Treatment options for androgenetic alopecia

Lydia Rudnitskaya , Professor of the Department of Dermatology at the Medical University of Warsaw (Poland)

Androgenetic alopecia is the most common cause of hair loss in both men and women. The prevalence of the disease increases with age. It is experienced by at least 50% of adult men over 50 years of age and 70% of men over 70 years of age. In women under 30 years of age, the prevalence is estimated to be 3–6%. The corresponding figures for women over 50 years of age are 30–40%.

The main pathogenic factor in the onset of androgenetic alopecia is dihydrotestosterone-triggered follicular miniaturization in androgen-dependent areas of the scalp.

Etiology of the disease

Androgenetic alopecia is provoked by a number of factors, the main of which is genetic predisposition. The disease is based on follicular miniaturization in androgen-dependent areas of the scalp, triggered by the steroid male sex hormone - dihydrotestosterone (DHT). In men with androgenetic alopecia, the manifestation of DHT in the frontal scalp is significantly higher compared to the control group. Inflammatory processes and multiple cytokines are also involved in the pathogenesis of androgenetic alopecia, although their role has not been defined in detail.

Both women and men with androgenetic alopecia have higher 5α-reductase activity in the hair follicles of the frontal region compared to the occipital region. Conversely, a higher concentration of aromatase is observed in the occipital hair follicles. Studies confirm the role of aromatase as a determining factor in reducing the sensitivity of follicles to androgens.

Clinical manifestation of the disease

Men are characterized by hair recession in the frontal region and on the crown. The clinical severity of the disease is assessed using the Norwood–Hamilton scale. In women, hair loss follows the so-called female pattern - in the frontal and parietal areas (Ludwig type, severity is assessed on a three-step scale), or limited to the mid-frontal area (Olsen type), or hair thinning of the “Christmas tree” type. At the same time, the frontal hairline remains unchanged. The above subtypes of female androgenetic alopecia should be differentiated from telogen effluvium, especially in the early stages of the disease.

Differential diagnosis

Telogen effluvium

The cause of hair loss in telogen effluvium is the synchronization of the growth cycle and an increase in the proportion of hairs in the telogen phase. There are three forms of telogen effluvium: acute, chronic and diffuse. Acute telogen effluvium is a self-limiting disorder of hair loss without scarring. Excessive hair loss usually begins 3 months after the initial episode, lasts 3 to 6 months, and ends with complete recovery. Telogen effluvium develops physiologically in the postpartum period. In pathological conditions, sudden hair loss begins several months after the initiating event, which leads to the rapid exit of a significant number of hair follicles from the anagen phase, but the etiological factor remains unknown in approximately 30% of cases. An important role in the diagnosis of acute telogen effluvium is played by a detailed history (infectious diseases, medications used, surgeries, stress), laboratory tests and trichoscopic examination. Laboratory tests recommended to rule out common causes of telogen effluvium are listed in Table 2.

Frontal fibrosing alopecia

Frontal fibrosing alopecia is characterized by recession of the frontal hairline. It differs from male and female androgenetic alopecia by the formation of scar tissue in the area of hair loss. The diagnosis is made on the basis of characteristic clinical manifestations and the results of trichological studies.

Involutional alopecia (alopecia senilis)

Involutional alopecia mainly affects women over 70 years of age. The disease usually involves gradual, progressive hair loss in the crown area. This type of alopecia often does not respond to antiandrogen treatment.

Other diseases

To make a diagnosis of androgenetic alopecia, differential diagnosis should also be carried out with diffuse focal alopecia, focal alopecia of unknown origin, congenital triangular alopecia, trichotillomania, lichen planus follicularis and other diseases in which the location of hair loss may be similar to androgenetic alopecia.

Diagnosis of androgenetic alopecia

In most cases, a well-collected history and clinical examination are sufficient to diagnose a man. In the case of female androgenetic alopecia, trichoscopy should be added to the above points, and in case of suspected telogen effluvium, laboratory tests and a trichogram should be added. If the diagnosis is still unclear, trichoscopic findings should be considered in correlation with histopathological evaluation of scalp biopsy specimens.

Trichoscopy

Trichoscopy can be performed using a portable dermatoscope or videodermatoscope. A portable dermatoscope helps to identify heterogeneity in the thickness of the hair shafts (when more than 20% of the hair shafts are thin), an increase in the proportion of vellus hairs (more than 10%), an increase in the proportion of follicular units with one hair shaft, associated with a decrease in follicular units with three or more hairs. These abnormalities are more noticeable in the frontal region than in the occipital region. Yellow dots are usually rare and have no diagnostic significance. They are empty follicular openings (hair follicles in the kenogen phase). Perifollicular hyperpigmentation is thought to correspond to the presence of inflammatory infiltrates and may be a negative prognostic sign.

Trichoscopy, performed using a videodermatoscope, allows you to evaluate the structures of the scalp at higher magnification. There is a set of symptoms that accompany androgenetic alopecia. The diagnosis is made if two main or one main and two minor signs are present.

Histological examination

For the study, a 4-mm sample is taken from the frontal region. Recently, specialists are abandoning the earlier technique, when several histological preparations were taken simultaneously from different areas. The criterion for diagnosis is the ratio of pigmented hair follicles to vellus hair follicles: a ratio close to 8:1 may be an indicator of telogen effluvium, and a ratio of less than 4:1 is characteristic of androgenetic alopecia.

Treatment of androgenetic alopecia

Drugs with approved indications for the treatment of androgenetic alopecia are minoxidil 2 and 5% for topical therapy and finasteride 1 mg/day. for systemic therapy in men. Other doses and treatments are used off-label, but provide good clinical results.

Minoxidil

Minoxidil 2 and 5% can be prescribed to treat both men and women. Men are usually prescribed minoxidil 5% once or twice daily, women are prescribed minoxidil 2% twice daily or minoxidil 5% once daily.

A temporary side effect after using minoxidil may be sudden telogen effluvium, which usually occurs in the 6th to 8th week of treatment and disappears after several weeks or months of continued therapy. Hair loss will also occur three months after completion of treatment.

The second most common side effect is facial hypertrichosis, which occurs more frequently in patients treated with minoxidil 5%. Patients are advised to take minoxidil at least 2 hours before bedtime to avoid getting the product on the face through the pillow. Scalp irritation and contact dermatitis are more commonly associated with the use of minoxidil 5%, most likely due to the higher concentration of propylene glycol in the formulation. If a contact allergy to propylene glycol is confirmed by a skin test, a slightly different formulation of minoxidil should be considered. Itchy scalp is present in approximately 5% of patients. Other side effects, such as headache, dizziness or tachycardia, are rare and may be due to the drug entering the bloodstream through damaged epidermis. Minoxidil should not be used during pregnancy or breastfeeding.

Finasteride

Finasteride is a selective 5α-reductase-II inhibitor. Finasteride in a single oral dose of 1 mg/day. reduces the concentration of DHT in the blood serum and scalp by approximately 70%. With long-term treatment, tachyphylaxis is not observed. Finasteride is rapidly absorbed from the gastrointestinal tract and reaches maximum concentration in the blood within 1-2 hours after administration. The half-life is six hours.

Read the full version of the article in the magazine Les Nouvelles Esthetiques Ukraine 2 (108)/2018