat clinical hyperandrogenism cosmetically, diminishing their apparent clinical severity • appreciate that self-assessment of unwanted excess hair growth, and possibly acne and female pattern hair loss, has a high degree of validity and merits close evaluation, even if overt clinical signs of hyperandrogenism are not readily evident on examination • be aware that only terminal hairs need to be considered in defining hirsutism, and these can reach > 5 mm if untreated, vary in shape and texture and are generally pigmented • note that new-onset severe or worsening hyperandrogenism, including hirsutism, requires further investigation to rule out androgen-secreting tumours and ovarian hyperthecosis • monitor clinical signs of hyperandrogenism, including hirsutism, acne and female pattern hair loss, for improvement or treatment adjustment during therapy.</td><td></td></tr><tr><td>1.4</td><td colspan="3">Ultrasound and polycystic ovarian morphology</td></tr><tr><td>1.4.1</td><td>EBR</td><td>Follicle number per ovary (FNPO) should be considered the most effective ultrasound marker to detect polycystic ovarian morphology (PCOM) in adults.</td><td>◊◊◊◊ ⊕⊕⊙⊙</td></tr><tr><td>1.4.2</td><td>EBR</td><td>Follicle number per ovary (FNPO), follicle number per cross-section (FNPS) and ovarian volume (OV) should be considered accurate ultrasound markers for PCOM in adults.</td><td>◊◊◊◊ ⊕⊕⊙⊙</td></tr><tr><td>1.4.3</td><td>CR</td><td>PCOM criteria should be based on follicle excess (FNPO, FNPS) and/or ovarian enlargement (OV).</td><td>◊◊◊◊</td></tr><tr><td>1.4.4</td><td>CR</td><td>Follicle number per ovary (FNPO) ≥ 20 in at least one ovary should be considered the threshold for PCOM in adults.</td><td>◊◊◊◊</td></tr><tr><td>1.4.5</td><td>CR</td><td>Ovarian volume (OV) ≥ 10 ml or follicle number per section (FNPS) ≥ 10 in at least one ovary in adults should be considered the threshold for PCOM if using older technology or image quality is insufficient to allow for an accurate assessment of follicle counts throughout the entire ovary.</td><td>◊◊◊◊</td></tr></tbody></table>

A series of clinical photographs documenting a case of severe hirsutism and its response to treatment. Panels (a) and (b) show the patient at presentation, demonstrating dense, dark terminal hair growth on the upper lip, chin, and submandibular region (jawline) extending toward the preauricular area, consistent with a high Ferriman-Gallwey score. Panel (a) also shows evidence of mild inflammatory acne on the cheeks. Panel (c) displays significant terminal hair growth on the abdomen, both supraumbilical and infraumbilical. Panels (d) and (e) provide a follow-up comparison at 6 months after pharmacological intervention, showing a dramatic clinical reduction in facial terminal hair density and improvement in skin texture. This comparison illustrates the visual manifestation of hyperandrogenism and the efficacy of hormonal management in reversing androgen-dependent hair patterns in female patients.

<table> <tr> <th>Table 1. Definition of Terms</th> <th></th> </tr> <tr> <th>Term</th> <th>Definition</th> </tr> <tr> <td>Hirsutism</td> <td>Hirsutism is excessive terminal hair that appears in a male pattern (excessive hair in androgen-dependent areas; <i>i.e.</i>, sexual hair) in women.</td> </tr> <tr> <td>Ferriman–Gallwey score</td> <td>The modified Ferriman–Gallwey score is the gold standard for evaluating hirsutism. Nine body areas most sensitive to androgen are assigned a score from 0 (no hair) to 4 (frankly virile), and these separate scores are summed to provide a hormonal hirsutism score (Fig. 1).</td> </tr> <tr> <td>Local hair growth</td> <td>This is unwanted localized hair growth in the absence of an abnormal hirsutism score.</td> </tr> <tr> <td>Patient-important hirsutism</td> <td>Unwanted sexual hair growth of any degree that causes sufficient distress for women to seek additional treatment.</td> </tr> <tr> <td>Hyperandrogenism</td> <td>Hyperandrogenism (for the purposes of this guideline) is defined as clinical features that result from increased androgen production and/or action.</td> </tr> <tr> <td>Idiopathic hirsutism</td> <td>This is hirsutism without hyperandrogenemia or other signs or symptoms indicative of a hyperandrogenic endocrine disorder.</td> </tr> </table>
| Domain | Points |
|---|---|
| Onset & progression | Sudden, rapid onset → suspect androgen-secreting tumor; gradual since puberty → PCOS or idiopathic |
| Menstrual history | Oligomenorrhea (<8 cycles/year) or amenorrhea → ovarian source more likely; regular cycles → idiopathic or adrenal |
| Age of onset | Teens/early 20s with onset around menarche → PCOS; adult onset with weight gain → insulin-driven PCOS |
| Cosmetic self-treatment | Waxing, shaving, threading underestimate clinical severity on examination - always ask |
| Drug history | Phenytoin, minoxidil, cyclosporine, valproic acid, diazoxide → hypertrichosis (not true HA); androgenic progestins in older OCP formulations |
| Family history | Hirsutism + infertility → non-classic CAH; PCOS in mother/sisters |
| Galactorrhea | → Hyperprolactinemia |
| Cushing features | Weight gain (central), easy bruising, striae, hypertension, proximal muscle weakness → Cushing syndrome |
| Acromegaly features | Headache, visual field defects, jaw changes, hand/foot enlargement (rare cause) |
| Fertility goals | Determines which treatment arm to pursue |
Red flag history: Sudden onset + rapid progression + virilization = androgen-secreting tumor until proven otherwise. - Harrison's 22E, p. 3183
| Sign | Significance |
|---|---|
| Hirsutism | Androgen-sensitive distribution (see mFG score below) |
| Acne | Comedonal/inflammatory, especially jawline; suggests androgen excess |
| Androgenic alopecia | Diffuse crown thinning (Ludwig pattern) in women; frontoparietal recession in severe cases |
| Acanthosis nigricans | Hyperpigmented, velvety skin at nape/axillae/groin → insulin resistance |
| Skin tags | Also suggest insulin resistance |
| Striae, easy bruising | → Cushing syndrome |
| Seborrhea | Oily skin → androgen-stimulated sebaceous glands |

| Score | Interpretation |
|---|---|
| < 8 | Normal (non-Hispanic White, African-American) |
| ≥ 8 | Hirsutism - warrants hormonal evaluation |
| ≥ 4-6 | Threshold for some ethnicities (Endocrine Society 2018) |
Note: Asian and Native American women may score <8 but still have significant biochemical HA manifesting only as acne or scalp hair thinning. - Harrison's 22E, p. 3184
| Test | What it Detects | Key Thresholds |
|---|---|---|
| Total testosterone (by LC-MS/MS specialty assay) | Ovarian source; PCOS; tumor | >200 ng/dL (>7 nmol/L) → strongly suggests tumor; >100 ng/dL → investigate further |
| Free / calculated free testosterone (from total T + SHBG) | Most accurate biochemical marker; elevated even when total T is normal due to low SHBG | Elevated in PCOS with hyperinsulinemia |
| SHBG | Low in insulin resistance/PCOS → increases free testosterone fraction | |
| DHEA-S | Adrenal androgen source | >7000 μg/L (>18.5 μmol/L) → adrenal tumor; modestly elevated in PCOS too |
| 17-Hydroxyprogesterone (17-OHP) - fasting, follicular phase | Screens for non-classic CAH (21-hydroxylase deficiency) | Basal >200 ng/dL → proceed to ACTH stimulation test |
| LH : FSH ratio | PCOS | Ratio >2-3 supportive of PCOS (but not required for diagnosis) |
| Fasting glucose + fasting insulin / HOMA-IR | Insulin resistance in PCOS | |
| Prolactin | Hyperprolactinemia | |
| TSH | Hypothyroidism |
Labs are most accurate when the patient is off oral contraceptives for 4-6 weeks and drawn before menses (follicular phase). - Fitzpatrick's Dermatology, Table 137-18
| Indication | Test |
|---|---|
| Testosterone >200 ng/dL or DHEA-S >7000 μg/L | CT abdomen/pelvis (adrenal) + transvaginal ultrasound (ovary) |
| Rapid-onset virilization at any testosterone level | Urgent pelvic ultrasound + CT adrenals |
| Cushing syndrome suspected | 24-hour urinary free cortisol; overnight 1 mg dexamethasone suppression test; late-night salivary cortisol |
| Non-classic CAH (basal 17-OHP 200-1000 ng/dL) | ACTH stimulation test (250 μg IV ACTH; 17-OHP >10,000 ng/dL at 60 min → confirms CAH) |
| Acromegaly suspected | IGF-1, oral glucose tolerance test with GH |
| Adolescent PCOS | Caution - diagnosis requires both persistent features of HA and ovulatory dysfunction; do not over-label |

| Condition | Key Clinical Clues | Key Lab Finding | Confirmatory Test |
|---|---|---|---|
| PCOS | Irregular periods + hirsutism since puberty, obesity, acanthosis nigricans | Elevated free T, low SHBG, elevated LH:FSH | Pelvic USS (PCOM) + Rotterdam criteria |
| Non-classic CAH | Hirsutism ± irregular cycles; family history; Ashkenazi/Hispanic/Slavic ethnicity | Elevated basal 17-OHP (>200 ng/dL) | ACTH stimulation test (17-OHP >10,000 ng/dL) |
| Androgen-secreting ovarian tumor | Rapid onset, virilization, severe hirsutism | Testosterone >200 ng/dL (>7 nmol/L) | Transvaginal ultrasound → MRI if needed |
| Adrenal tumor | Rapid onset, virilization | DHEA-S >7000 μg/L | CT adrenals |
| Cushing syndrome | Centripetal obesity, striae, easy bruising, hypertension, moon face | Elevated urinary free cortisol | 1 mg DST, late-night salivary cortisol, CRH test |
| Hyperthecosis | Marked virilization, postmenopausal, testosterone >200 ng/dL, normal imaging | Testosterone >200 ng/dL | Bilateral oophorectomy confirms |
| Hyperprolactinemia | Galactorrhea, amenorrhea | Elevated prolactin | MRI pituitary |
| Idiopathic hirsutism | Normal menses, normal androgens, positive mFG | All labs normal | Diagnosis of exclusion |