Androgenetic alopecia is a common disorder in Malaysia. It is estimated that at least 50% of men develop androgenetic alopecia or male pattern hair loss at some point in their lives. Androgenetic alopecia has important psychosocial impact on patients.

The basic pathophysiology of androgenetic alopecia involves the miniaturization of scalp hair follicles in site specific areas due to a genetic predisposition being translated by a hormonal mechanism. Current evidence indicates that dihydrotestosterone(DHT) is the hormonal messenger. Currently, the only pharmacological agents that are scientifically proven effective are oral Finasteride and topical Minoxidil. Surgical treatment is an option for selected patients. Except for surgery, currently available pharmacological treatments are suppressive and not curative. Supporting the patients emotionally and ensuring that they understand the limitation of these treatments remains an important component of the management of androgenetic alopecia.

Definition

Androgenetic Alopecia (AGA) is a genetically determined pattern of baldness mediated by increased follicular androgen sensitivity leading to follicular minituarization with characteristic and progressive pattern of baldness in males and females.

Clinical Features

In both sexes the essential feature is replacement of terminal hair by progressively finer and shorter vellus hair in a frontovertical distribution. The onset may be any time after puberty and may be clinically apparent by age 17 in normal Caucasian males and 25-30 years in normal Caucasian females.

In our Asian context, the prevalence of AGA. in Chinese is less common than in Caucasians, milder and of later onset . Japanese males for instance develop AGA. 10 years later than Caucasoids and have 1.4 times less AGA in each decade of life. In all races, the reduction in follicle size is associated with shortened anagen and increased shedding of telogen hair .

Males

The distinctive pattern as described by Hamilton and later modified by Norwood spares the posterior and lateral scalp even in the most severe cases. (see figure 1) The sequence and rate of progression can be vacariable but usually starts with bitemporal recession, balding of the vertex, then uniform balding of the frontal area which merges with the bald vertex. Eventually the frontovertical area contains only sparse vellus hairs which are finally lost.

Females

The pattern of A.G.A in women is likely to be that of a diffuse vaultal alopecia – the Ludwig pattern or ‘female pattern baldness’. The progression from Ludwig I-III is usually very slow but accelerates around menopause. Abnormal androgen excess needs to be excluded in premenopausal female with Ludwig IIIII baldness, Hamilton pattern IV or more. The Hamilton type of baldness is more common after menopause. In pre-menopausal women, 13% Hamilton type II-IV, while in post-menopausal women, the

frequency of Hamilton type II-V increase to 37%.

Diagnosis

Males

The characteristic Hamilton-Norwood pattern of alopecia , history of increased shedding, and a strong

family history makes the diagnosis easy. Other causes of hair loss have to be considered .

Females

Diagnosis may be more difficult in women with AGA. but generally before menopause the Ludwig pattern of alopecia is seen . In difficult cases where there is no family history of AGA, together with evidence of androgenic excess eg. acne, hirsutism, a menstrual disturbance, it may be necessary to evaluate the patient over a period of weeks, perform endocrinological assessments, and even scalp biopsies (eg to exclude diffuse alopecia

areata, and to prognosticate A.G.A.)

Assessment of severity

The following features indicate a more severe disease :

1. Early age of onset of hair thinning.

2. Family history of AGA in parents, siblings, aunts, uncles and grandparents on both sides of the family.

3. Pattern and distribution of hair thinning /loss:
4. i) Hamilton-Norwood classification for male pattern hair loss (Refer fig. 1)

Mild : pattern I and II

Moderate : pattern IIa to IV

Severe : pattern IV a to VII

1. ii) Ludwig classification for female pattern hair loss (Refer fig. 2).

Mild : Ludwig I

Moderate : Ludwig II

Severe : Ludwig III

Females

The pattern of A.G.A in women is likely to be that of a diffuse vaultal alopecia – the Ludwig pattern or ‘female pattern baldness’. The progression from Ludwig I-III is usually very slow but accelerates around menopause. Abnormal androgen excess needs to be excluded in premenopausal female with Ludwig IIIII baldness, Hamilton pattern IV or more. The Hamilton type of baldness is more common after menopause. In pre-menopausal women, 13% Hamilton type II-IV, while in post-menopausal women, the

frequency of Hamilton type II-V increase to 37%.

Investigations

This is a clinical diagnosis based on recognizing a pattern of alopecia and a family history of AGA. If there is any doubt in diagnosis investigations may be done to includfe out other causes of alopecia. The investigations include :

Microscopic examination of hair shaft and bulbs(clip test).

About 25 to 30 hairs are cut above the scalp surface and examined on a wet microscopic slide.

 Hair pull test

About 60 hairs are pulled with constant traction and the bulbs of extracted hairs examined.

Normally there should be less then 6 club hairs extracted.

Hair pluck test

Abruptly extract hairs from scalp with rubber tipped needle holder and examine the roots. In telogen effluvium > 20% telogen hairs noted.

Blood examination to exclude any systemic disorder

Full Blood Count

VDRL

Serum iron, serum, Ferritin, Total Iron Binding Capacity

Thyroid function test

Anti Nuclear Factor

Scalp biopsy

This is done if the diagnosis of AGA remains questionable. It helps in distinguishing AGA from telogen effluvium, alopecia areata and a concomitant primary scarring alopecia.

MANAGEMENT

Goals of Therapy

1. To slow down further hair thinning
2. To increase hair coverage of the scalp
3. To assist patients to function normally in society as it may have marked psychological impact

People concerned about their androgenetic alopecia have 4 options

1. Do nothing
2. Get aesthetic aids
3. Seek medical treatment
4. Seek surgical treatment

This articles originates from CONSENSUS ON MANAGEMENT OF ANDROGENETIC ALOPECIA MINISTRY OF HEALTH MALAYSIA