AGA onset may be at any age following puberty, showing an increasing frequency with age.

The etiology of AGA is multifactorial and polygenic with, as of this writing, 12 genetic regions
recognized to associate with AGA in men. In men, AGA is an androgen-dependent trait. Even
though the role of androgens in female AGA is less certain than in men, there is a subset of
women with AGA and associated hormonal dysregulation.

Generally, diagnosis of AGA is based on history and clinical examination. Depending on

patient history and clinical evaluation, however, additional diagnostics may become
necessary to exclude differential diagnoses; for example, ferritin level or thyroid-stimulating
hormone in diffuse effluvium or endocrinologic workup in women with signs of
hyperandrogenism. Biopsy is very rarely indicated in AGA. Biopsy is indicated only if, for
example, the differential diagnoses cicatricial alopecia or diffuse alopecia areata are
suspected.

AGA has a naturally progressive course, meaning that the main therapeutic aim is the
prevention of disease progression or enhancement of hair growth during the early, mild to
moderate stages of the disease. The best clinical evidence according to current study data
exists for topical application of minoxidil in both genders and for the oral intake of
finasteride in men. Alternatively, cosmetically satisfactory results can be achieved using hair
transplantation in nonprogressive stable AGA wwith sufficient available donor area.

Patient and family history of the first manifestation of hair loss and of the course of hair loss
(chronic or intermittent) should be documented. Patients with AGA usually complain about
a longstanding, slowly progressing reduction of hair density, sometimes even without
noticing significant hair loss. Patients typically describe hair thinning with an accentuation of
the frontal, parietal, or vertex region, but diffuse thinning is possible as well. Pruritus and
trichodynia may present as initial signs of AGA. The family history for AGA is often positive.
A positive family history for other hair disorders may facilitate differential diagnostic
conclusions and lead to further diagnostic procedures.

In women, especially in those with peripheral signs of hyperandrogenism, a gynecologic

history is recommended, including among other possibilities, menstrual cycle disturbances
and intake of hormonal contraception.
Furthermore, a detailed patient history should be performed to rule out other causes for the
hair loss or aggravating factors.
Patient interview should include systemic and newly diagnosed diseases (eg, infections,
thyroid function disorders, and surgical procedures) that occurred 6 months to 1 year prior
to the first signs of hair loss, and nutritional behavior (especially chronic deficient diet or
rapid significant weight loss) possibly leading to diffuse effluvium.

Lifestyle procedures, such as special hairstyles causing traction, and environmental factors
like smoking and ultraviolet radiation exposure should be considered. A drug history should
be taken to identify a possibly drug-related hair loss, such as after treatment with
chemotherapeutic agents, hormones with proandrogenic or antithyroid action, intake of
anabolic steroids, or supplemental androgens. Allergies and intolerances should be recorded
as they might be important for the choice of the appropriate therapy (eg, contact dermatitis
caused by propylene glycol in topical solutions)1 as well as cosmetic habits (eg, hair care and
color, hair style).

MALE PATTERN HAIR LOSS / MALE PATTERN, HAMILTON NORWOOD TYPE

This is the most frequent clinical pattern in men with AGA, and only occasionally observed in
women. Recession of the frontal hairline, mainly in a triangular pattern is the characteristic
finding, later followed by a vertex thinning with progression until the top of the scalp is
completely bald (Figs. 85-1 and 85-2). Occipital area and sides of the scalp are spared even
in longstanding male pattern hair loss.

FEMALE PATTERN HAIR LOSS FEMALE PATTERN, LUDWIG TYPE

The so-called female pattern hair loss is characterized by a diffuse thinning of the
centroparietal region with maintenance of the frontal hair line (Fig. 85-3). It is the most
common type of AGA in women; it is occasionally observed in men. There are 2 scales
describing this pattern, the 3-point Ludwig scale (Fig. 85-4) and the 5-point Sinclair scale
(Fig. 85-5).

Telogen effluvium (TE) was originally described by Kligman in 1961. TE is best characterized
by a premature termination of the anagen (growing) phase of hair follicles, with a resultant
increase in telogen (resting) phase hairs leading to excessive and diffuse loss of club hairs.

Classically, TE refers to an acute hair loss subsequent to a variety of stresses including those
caused by febrile diseases, childbirth, emotional disturbance, chronic systemic diseases, or
the administration of heparin. TE can be a physiologic event in the newborn. Later studies
revealed that the trigger and manifestation of TE were variable. TE represents the most
common cause of diffuse hair loss. In clinics, truly diffuse hair loss is not often encountered.

The most common reason bringing TE patients to the clinic is the increase in hair shedding
after shampooing or brushing alone. Typically, TE is self-limiting, and full recovery can be
expected once the specific causes are identified and corrected. However, especially in
nonclassical chronic TE in women, distinction between female pattern hair loss is often
challenging. In this chapter, the clinical features, pathophysiology, and differential diagnoses
of TE are discussed.

Depending on the clinical course and symptoms, TE can be subdivided into 3 subgroups:
classic acute TE, chronic diffuse telogen hair loss, and chronic telogen effluvium.

Irrespective of clinical subtypes, the most representative manifestation of TE is diffuse

excessive shedding of club hairs. It should be noted that in severe TE cases, apparent diffuse
or bitemporal hair thinning can be observed; however, hair loss is often subclinical and
increased hair shedding can be the only objective sign in TE. In some cases, hair shedding
has already peaked out and shed hairs carried by a patient alone is indicative of TE history.
The clinical features of each subset are listed below.

Acute telogen
Efluvium of the newborn
Febrile illness
Surgery
Pregnancy
Weight loss (crash diet)
Drugs (may cause CDTHL)

Chronic diffuse telogen hair loss (CDTHL)

Thyroid disease
Aging
Malnutrition
Iron deficiency (controversial)
Zinc deficiency (severe cases)
Systemic illness
Psychological stress (controversial)
STD (HIV infection and syphilis)
Miscellaneous

Chronic telogen effluvium

Idiopathic (shortening of anagen)