A prescription vitamin A derivative for the skin, with an unusually deep base of human evidence. It improves fine and coarse lines, uneven brown coloring and rough texture, and rebuilds the supportive layer beneath. Change is gradual, modest, and fades after treatment stops. Early redness, flaking, dryness and stinging are the main reason it is abandoned. Avoided in pregnancy. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Serum beta-hCG | Negative | Rules out the one absolute contraindication |
| Serum retinol | 1.5–2.4 µmol/L | Establishes total vitamin A burden before adding any retinoid |
| 25-hydroxyvitamin D | 40–60 ng/mL | Strict photoprotection required by the protocol reduces cutaneous synthesis |
| hs-CRP | < 0.5 mg/L | Elevated systemic inflammation predicts poorer barrier recovery and worse irritation |
| HbA1c | 4.8–5.2% | Glycated collagen does not remodel, capping achievable dermal improvement |
| Fasting insulin | 2–5 µIU/mL | Insulin resistance drives glycation and impairs wound healing |
| Ferritin | 50–125 ng/mL (women), 50–150 ng/mL (men) | Iron status affects collagen synthesis, which requires iron-dependent hydroxylases |
| TSH | 0.5–2.0 mIU/L | Hypothyroidism produces xerosis that tretinoin will compound |
| Comprehensive metabolic panel including ALT and AST | ALT and AST 10–26 U/L | Establishes hepatic baseline before any retinoid exposure, including concurrent oral vitamin A |
Cadence: Baseline panel drawn before initiation. Photographic and instrumented monitoring at baseline, 4 weeks, 12 weeks, 6 months, then every 6 months. Laboratory markers re-checked only if abnormal at baseline or if a systemic condition changes, typically every 6–12 months; pregnancy status re-confirmed whenever there is any possibility of conception.