Low-dose oral minoxidil is gaining popularity for treating hair loss, but requires expert guidelines to balance effectiveness with potential cardiovascular risks.

Hair loss can greatly affect a patient’s quality of life and may be nonscarring or scarring. It can be caused by various factors, including hereditary conditions like androgenetic alopecia (AGA), aging, congenital disorders affecting the hair shaft, traction, inflammatory conditions (primary scarring alopecia), autoimmune diseases (alopecia areata), or as a result of medical, surgical, or emotional stress (telogen effluvium). It can also be triggered by infections (e.g., tinea capitis) or certain medications, including those used in cancer treatments (1^✔ ✔Trusted Source
Low-Dose Oral Minoxidil Initiation and Monitoring (LOMI) For Hair Loss: A Modified Delphi Consensus of Experts

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FDA-Approved Use of Topical Minoxidil for AGA Treatment

Topical minoxidil is approved by the US Food and Drug Administration (FDA) as an over-the-counter drug designed to treat male patients with AGA (minoxidil, 5% solution, or minoxidil, 5% foam, twice daily) and female patients with AGA (minoxidil, 2% solution, twice daily, or minoxidil, 5% foam, once daily). It is also frequently prescribed off-label for other types of hair loss in children and adults. Common adverse effects include transient shedding with initiation, hypertrichosis, and contact dermatitis, most commonly secondary to nonactive formulary ingredients, such as propylene glycol.

Minoxidil, a potent peripheral vasodilator, was originally approved by the FDA in 1979 as an oral agent for patients with severe refractory hypertension with antihypertensive dosing ranging from 10 mg to 40 mg daily. Interestingly, a significant adverse effect of oral minoxidil was hypertrichosis, leading to the development of topical minoxidil as a hair growth agent in the 1980s.

Mechanisms of Action: How Minoxidil Works

Minoxidil exerts its effects via various proposed pathways: a vasodilator acting on adenosine triphosphate–sensitive potassium channels, an anti-inflammatory agent, inducer of the Wnt/β-catenin signaling pathway, a 5-α reductase inhibitor and antiandrogen, and an anagen extender. Topical minoxidil is converted into its active form, minoxidil sulfate, via sulfotransferase enzyme activity in the outer root sheath of hair follicles, and oral minoxidil is absorbed in the gastrointestinal tract and converted to its activated sulfated form in the liver. The systemic absorption of topical minoxidil is negligible, well below the minimum level of 20.0 mg per millimeter, at which hemodynamic changes in blood pressure have been documented. Oral minoxidil reaches peak levels in plasma within an hour, has a half-life of 3 to 4 hours, and is excreted by the kidneys within 12 to 20 hours.

Off-Label Use of Low-Dose Oral Minoxidil

Oral minoxidil is not a first-line antihypertensive agent due to the risk for fluid retention, tachycardia, and other potential adverse effects, such as pericardial and pleural effusion, cardiac tamponade, and angina pectoris, with antihypertensive dosing. However, a growing number of research groups have reported on the off-label use of low-dose oral minoxidil (LDOM), ranging from 0.25 mg to 5 mg daily, as a safe and effective treatment option for male and female patients with AGA, age-related patterned thinning, traction alopecia, alopecia areata, telogen effluvium, scarring, and other forms of hair loss; though some serious adverse effects have been reported. This correlates with an increased demand for LDOM prescriptions in recent years. As the current data on LDOM initiation and monitoring for hair loss are limited, there is a pressing need for an expert consensus–based statement for common use to maximize hair growth and minimize cardiovascular and other adverse effects.

Expert Input and Anonymous Responses

Dermatologists with hair loss expertise, identified by clinical experience, research activities, and participation in recognized professional societies, including the North American Hair Research Society, International Federation of Hair Research Societies, and World Congress for Hair Research, were invited via email to join the LOMI expert panel and engage in multiple survey rounds addressing LDOM safety, efficacy, dosing, and monitoring for treating patients with hair loss. Experts were encouraged to answer items based on their clinical expertise and experience with LDOM; relevant literature was provided for review. To minimize bias, individual expert responses were anonymous from all except the study coordinator (Y.M.A.). Based on consensus parameters set by prior Delphi studies, consensus for a LOMI item was defined as at least 70% of experts indicating agree or strongly agree on a 5-point Likert scale.

Review and Feedback Process After Each Survey Round

The initial survey round included items that were non–Likert scale (demographic, open-ended, or multiple choice), as well as items requiring a Likert scale response (strongly disagree, disagree, neutral, agree, strongly agree); after each round, aggregated responses were reviewed by the multidisciplinary LOMI steering committee, and feedback was provided to the LOMI expert panel. When indicated, survey items were revised for clarification or to incorporate expert comments and submitted for expert review in subsequent rounds. In rounds 2, 3, and 4 survey items were calibrated, or did not achieve at least 70% consensus, were either revised or reconsidered in subsequent rounds or eliminated.

Reference:

1. Low-Dose Oral Minoxidil Initiation and Monitoring (LOMI) For Hair Loss: A Modified Delphi Consensus of Experts – (https://www.jaad.org/article/S0190-9622(24)01059-4/fulltext)

Source-Eurekalert