About Androgenetic Alopecia
Androgenetic alopecia, or common baldness, is a genetically determined sensitivity of the hair follicle to androgens. It occurs post-pubertally in both males and females and is manifest by the non-scarring loss of hair in the vertex and frontotemporal areas. Terminal hairs are first replaced by thin, small vellus hairs. Eventually the follicles become completely atrophic. Hair loss can begin at any age after puberty and exposure to increased levels of androgens, but onset is highly variable.
With what can androgenetic alopecia be confused?
In men, the diagnosis of androgenetic alopecia is usually obvious. In women, a hormonal abnormality, especiallypolycystic ovary syndrome (PCOS) should be considered, especially if accompanied by irregular periods, infertility, hirsutism, or acne. Hypothyroidism can also be a cause of thin brittle hair. Other conditions that can cause non-scarring alopecia include: alopecia areata, telogen effluvium, secondary syphilis, hyperthyroidism, anemia, and trichotillomania. Seborrheic dermatitis and tinea infection of the scalp can also cause hair loss.
How is androgenetic alopecia diagnosed?
Hair loss, notably temporal recession in men, is usually first noticed in the third decade of life, but can begin as early as the second decade. It progresses in a distinct pattern, hence its other designation “male pattern baldness”, involving in men the vertex and frontotemporal areas but sparing the posterior and lateral aspects of the scalp. In women, the vertex is involved but the frontotemporal aspect may be spared. Scalp examination reveals replacement of dark terminal hairs with vellus hairs or with atrophic hair follicles; the number of follicles remains unchanged, but they may be difficult to perceive. There is no scarring or inflammation. A family history of baldness is usually present. In most cases, laboratory tests and biopsy are unnecessary. In women, a thyroid stimulating hormone assay and androgen levels, including total testosterone, free testosterone, androstenedione, and DHEA-S should be ordered. If considering polycystic ovary syndrome, follicle stimulating hormone, lutenizing hormone, prolactin levels, and tests of insulin resistance may be appropriate. Iron studies and an ANA test for autoimmune disease may be warranted as well. Severity of androgenetic alopecia is classified in men by the Hamilton classification, and in women by the Ludwig classification.
How is androgenetic alopecia treated?
Topical minoxidil (Rogaine), as either a 2% or 5% solution or foam, is moderately effective in stimulating regrowth of terminal hairs on the vertex, and less so in the frontal area. However, treatment must be continued indefinitely for results to be maintained. Minoxidil can be used in women as well. Finasteride (Propecia) is a type II 5 alpha-reductase inhibitor that prevents the peripheral conversion of testosterone into the more active dihydrotestosterone. In the clinical trials for Propecia, 83% of men maintained or increased their hair counts after two years of treatment. Propecia cannot be used in women of child-bearing age since it is teratogenic. In women with androgenetic alopecia and elevated androgens, androgen-blocking agents such as spironolactone, flutamide, cimetidine, and cyproterone acetate can be used. These agent block the peripheral effects of testosterone and should not be used in men. Non-pharmaceutical approaches include various methods of hair transplantation, including punch grafts and scalp reductions, wearing a toupee or wig, or to go bald gracefully (more an option for men than for women). Recently, prostaglandin analogs, such as bimatoprost (Latisse), have come in to use to promote eyelash growth. These drugs are now being investigated in scalp hair loss as well.
What is the prognosis for androgenetic alopecia?
The balding process is substantially complete by the age of 50, though additional thinning continues throughout life.
Other resources for androgenetic alopecia