Dermatology

Alopecia - androgenetic

Male and Female Pattern Hair Loss

Are You Confident of the Diagnosis?

Male and female pattern hair loss presents with the characteristic patterns of hair thinning. The authors prefer the term male/female pattern hair loss, in place of androgenetic alopecia, because serum androgen levels are normal in the majority of patients and 50% of the time there is no family history.

  • Characteristic findings on physical examination

In male pattern hair loss, the frontal hairline will take on a classic “M” shape or develop varying degrees of thinning of the vertex, crown and frontal scalp. The anterior hairline is often reshaped (Figure 1). The peripheral scalp is often unaffected.

Figure 1.

Typical male pattern hair loss.

Female pattern hair loss characteristically spares the anterior hairline (in other words the hairline is retained) (Figure 2) and women typically first notice an increase in the width of their part over the crown. A useful physical examination technique is to compare the quality of the part width on the crown of the scalp compared to the occipital scalp. The part width on the crown is wider or more prominent when compared to the part width on the occipital scalp (Figure 3, Figure 4). Note that 10-20% of females have diffuse thinning of the entire scalp.

Figure 2.

Note retained anterior hairline with is classic in female pattern hair loss.

Figure 3.

Part width on crown is wider compared to part width on occiput - see other figure.

Figure 4.

Occipital part width is wider compared to crown part width.

A family history of male or female pattern hair loss is present in only 50% of female patients; focus on first-degree relatives.

A pull test performed on scalp hair is typically negative. In most cases of patterned hair loss, the combination of history and physical examination is enough to confirm the diagnosis.

  • Expected results of diagnostic studies

In females, any evidence of androgen excess warrants further work-up. This includes a history or physical findings of persistent acne, irregular menstrual cycles, infertility, hirsutism, galactorrhea or virilization. These patients should have an evaluation of their serum total testosterone, serum free and total testosterone, serum dehydroepiandrosterone sulfate (DHEAS) and serum prolactin.

I normally do not check a thyroid-stimulating hormone (TSH) as hair loss related to hypo/hyperthryoidism most commonly presents with diffuse hair thinning, as opposed to "patterned" hair thinning. However, there are reports of patterned hair thinning presenting with hypothryoidism-induced hair loss and a TSH can be checked in the appropriate historical context.

Scalp biopsy is rarely needed. However, in cases where the diagnosis is uncertain, a simple biopsy of the scalp is confirmatory. A 4mm punch sent for horizontal sectioning will reveal most markedly a change in the ratio of terminal to vellus hairs from the normal 9:1 to a ratio lower than or equal to 4:1 (Figure 5).

Figure 5.

Temporal recession does not respond to medically approved treatments for male and female pattern hair loss.

  • Diagnosis confirmation

For male pattern hair loss, it is rare to have a differential diagnosis as the history and physical examination is straightforward. Occasionally scarring alopecias, specifically central centrifugal cicatricial alopecia, can present similarly to male pattern hair loss. However, in scarring alopecia, the follicular orifices are obliterated and the skin has the feeling of “slick cement.”

For female pattern hair loss, there is a differential diagnosis. Central centrifugal cicatricial alopecia can involve only the crown of the scalp. Lack of follicular orifices distinguishes this condition from female pattern hair loss, where the follicular orifices are visibly recognized.

Two variants of lichen planopilaris, namely frontal fibrosing alopecia (FFA) and fibrosing alopecia in a patterned distribution (FAPD), can be confused with female pattern hair loss. FFA affects the frontal rim of the scalp, with females often noting recession of the hairline. This condition typically starts after the age of 40. FAPD involves the crown of the scalp, and like other scarring conditions, results in loss of follicular orifices.

Rarely, trichotillomania can present in a pattern similar to female pattern hair loss. Look for broken hairs and hairs of variable length. Often times, a psychiatric disease accompanies trichotillomania in an adult.

Who is at Risk for Developing Alopecia - androgenetic?

Both males and females of all races are equally affected by pattern hair loss. It is estimated that 50% of males and females have some degree of pattern hair loss by age 50. Male and female pattern hair loss can express itself any time after puberty, most often appearing between 20 and 30 years of age. Expression can also occur during or after the fifth decade in both genders. Male and female pattern hair loss is thought of as autosomal dominant disease with variable penetrance.

What is the Cause of Alopecia - androgenetic?

  • Pathophysiology

Male pattern hair loss is caused by a genetically programmed follicular sensitivity to androgens in select regions of the scalp, most notably dihydrotestosterone (DHT). The intracellular enzyme 5α-reductase converts circulating testosterone to DHT which then acts on specific intracellular receptors within the follicle to produce a shortened anagen phase, resulting in follicular atrophy (Figure 6). The role of androgens in the pathogenesis of female pattern hair loss remains to be elucidated.

Figure 6.

Androgenetic alopecia showing miniaturization of the hair shafts. (Courtesy of Bryan Anderson, MD)

Systemic Implications and Complications

Hair loss can have a dramatic impact on an individual's psychosocial well-being. It is important to assess how well a patient is coping with her or his loss. This can be done with simple questioning.

Treatment Options

Treatment options are summarized in Table I.

Table I.

Therapeutic options
Medical Treatment Surgical Procedures Physical Modalities
Minoxidil 2% topical solution BID (FDA approved for males and females) Follicular unit hair transplantation Hair piece
Minoxidil 5% topical solution or foam BID (FDA-approved for males only)
Finasteride 1mg PO Daily (FDA-approved for males only) Improved coverage with hair styling and coloring
Antiandrogens (females only):
Spironolactone 100-200mg PO Daily
+
Oral contraceptive pills

Optimal Therapeutic Approach for Alopecia - androgenetic

- Patients should be counseled that hair washing and styling will not expedite loss.

- Patients should also be informed that 6 months to a year of treatment may be necessary before results are seen.

- Baseline photographs of the scalp for both men and women should be taken at the time of initial visit for comparison at return appointments.

Men

- FDA approved therapies: topical minoxidil and oral finasteride

- Minoxidil is available in 2% and 5% topical solutions and a more cosmetically appealing 5% foam vehicle. Minoxidil should be applied directly to the scalp, not to the hair itself. Minoxidil is best at maintaining the current density of hair, and reports show that 40% of men will experience at least moderate regrowth. If the drug is discontinued, its benefits will be lost in 3 to 6 months. Minoxidil is not effective in treating regression of the bitemporal hairline. The most common side effect is scalp irritation, which generally improves with repeated applications.

- Finasteride 1mg by mouth daily. Reports show that 90% of men will maintain the hair they have, and approximately 67% will see regrowth. Like topical minoxidil, a 6-month trial of treatment is warranted before declaring treatment failure. If the drug is stopped, benefits will be lost within a year. Males over the age of 40 years need a baseline PSA level. Finasteride will decrease the PSA level by 1/2. Sexual side effects such as impotence are rare and often improve with treatment continuation. However, there are rare cases where decreased libido may not improve and appropriate referral is warranted for further investigation.

Women

- Minoxidil 2% solution is the only FDA-approved treatment for female pattern hair loss. Minoxidil is most effective at slowing the progression of hair thinning and in approximately 40% of cases improvement in density is expected after 4 months of treatment. Seven percent of women using minoxidil can develop symmetrical facial hypertrichosis that readily reverses once the medication is stopped. Scalp irritation can develop but often improves with continued treatment.

Some clinicians recommend 5% solution to use daily, but this is off label and should be appropriately discussed with the patient. Most of my female patients use the 5% minoxidil foam on a nightly basis. The foam is less messy compared to the solution and once-daily application promotes compliance. This is an off-label use of this over-the-counter medication.

- Antiandrogen therapy is particularly important in cases where systemic androgen excess is associated with female pattern hair loss, but may also be used in conjunction with topical minoxidil in resistant cases. Spironolactone is prescribed at a dose of 50-100mg twice daily. In order to avoid the two most common side effects of spironolactone, breast tenderness and menstrual irregularity, an oral contraceptive should be prescribed concomitantly. Results should be expected in 6 months.

Female patients must not become pregnant on spironolactone. In addition, if there is a personal or family history of breast cancer in a first degree relative, I recommend consultation with the primary care physician or gynecologist. However, there is not a clear link between spironolactone use and increased risk of breast cancer.

- The goal of treatment is maintenance and/or improvement of hair density.

- Follicular Unit hair transplant - Follicles from androgen insensitive regions such as the occiput and inferior temporal vicinity, are transplanted to affected areas. Patients must have sufficient density of hair in donor sites. The procedure is expensive but can achieve very cosmetically pleasing results. It is important to select the proper candidate, as females with diffuse thinning are not candidates.

- Hair pieces - There are a variety of hair pieces available capable of achieving a natural appearance.

Patient Management

Patients should be followed routinely to monitor the efficacy of therapy. Comparison photographs can be useful in demonstrating a course of improvement. The impact of the hair loss on the patient's well-being should be observed.

Unusual Clinical Scenarios to Consider in Patient Management

The results of recent retrospective studies indicate that patterned hair loss may be associated with a higher incidence of risk factors for cardiovascular disease. These risk factors include the presence of the metabolic syndrome and carotid atheroma. Patients should be encouraged to seek age-appropriate screening for cardiovascular disease risk factors from their primary care physicians.

Both finasteride and dutasteride do not appear to prevent prostate cancer. Both drugs shrink prostate tumors temporarily in patients with tumors that have low potential for being lethal. Furthermore, both drugs lower PSA levels and may delay diagnosis of prostate cancer, but further analysis is ongoing and should continue to be looked at based upon the "prostate cancer prevention trial."

What is the Evidence?

Johnson, R, Wolff, K. "Color atlas and synopsis of clinical dermatology, common and serious diseases". McGraw Hill. 2009. pp. 965-70.

(An excellent text detailing history, pathophysiology, epidemiology, diagnosis and treatment of male and female pattern hair loss.)

Marks, J, Miller, J. "Lookingbill and Marks' principles of dermatology". Saunders Elsevier. 2006. pp. 265-7.

(An excellent text detailing history, pathophysiology, epidemiology, diagnosis and treatment of male and female pattern hair loss.)

Mounsey, AL, Reed, SW. "Diagnosing and treating hair loss". Am Fam Physician.. vol. 80. 2009. pp. 356-62.

(A broad review of nonscarring alopecia separated into focal and non-focal causes. Details pathophysiology, physical exam findings and current standards of treatment.)

Price, VH. "Treatment of hairloss". N Engl J Med. vol. 341. 1999. pp. 964-73.

(An excellent review of treatment options for different types of hair loss that includes a discussion on when laboratory testing would be indicated for diagnostic purposes.)

Salvador, AS, Gutierrez-Salmeron, MT. "Androgenetic alopecia and cardiovascular risk factors in men and women: A comparative study". J Am Acad Dermatol. vol. 63. 2010. pp. 420-38.

(A retrospective case control study comparing risk factors for cardiovascular between androgenetic alopecia patients and controls presenting to a dermatology practice in Spain. The authors found a higher incidence of the metabolic syndrome, carotid atheroma, insulin resistance, elevated concentrations of inflammatory markers, and decreased concentrations of sex hormone binding globulin in patients with patterened hair loss when compared to controls. The piece also includes a discussion of the possible pathophysiology underlying the association.)

Shapiro, J. "Hair loss in women". N Engl J Med. vol. 357. 2007. pp. 1620-30.

(Another excellent and up to date review on hair loss, including a discussion tailored to female pattern hair loss.)

Sinclair, R, Wewerinke, M, Jolley, D. "Treatment of female pattern hair loss with oral antiandrogens". Br J Dermatol. vol. 152. 2005. pp. 466-73.

(An uncontrolled study testing cyproterone acetate and spironolactone as therapies for female pattern hair loss. Also includes background discussion on the use of antiandrogens in female pattern hair loss. Eighty female patients with patterned hair loss were given either spironolactone or cyproterone and reevaluated at least 12 months later. Eighty-eight percent maintained the hair they had or experienced regrowth. No significant difference was appreciated between cyproterone acetate and spironolactone.)

Rinaldi, S, Bussa, M, Mascaro, A. "Update on the treatment of androgenetic alopecia". Eur Rev Med Pharmacol Sci. vol. 20. 2016 Jan. pp. 54-8.

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