| **Section** | **Key Points** | |-------------|----------------| | **What it is** | Synthetic anabolic–androgenic steroid (AAS) – a modified testosterone that promotes protein synthesis and cell proliferation. | | **Formulation** | Injectable oil solution (typically 25 mg/mL). The ester (decanoate) prolongs release, giving a half‑life of ~12–14 days. | | **Why it’s used** | • Clinical: to treat anemia, osteoporosis, delayed puberty, some cancers. • Off‑label/athletic: to increase lean body mass, strength, and recovery. |
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## How It Works (Mechanism)
1. **Cellular Entry** *N*‑acetyl‑testosterone diffuses into muscle or other tissues.
2. **Receptor Binding** - Binds intracellular androgen receptors (AR). - The AR–ligand complex dimerizes and translocates to the nucleus.
3. **Gene Activation** - The complex binds DNA at androgen response elements (AREs). - Activates transcription of genes involved in protein synthesis, satellite‑cell proliferation, glycogen storage, etc.
| Parameter | Typical Value | |-----------|---------------| | **Absorption** | Oral bioavailability ~10–20% due to first‑pass metabolism. | | **Half‑life** | 1–4 h; depends on dosage form (immediate vs extended release). | | **Metabolism** | CYP3A4 predominant; glucuronidation via UGT enzymes. | | **Excretion** | Renal (~70% unchanged) and fecal (~20%). |
> **Clinical Note:** Because of extensive metabolism, drug–drug interactions are common (e.g., with ketoconazole or rifampicin).
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## 4. Clinical Indications
| Condition | Evidence Level | Notes | |-----------|-----------------|-------| | **Severe acne vulgaris** | **Strong** | First‑line systemic therapy; effective in cystic/comedonal types. | | **Androgen‑induced alopecia (female pattern)** | Moderate | Improves hair density; used as monotherapy or adjunct to topical minoxidil. | | **Hirsutism secondary to PCOS** | Strong | Reduces terminal hairs on face, chest, abdomen. | | **Cushing’s syndrome (androgen‑producing adrenal tumor)** | Weak | Limited case reports; primarily for symptom control. | | **Other hyperandrogenic states** | Variable | Evidence is scarce and inconsistent. |
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## 4. Summary of Evidence
| Outcome | Key Findings | Limitations | |---------|--------------|-------------| | **Hair growth in women with androgenetic alopecia** | RCTs (e.g., *J Clin Endocrinol Metab* 2015) show significant increase in hair count and thickness vs placebo after 12–24 weeks. | Small sample sizes; short follow‑up; variable outcome measures. | | **Hair growth in hirsutism or androgen excess** | Limited crossover studies (e.g., *Int J Womens Health* 2020) report modest improvements in terminal hair density. | No large RCTs; many rely on self‑reported outcomes. | | **Safety** | Adverse events include mild injection site pain, transient bruising; no systemic side effects reported. | Long‑term safety data lacking due to short duration of studies. |
Overall, the evidence supports use for localized cosmetic indications (fine hair removal or thick terminal hair growth) but is insufficient for widespread clinical recommendations in hirsutism or androgen excess disorders.
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## 3 – Clinical Scenario **Patient:** Female, 35 yrs old, regular menses, presents with excessive terminal hair on the upper lip and chin. She has tried waxing and laser therapy without satisfactory results.
### a) First‑Line Management
| Step | Intervention | Rationale | |------|--------------|-----------| | **1. Verify diagnosis** | Full physical exam + review of growth pattern; rule out other causes (e.g., hirsutism secondary to PCOS). | Ensures correct target for therapy. | | **2. Discuss options** | - *Topical depilatories* (e.g., potassium hydroxide) - *Trichloroacetic acid (TCA)* peeling - *Laser hair removal* (diode or Nd:YAG). | Provides evidence‑based alternatives; informs patient choice. | | **3. Offer *trichloroacetic acid* peel** | Use 30–40% TCA in a controlled fashion; apply to the area, leave until frosting, then remove. Perform multiple sessions (2–4) spaced ~1 month apart. | Minimally invasive, suitable for small facial areas; may require careful skin cooling and post‑care. | | **4. Follow up** | Monitor for epidermal damage or hyperpigmentation; provide sun protection, moisturizers, and optional topical treatments (e.g., tretinoin). | Ensures safety and optimal healing. |
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### 5. General Precautions & Post‑Care
| Topic | Recommendation | |-------|----------------| | **Sun Protection** | Use SPF 50+ daily; reapply every 2–3 h when outdoors; wear hats, sunglasses, protective clothing. | | **Moisturizing** | Non‑comedogenic, fragrance‑free moisturizers (e.g., ceramide‑based). | | **Avoid Over‑Cleansing** | Use gentle cleansers (pH 4.5–6); avoid hot water and scrubbing. | | **Monitor for Irritation** | Discontinue or reduce frequency if redness, burning, scaling > 2 weeks. | | **Regular Follow‑Up** | Dermatology visits every 3–6 months to assess progress; adjust therapy accordingly. |
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## Summary
- **Skin Type:** Oily/combination with visible acne and occasional hyperpigmentation. - **Treatment Plan (12‑Month Timeline):** 1. **Months 0‑3:** Retinoid + Benzoyl Peroxide + Azelaic Acid (spot) + Gentle cleansing, moisturizer, SPF. 2. **Months 4‑6:** Add Salicylic Acid wash; consider low‑dose oral doxycycline if needed. 3. **Months 7‑9:** Introduce chemical exfoliation (AHA/BHA), maintain retinoid regimen, adjust topical therapies based on response. 4. **Months 10‑12:** Evaluate for laser/IPL therapy or further systemic options; continue maintenance with topical actives and sunscreen.
Throughout, monitor for irritation, patch test before new ingredients, keep a skincare diary, and schedule quarterly follow‑ups to reassess efficacy and safety. This structured, progressive plan balances immediate acne control with long‑term skin health and prevention of future breakouts.
