A plethora of options is available for the treatment of androgenetic alopecia (AGA), including topical and systemic drugs, over-the-counter products and interventional therapies. The range of products is wide and reaches from pharmaceutical to cosmetic agents, natural products, different herbal preparations, functional food, etc. Currently, topical minoxidil and oral finasteride are the only Food and Drug Administration (FDA)-approved drugs and low-level laser light therapy (LLLLT) the only FDA-cleared device for the treatment of AGA.
The decision for the best-suited individualized therapeutic approach must be taken by physician and patient together, taking under consideration available evidence, expected therapeutic results, practicability, adverse effects, compliance and costs.1 Monotherapy or combination therapy can be considered.
In order to achieve best results, treatment of AGA should be started as early as possible, when miniaturization of hair follicles has not progressed yet. The therapeutic objective is stabilization of the clinical course, deceleration of hair loss and in best case hair regrowth, thus contributing to an improved quality of life.1 The response to treatment (defined as maintenance of stable condition and in best case induction of hair growth) should be assessed at approximately 6 months. Since AGA is a naturally progressive condition, successful treatment needs to be continued to maintain efficacy.1 See Table 77-1.
Table 77-1Androgenetic Alopecia Treatment Table ||Download (.pdf) Table 77-1 Androgenetic Alopecia Treatment Table
|MEDICATION NAME ||INDICATION ||MECHANISM OF ACTION ||DOSING ||ADVERSE EFFECTS ||SUGGESTED MONITORING ||LEVEL OF EVIDENCE (REFERENCE) |
|Topical Therapy |
|Minoxidila ||AGA in men (first-line treatment) ||Induction and prolongation of anagen, hair follicle size increase. Possible mechanisms of action include vasodilation, stimulation of cell proliferation, inhibition of collagen synthesis, and stimulation of vascular endothelial growth factor and prostaglandin synthesis ||5% BID (1 mL of solution or half a cap of foam) ||Transitory increased telogen hair shedding during the first months of treatment, “post-minoxidil rebound”: increased hair loss following interruption of topical minoxidil, ectopic (mostly facial) hypertrichosis, irritant and allergic contact dermatitis ||None ||IA1-3 |
|Minoxidila || |
AGA in women (first-line treatment)
Pause during pregnancy and lactation recommended due to lack of data during this period
| ||2% BID (solution) or 5% QD (foam) || ||None ||IA1,3 |
|Finasteride ||AGA in men ||5α-reductase (type 2) inhibition ||0.1%-0.25% QD-BID ||Limited safety data so far; reports of scalp irritation, contact dermatitis, single cases of increased liver enzymes, bed-wetting, testicular pain, headaches, presyncope and oropharyngeal pain reported (causality unclear) || |
Caveat: dosis-dependent serum DHT reduction
|17α-estradiol (alfatradiol) ||Limited current data. Adjunctive therapy within an individually tailored management approach at the discretion of the treating dermatologist and the decision of the patient for deceleration/stabilization of hair loss, e.g., if first-line therapies were ineffective or not well tolerated ||5α-reductase inhibition ||0.025% QD ||Topical reactions, such as erythema, tingling sensation, pruritus and desquamation ||None ||IB-IIA...|