 |  | Androgenetic alopecia in men and women |  |
Copyright 1997
Information Access Company, a Thomson Corporation Company;
ASAP Copyright 1997 Jannetti Publications, Inc. Dermatology Nursing
December, 1997
SECTION: No. 6, Vol. 9; Pg. 379; ISSN: 1060-3441
LENGTH:
3380 words
HEADLINE:
Androgenetic alopecia in men and women: an overview of cause and treatment;
Continuing Education Series, with test
BYLINE:
Roberts, Janet L.
AUTHOR-ABSTRACT:
Hair loss is a cause of anxiety and distress in both men and women. New
understanding of the causes of androgenetic alopecia is leading to potential
new medical therapies. Pathophysiology, clinical presentations, diagnosis,
current and future treatments are discussed.
BODY:
Objectives
This independent study offering is designed for nurses and other health care
professionals who care for and educate patients regarding androgenetic
alopecia. A multiple choice examination follows this article and is designed to
test the reader's achievement of the objectives listed below. After studying
the information presented in this article, the reader will be able to:
1. Understand the causes of androgenetic alopecia.
2. Distinguish androgenic alopecia in men and women.
3. Describe the psychological effects of androgenetic alopecia.
4. Distinguish androgenetic alopecia from other causes of hair loss.
5. List current and potential treatments.
A brief review of the anatomy of hair follicles and the continuous cycles they
undergo will provide the basis for describing the alterations that occur in
androgenetic alopecia. The hair follicle comprises the dermal papilla which
invaginates into the base of the follicle where rapidly dividing matrix cells
are located (see Figure 1). Matrix cells differentiate into the hair shaft and
several specialized layers. The rich environment of the dermal papilla provides
nutrients and signals for differentiation and proliferation.
[Figure 1 ILLUSTRATION OMITTED] PAGE 2 Dermatology Nursing December, 1997
Each hair follicle undergoes continuous cycles of growth, rest, and regrowth.
The timing of these phases varies from site to site on the body. The growth
cycle is called the anagen phase which lasts from 2 to 8 or more years on the
scalp. This is followed by a brief transition phase called the catagen phase
lasting no more than 2 to 3 weeks, progressing into the telogen (resting) phase
lasting 2 to 3 months on the human scalp. The hair then immediately begins a
new anagen growth phase (see Figure 2).
[Figure 2 ILLUSTRATION OMITTED]
Clinical Presentation of Androgenetic Alopecia
Alopecia is a general term for hair loss and requires further description.
Androgenetic alopecia (AGA) is the most common cause of hair loss, presenting
as loss of hair over the top (vertex) of the scalp in affected men and women.
AGA is associated with normal levels of estrogens and androgens in both men and
women. The term androgenetic alopecia denotes that both a genetic
predisposition and the presence of androgens are necessary to cause expression.
The specific mode of inheritance is not known.
Androgenetic Alopecia in Men
In men, androgenetic alopecia, also called male pattern hair loss, is
characterized by hair loss in the frontal and vertex areas of the scalp.
Several patterns are commonly recognized and classified according to the
Hamilton (Hamilton, 1942) and Norwood classifications (Norwood, 1975). These
classifications are based on the degree of hair thinning and the affected areas
of the scalp (see Figure 3). AGA in men begins anytime after onset of puberty.
[Figure 3 ILLUSTRATION OMITTED]
Androgenetic Alopecia in Women
In women, androgenetic alopecia, also called female diffuse thinning, presents
with more diffuse thinning in a mosaic pattern over the vertex of the scalp.
The frontal hairline is usually retained. Occasionally there is a prominent
triangle of thinning behind the retained frontal fringe (see Figure 4). Part
width over the vertex is widened when compared to the back of the scalp (see
Figures 5 and 6). Onset is generally in late 20s to 30s. The hair loss in women
is usually less dramatic than that seen in men. Originally, the degrees of
thinning were divided into three categories by Ludwig (1977) (see Figure 7).
More recently, Savin (1994) devised a scale based on eight categories of
density and part width over the vertex of the scalp. Affected women are not
virilized. Onset and exacerbation of hair loss often occurs at times of
hormonal upheavals such as puberty, postpartum, use of oral contraceptives, and
the early post-menopausal period. See Figures 8 and 9 for comparisons of AGA in
men and women.
[Figures 4-9 ILLUSTRATION OMITTED]
Prevalence
Approximately 20% of Caucasian men are affected by the age of 20 with incidence
increasing 10% per decade. Fifty percent of Caucasian women are affected by age
50. Racial differences are noted with more Caucasians affected PAGE 3
Dermatology Nursing December, 1997
than Asian and Negroid races (Olsen, 1993).
Psychosocial Aspects
Recent studies on the quality of life in men and women with AGA show that loss
of scalp hair can have major psychologic effects. Men with AGA may feel less
attractive and older than their peers leading to diminished self-esteem,
stress, anxiety, depression, and social inadequacy (Cash, 1992). Women with AGA
have both social and emotional concerns. They may be frustrated at the time and
trouble necessary to camouflage thinning hair and the inability to style their
hair as they would like. They may feel self-conscious that others will notice
hair loss, embarrassment, decreased self-esteem, and jealousy of other women
who are blessed with bountiful scalp hair (Cash, Price, & Savin 1993;
Girman, Hartmaier, Roberts, Bergfeld, & Waldstriecher, 1996).
Pathophysiology of Androgenetic Alopecia
Although the clinical presentation is different in men and women, the
underlying cellular processes causing AGA are thought to be similar. AGA is
caused by androgens in both men and women. Androgens are produced in men by the
testes and adrenal glands. In women, androgens are produced by the ovaries and
adrenal glands. Androgens produced peripherally by endocrine-sensitive hair
follicles and sebaceous glands also contribute significantly to circulating
androgens in both men and women. All men and women with AGA have normal levels
of circulating androgens.
The androgen dihydrotestosterone (DHT), a potent metabolite of the androgen
testosterone (T), causes a gradual, progressive shrinkage in the length and
caliber of genetically programmed hair follicles. This process is called
miniaturization. Miniaturization results from shortening of the anagen phase
and a decrease in the sit of the dermal papilla and volume of matrix cells.
Consequently, each succeeding hair cycle results in production of smaller,
finer hairs which contribute less to the overall appearance and density of the
hair (Messenger, 1993) (see Figure 10). Increased shedding of miniaturized
hairs and minor inflammation, as manifested by seborrheic dermatitis, may
occur.
[Figure 10 ILLUSTRATION OMITTED]
These biochemical events occur at the cellular level of the hair follicle.
Because the dermal papilla is highly vascular, it is continuously bathed in
circulating androgens. It has been demonstrated that the dermal papilla is rich
in androgen receptors and is the primary target of androgen action (Choudhry et
al., 1996; Randall, Thornton, Hamada, & Messenger, 1992). Cells in
genetically programmed hair follicles contain the enzyme 5[Alpha]-reductase
(5[Alpha]R). 5[Alpha]R converts T into the more potent DHT (Chen, Zouboulis,
& Orfanos, 1996) (see Figure 11). 5[Alpha]R is found in higher quantities
in the scalp follicles of affected men and women (Sawaya & Price 1997).
Androgen receptors in the cells of the dermal papilla bind with circulating
DHT, forming androgen-receptor complexes. These complexes are presented to
binding sites on the DNA in the cell nuclei of the dermal papilla. Modified DNA
sends messages via messenger RNA to the matrix cells, creating proteins to
carry out the androgen effects of miniaturization on the hair follicle (Randall
et al., 1992) (see Figure 12).
[Figures 11-12 ILLUSTRATION OMITTED] PAGE 4 Dermatology Nursing December, 1997
Aromatase, present in the outer root sheath of the hair follicle, is another
enzyme that plays an important function in androgenetic alopecia. This enzyme
converts testosterone and dihydrotestosterone back into estrogens. Aromatase is
approximately six times more abundant on the female frontal scalp as compared
to males, and may be responsible for the less severe expression of AGA in women
(Sawaya & Price, 1997). It may also explain retention of the anterior
hairline in women.
Differential Diagnosis of Androgenetic Alopecia
In general, the clinical appearance and history of AGA in men is
straightforward and does not present a diagnostic challenge. Because the
pattern is more ambiguous in women, several other types of hair loss may mimic
AGA and should be kept in mind when evaluating patients.
Telogen effluvium. Women are especially prone to increased shedding of telogen
hairs from various physical insults, a condition called telogen effluvium.
Acute and chronic illnesses, abrupt hormonal changes, iron and dietary protein
deficiency, and many medications can all cause an increased shift of hairs into
the telogen phase with a resultant increase in shedding. This shedding is
accentuated along the frontal hairline and vertex of the scalp and can easily
mimic AGA. Sometimes an episode of telogen effluvium hastens expression of AGA
in genetically prone individuals (see Figure 13).
[Figure 13 ILLUSTRATION OMITTED]
Alopecia areata. Alopecia areata is an autoimmune condition which usually
presents as patchy hair loss, but occasionally presents initially as increased
shedding and diffuse hair loss. The onset tends to be more dramatic and severe
than AGA and alopecia areata is usually progressive to a patchy hair loss
pattern (see Figure 14).
[Figure 14 ILLUSTRATION OMITTED]
Scarring or permanent alopecia. There are several types of hair loss which
cause permanent destruction of the follicles. Hair loss is usually patchy with
obvious signs of scalp inflammation. However, hair loss can be diffuse and the
scalp may not appear clinically inflamed. Early recognition and treatment are
important to prevent permanent hair loss (see Figure 15).
[Figure 15 ILLUSTRATION OMITTED]
Androgenic alopecia. Androgenic alopecia is caused by increased androgen
production in women. It is usually accompanied by other signs of androgen
excess such as irregular menstruation, infertility, hirsutism (increased
secondary sexual hair in the male distribution), acne, and oily skin. Onset is
generally earlier than AGA. Hair loss is more severe and may mimic the pattern
of AGA in men (see Figure 16). Women with suspected androgenic alopecia should
be evaluated by an endocrinologist or by a dermatologist with special expertise
in androgen-related hair conditions.
[Figure 16 ILLUSTRATION OMITTED]
Clinical evaluation. Evaluation of women with hair loss should include
documentation increased hair loss by actual hair counts. An average daily PAGE
5 Dermatology Nursing December, 1997
count of 50 to 100 hairs is normal. A careful medical history should be taken,
including recent surgeries or illnesses, dietary habits, weight loss,
medications, menstrual and pregnancy history. Clinical examination of the
patient includes evaluating hair density, pattern, length, and evidence of
regrowth. The scalp should be checked for signs of scarring alopecia including
inflammation, obliteration of follicular orifices, and atrophy. At a minimum,
laboratory examinations, including thyroid and iron evaluation, should be
obtained. Serum ferritin levels are the most helpful; desired values are 40-300
ng/ml. Women with AGA having regular menses, normal fertility, and no stigmata
of virilization do not require endocrinologic evaluation.
Treatments for Androgenetic Alopecia
Surgical treatments. Surgical treatments for AGA, including hair follicle
transplantation, have been increasingly refined in the past several years and
are beyond the scope of this article. Readers are referred to the September
1997 issue of Dermatologic Surgery for a complete review of this subject
(Slough, 1997).
Medical treatments. Medical therapy for androgenetic alopecia can be divided
into the following categories: (a) nonspecific promoters of hair growth, (b)
topical and systemic anti-androgens, (c) 5-reductase inhibitors.
Nonspecific promoters of hair growth. Minoxidil is the best known drug in this
category. Minoxidil is an oral medication used to treat refractory
hypertension. It was noted to cause hypertrichosis (increased nonsexual hair
growth). Mechanism by which it stimulates hair growth is unknown. Clinical
trials have shown that a 2% solution applied topically to the scalp can
stimulate hair growth in some men and women. Fewer than 5% of patients have
dense regrowth while approximately 30% have moderate regrowth (Olsen, Weiner,
DeLong, & Pinnell, 1985; Roberts, 1987). Continued use is required to
maintain hair growth. Currently, it is the only drug FDA approved for treating
AGA. Five-percent topical minoxidil solution has proven more effective than the
2% solution in men and has been approved by the FDA for sale over-the-counter
in the United States. (It has been available in Canada).
Anti-androgens. This term describes topical or systemic drugs which reduce
production of androgens, interfere with androgen metabolism, or prevent
androgen activity at target sites such as endocrine-sensitive hair follicles.
Because systemic anti-androgens reduce circulating testosterone, which is
required for normal male sexual functioning, their use is limited to women
(Straw, 1996). Numerous topical preparations, such as estrogen, progesterone,
and cyoctol have not been thoroughly tested in clinical studies (Olsen, 1993).
Spironolactone is a potassium-sparing diuretic used for treating mild
hypertension. Oral spironolactone is used fairly widely for treating women with
AGA although literature documentation of efficacy is sparse. Spironolactone
works by decreasing adrenal and ovarian androgen production. It also competes
with T and DHT for androgen receptors in the hair follicle cells. Doses in the
range of 100 to 200 mg are used. Side effects can include breast tenderness and
menstrual irregularities. Women using spironolactone should be protected from
pregnancy and have yearly Pap smears and mammograms (Straw, 1996).
Oral contraceptive pills (OCP) decrease production of ovarian androgens (Shaw,
1996). The progestin component also competes with T and DHT for PAGE 6
Dermatology Nursing December, 1997
androgen-receptor binding in the hair follicles. Oral contraceptive pills can
be relatively estrogenic or androgenic. Estrogenic OCPs are suggested if used
for women with AGA (see Table 1).
Table 1. Oral Contraceptive Pills
Progestins (Most to Least Estrogenic) Brand Names
Desogestrel Desogen, Ortho-Cept
Norgestimate Ortho-Cyclen,
Ortho-Tri-Cyclen
Norethindrone Micronor, Nor-QD,
Ovcon-35, Brevicon,
Modicon
Ortho-Novum 7/7/7,
Ortho-Novum 10-11.
Tri-Norinyl, Norinyl,
Ortho 1/35
Ethnodiol diacetate Demulen 1/35
Levonorgestrel Triphasal, Tri-Leviin,
Nordeue, Alesse-28
Norgestrel Lo/Ovral, Ovreue, Ovral
Norethindrone acetate Loestrin 1/20, Loestrin
1.5/30 PAGE 7 Dermatology Nursing December, 1997
5[Alpha]-reductase inhibitors. Drugs in this class work by inhibiting the
enzyme 5[Alpha]R, which limits the conversion of T to DHT (Chen et al., 1996).
Finasteride is the first drug in this class to undergo extensive clinical
trials in men. Finasteride has selective activity against 5[Alpha]R. As a
result, serum and follicular DHT levels are significantly reduced (Dallob et
al., 1994). Finasteride has no androgenic or estrogenic hormonal activity.
Because testosterone levels are not significantly affected, finasteride is not
considered an anti-androgen and may be safely used in men.
Summary
Androgenetic alopecia occurs frequently in both men and women. It is caused by
the action of dihydrotestosterone, a potent metabolite of testosterone, on
endocrine-sensitive hair follicles. It can be the cause of significant social
and emotional distress. Dermatology nurses can help educate their androgenetic
alopecia patients by understanding the clinical presentation, differential
diagnosis, pathophysiology, and current and future therapies related to this
condition.
References
Cash, T.F., Price, V.H., & Savin, R.C. (1993). Psychological effects of
androgenetic alopecia on women: Comparisons with balding men and with female
control subjects. Journal of the American Academy of Dermatology, 29(4),
568-575, 926-931.
Cash, T.F. (1992). The psychological effects of androgenetic alopecia in men.
Journal of the American Academy of Dermatology, (26), 926-931.
Chen, W., Zouboulis, Ch.C., & Orfanos, C.E. (1996). The 5-reductase system
and its inhibitors. Dermatology, 193, 177-184.
Choudry, R., Hodgins, M.B., Van der Kwast, T.H., Brinkmann, A.O., &
Boersma, W.J.A. (1992). Localization of androgen receptors in human skin by
immunohistochemistry: Implications for the hormonal regulation of hair growth,
sebaceous glands and sweat glands. Journal of Endocrinology, 133 467-475.
Dallob, A.L., Sadick, N.S., Unger, W., Lipert, S., Geissler, L.A., Gregoire,
S.L., Nguyen, H.H., Moore, E.C., & Tanaka, W.K. (1994). The effect of
finasteride, a 5-reductase inhibitor, on scalp skin testosterone and
dihydrotestosterone concentrations in patients with male pattern baldness.
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Girman, C.J., Hartmaier, S., Roberts, J., Bergfeld, W., & Waldstreicher, J.
(1996). Patient-perceived importance of negative effects of androgenetic
alopecia in women. Unpublished manuscript.
Hamilton, J.B. (1942). Male hormone is a prerequisite and an incitant in common
baldness. American Journal of Anatomy, 71, 451-480.
Ludwig, E. (1977). Classification of the types of androgenetic alopecia (common
baldness) occurring in the female sex. British Journal of Dermatology, 97,
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Messenger, A.G. (1993). The control of hair growth: An overview. Journal of
Investigative Dermatology, 101, 4S-9S.
Norwood, O.T. (1975). Male pattern baldness: Classification and incidence.
Southern Medical Journal, 68, 1359-1365.
Olsen, E.A., Weiner, M.S., Delong, E.R., & Pinnell, S. (1985). Topical
minoxidil in early male pattern baldness. Journal of the American Academy of
Dermatology, 13, 185-192.
Olsen, E.A. (1993). Androgenetic alopecia. In E.A. Olsen (Ed.), Disorders of
hair growth: Diagnosis and treatment (pp. 257-283). New York: McGraw-Hill, Inc.
Randall, V.A., Thornton, M.J., Hamada, K., & Messenger, A.G. (1992).
Mechanism of action in cultured dermal papilla cells derived from human hair
follicles with varying responses to androgens in vivo. The Journal of
Investigative Dermatology, 98(6), 86-91.
Roberts, J. (1987). Androgenetic alopecia: Treatment with topical minoxidil.
Journal of the American Academy of Dermatology, 16(3), 705-710.
Savin, R.C. (1994). Upjohn Dermatology Division. Kalamazoo, MI: Upjohn Company.
Sawaya, M.E., & Price, V.H. (1997). Different levels of 5[Alpha]-reductase
type I & II, aromatase, and androgen receptors in hair follicles of women
and men with androgenetic alopecia. The Journal of Investigative Dermatology,
10(3), 296-300.
Shaw, J.C. (1996). Antiandrogen therapy in dermatology. International Journal
of Dermatology, 35(11), 770-776.
Stough, D. (Ed.). (1997). Special issue: Hair. Dermatologic Surgery, 23(9).
Janet L. Roberts, MI), is Clinical Professor of Dermatology, Oregon Health
Sciences University, Portland, OR; and is in Private Practice in Portland.
GRAPHIC: Photograph; Table; Chart; Diagram; Illustration
LANGUAGE: ENGLISH
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