Dr Z. Shahmoradi
Dermatologist
Hair follicle:
 5 million hair follicles on the human skin
 100,000 on the scalp(plus eyelashes & eyebrows)
 Three types: lanugos, vellus, terminal
 Anagen: 90-95% of normal scalp hairs (3 yrs=1000 days)
 Catagen: 1-2% (3 weeks)
 Telogen: 5-10% (3 months=100 days)
Alopecia:
 1) Cicatricial: lichen planus, DLE, kerion, Favus,
Morphea, Burning,….
 2) Non cicatricial: male pattern alopecia, alopecia
areata, psoriasis, seborrheic dermatitis, ….
Shedding in telogen effluvium.
Non CA
 Androgenetic alopecia
 Alopecia areata
 Traction alopecia
CA
Synonyms
 Male pattern hair loss (MPHL)
 Male pattern baldness (MPB)
 Androgenetic alopecia (AGA)
 Common baldness
Androgenetic alopecia
 -At least 80% of Caucasian men show some signs of AGA
by age 70.
 Although testosterone is the major circulating androgen in
men, the testosterone metabolite, DHT, plays a dominant
role in AGA.
 In scalp biopsy: in men with MPHL: 5aR activity & DHT
levels are increased
AGA
 The conversion of T to DHT is catalyzed by 5aR
 DHT: temporal scalp hair recession, acne, growth of
prostate, development of terminal hairs in the beard
region, external ears, nostril & on the limbs.
Type 1 5aR is widely expressed but its physiological
function is uncertain (in sebaceous glands & liver)
Type 2 5aR is expressed in androgen-dependent tissues
such as the prostate & hair follicle (scalp, beard& chest)
AGA
 MPHL is absent in men with genetic deficiency of type 2
5aR.
 Treatment with finasteride, a selective inhibitor of type 2
5aR, slows the progression of MPHL and produces some
regrowth of hair in about 2/3 of men.
 The primary target of androgen action in the hair follicle:
in dermal papilla & dermal sheath.
AGA
 Genetic factors predispose to AGA, but their nature and the
mode of inheritance is uncertain.
 Inheritance is most likely polygenic.
 There is increased frequency of AGA in sons of men with
AGA. The maternal influence on AGA is less well defined.
 Women with FPHL are less likely than men to have a strong
family history of the disorder
Female pattern hair loss (FPHL)
 FPHL undoubtedly, but not necessarily, occurs in women
with hyperandrogenism (MPHL, hirsutism and/or
menstrual disturbance)
 FPHL with hyperandrogenism may respond to treatment
with finasteride, or cyproteron acetate
 Most of women with FPHL show no other clinical or
biochemical evidence of androgen excess.
 There was no response in postmenopausal women to
treatment with finasteride or in women without signs of
androgen excess to cyproteroterone acetate.
Clinical finding
In men
 Onset: may begin anytime post-puberty, usually by age 40.
 14% in 15-17 yrs.
 Pattern: most common: bitemporal, frontal, mid scalp,
vertex
 Uncommon: diffuse scalp hair loss or female pattern with
diffuse central scalp hair thinning
 Hair pulling: may be positive in active early hair loss in the
central scalp but generally negative in long-standing hair
loss
…MPHL
 Affected hair: miniaturization (finer, shorter) and decreased
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hair density
Scalp: generally normal, concomitant seborrheic is common.
If perifollicular erythema or hyperkeratoses = biopsy for R/O
cicatricial alopecia
Associated finding: high incidence coronary artery dis.
(CAD), Hypertension, hypercholesterolemia.
Family history: commonly positive but in 20%, not have a
FH of MPHL.
Clinical finding (women)
 Onset: may begin any time post menarche
 In central scalp +/-sides of scalp
 Pattern: A- diffuse central thinning of the crown with
preservation of the frontal hair line
 B- frontal accentuation (Christmas tree)
C- Fronto-temporal recession/vertex loss (male pattern) is
uncommon.
 Bitemporal thinning is commonly associated with, but not
necessarily indicative of FPHL.
 Pulling test : may be positive in active early loss in the
central scalp, but generally negative in long-standing hairloss
…FPHL
 Affected hair: miniaturization of hair
 Scalp: generally normal, seborrhea, R/O Cicatricial
alopecia
 Associated finding: sign or symptoms of hyprndrogenism
(hirsutism,severe acne, galactorrhea, infertility, irregular
mense, A.Nigricance)
 Family history: FPHL are less likely than men with MPHL
to have a history of first-degree relatives with MPHL.
Evaluation
 R/O other cause of hair loss (iron def., acute & chronic
telogen effluvium, Sisaipho,…)
 In men: anabolic steroids or supplemental androgens may
worsen MPHL
 Consider check TSH if the hair loss is diffuse & not
localized exclusively to typical MPHL
 Consider iron (in vegetarian or otherwise deficient diet,..)
…Evaluation
 In hyperandrogenism, blood test should be include:
1 -free and/or total T +/- DHEAS at a minimum=done off of
OCP (inhibit both ovarian & adrenal source of androgens). If
these tests are normal on OCPs, but the suspicion is high for
hyper A, they should be repeated at least one month after
cessation of OCPs.
2 –if T is greater than 2.5x normal or >200ng/dl, or DHEAS is
greater than 2x normal or >700 micro g/dl in pre or >400 in
postmenopausal women, a work up for tumor with
radiographic test.
…Evaluation
 If galactohhhea or increased T or free T = check prolactin
 If T or DHEAS is elevate = screen for CAH. An early
morning serum 17-OH progesterone during the follicular
phase of the cycle (day 1-14) would be a reasonable
screening test for the most common form of CAH, ie, 21hydroxylase def.
If prolactin or 17-OH progesterone is increased = refer to
endocrinologist.
…Evaluation
 In women: screening blood work is generally recommended in
all of women
 In otherwise healthy women, check TSH & serum ferritin
 R/O Iron def.:by serum ferritin or serum iron and TIBC. Low
serum ferritin is diagnostic of iron def. depleted iron stores in
patients with chronic dis. May not be detected by serum
ferritin (ferritin is acute phase reactant and inflammatory
disorders, malignancy, infections increase its synthesis)
 If check iron & TIBC: pts. Should not be taking iron
preparations (multivitamin with iron or OCP with iron) for at
least 24h
…Evaluation
 Iron supplements taken for > 3 wk can falsely elevated
ferritin levels in the face of iron def.
 Iron def. is associated with low serum iron & relatively
high TIBC & low percent saturation.
 Other screening test may be indicated by history = CBC
and/or T4
 The majority of FPHL have no clinical or biochemical
evidence of androgen excess.
Specific investigations:
 Often non required
 Scalp biopsy
 Iron studies, serum electrolytes, Urea, Cr
 Thyroid function tests
 Androgen profile (if suspicious of virilization)
 Testosterone, DHT
 SHBG
 LH, FSH
 ANA
 Scalp photography
Histopathology
A- indication for biopsy:
 Diagnosis: Males: usually not necessary unless a FPHL,
diffuse HL or scalp changes suggestive of scarring alopecia
or prepubertal boy with a Ludwig PHL.
-Females: sometimes necessary to exclude chronic T.E,
diffuse AA or cicatricial hair loss
 Site of biopsy: central scalp (should not be from the
bitemporal =miniaturized hair independent of MPHL or
FPHL)
 A punch biopsy (not less than 4 mm), into the
subcutaneous fat. Many dermatopathologists favor
horizontal sectioning of biopsy.
…histology
 The ratio of terminal to vellus or vellus-like hair normally
is 7:1. in PHL , decrease to 2:1
 The total number of hairs per unit area is usually normal in
PHL (30-50 / 4mm punch), but reduced in severe baldness
 A perifollicular infiltrate, lymphohistiocytic
 Perifollicular fibrosis
First line therapies:
 Topical minoxidil
 Finasteride
 Dutasteride
 Spironolactone
 Cyproteron acetate
 Camouflage
A
A
C
B
B
D
Second line therapies:
 Scalp surgery or transplantation
C
Treatment
 Prevent further hair loss & if possible stimulate hair growth
 General: pts should avoid hair care products likely to damage
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scalp/hair.
Pts should maintain an adequate diet (especially protein)
Topical medications work only where the medication is
applied
If possible, any drugs that could negatively affect hair growth
should be stopped.
Treat any underlying scalp disorder (seborrhea, pso,..)
Treatment (men)
 Finasteride 1mg/d & minoxidil 2-5% =FDA approved for
men > 18 years old. 5% is a more rapid onset of action.
 Treatment should be used for 12 mo before making a
decision about efficacy although benefit may be seen
sooner.
 Finasteride : 2/3 decreased DHT in serum & scalp
 Efficacy: target area hair counts (TAHC): are circular target
areas 1cm to 1 inch in diameter typically at the anterior
leading edge of the vertex balding area where the terminal,
non-vellus, or visible hairs are counted pre & post
treatment.
…Finasteride
 TAHC increase over the first year and peak by 12 mo. : in
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men age 18-41, hair counts increase 17/cm2 for those on 1
mg finasteride vs-4/cm2 for placebo.
Hair growth continue to improve for at least the first 24 mo
of treatment .in 18-41 yr, 50% of men showed an increase in
hair growth by 1 yr, and 66% by 2 yr, compared to 7% & 7%
by placebo (1 yr=10% increase)
In 41-60 yr, 39% on finasteride versus 3% on placebo in 2 yr.
(90% stop hair loss in men for at least 5 yrs, hair
regrowth in 65%)
Discontinue: any positive effect will be lost in 12 mo.
superficial subcutis, variability in the caliber of hair follicles, with
an increased number of miniaturized hairs, is apparent. Several
fibrous streamers are also seen.
...Finasteride
 Safety: no known drug interaction, no effect on liver, BM,
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kidney,…, no effect on spermatogenesis
Reversible sexually related side effects (decreased libido ,
erectile dysfunction, decreased ejaculate volume): in 2%
versus 1% with placebo. In 41-60 yr : increased side effect in
8% vs 5% on placebo.
Painful gynaecomastia (0.001%)
This side effects often resolve during continued treatment
or within days to wks after discontinued.
The level of drug in semen is very low, and semen no risk to a
pregnant women or her fetus.
…Finasteride
 F. is teratogen. In male fetus : hypospadias with cleft prepuce,
decreased anogenital distance, reduced prostate weight,
altered nipple formation.
 F. has not effect on spermatogenesis or semen production
 No effect on bone density
...Finasteride
• Reduction in PSA is based on the effect decreased DHT on
the prostate. Recommendation is that any PSA test value
should be doubled for any man taking finasteride to
compensate for the effect of the drug.
• (40% reduced PSA in 40-49 yrs & 50% in 50-59 yrs.)
• Finasteride may selectively inhibit low grade prostate
tumors (Gleason stage 2-6) ,25% reduce among men aged
55 and over.
- low DHT may induce histologic changes that mimic high
grade disease
-low DHT may induce higher grade prostate cancers
(Gleason stage 7-10)
(5mg/d: high grade prostatic carcinoma in elderly men
(or reduced?)
...Finasteride
 Finasteride & dutasteride are both teratogens with very
long biological half-lives (activity may persist into second
trimaster), but pharmacokinetic half-life is 8 h.
 Photography is useful for monitoring, but unlikely to detect
changes of less than 20% in hair density.
 Max increase occur after 1 yr
 Further improvement : increase in hair length, diameter &
pigmentation.
Dutasteride
 D. is a combined type 1 & 2 5aR inhibitor. 0.5 mg/d a 53%
reduction is scalp DHT and at 2.5 mg/d the reduction is
83%.
 Sexual side effects are more common but reversible.
Minoxidil
 FDA approved for upper 18 yrs old (in adolescents)
 Mode of action: increases duration of anagen & enlarges
miniaturized follicles(enlargement of shaft diameter)
- K channel opener & vasodilator
 1 ml twice daily, require 1h for absorption
 Best result in early case (<10 yrs), limited extend(<10 cm, on
the vertex), hair density above 20 hairs/cm2)
 Efficacy: TAHC & photographs confirm a significant
increase in hair density, hair growth appears to peak at 16
wk, 5% is superior to 2%, TAHC increases are 19/cm2 for
5% & 13/cm2 for 2% & 4/cm2 for placebo at 6 mo.
…Minoxidil
 photography: 58% increased hair growth on 5% & 41% for
2% & 23% on placebo at 1 yrs.
 Conversion of vellus to terminal hair (30%), complete
remission (10%)
..Minoxidil
 Discontinue: any positive effect will be lost in 4-6 mo.
 Initial telogen effluvium, begin 2-8 wk after treatment
initiation ( result from release of telogen hair as anagen
promotion begins), self limiting with continued treat.
 Safety: side effects are mainly dermatologic: scalp
irritation, dryness, scaling, itching, redness (more common
with 5%)
-Allergic C.D: is uncommon (with minoxidil or PG)
Combination therapy
 -Additive effect
 For switch from treatment with one of these agents to other
should continue for at least 3 mo together.
Treatment for women
 Women with or without hyperandrogenism:
- no androgen therapy
-FDA : only 2% minoxidil approved for women (60% arrested
hair loss or mild to moderate hair growth)
- treatment should be used for 12 mo before making a decision
about efficacy although benefit may be seen sooner.
- minoxidil in those women with FPHL both with or without
hyperandrogenism, in young & old, in pre & postmenopausal
women alike.
..Minoxidil
 Safety: either 2 or 5% appears safe to use in women with
FPHL, with the only additional risk of the 5% for face
hypertrichosis (3-5%). The hypertrichosis tends to occur
over the cheeks & forehead as vellus, not terminal, hair and
disappears within 4 mo. of stopping the drug.
- hypertrichosis due to spreading to the face or may also be a
result of hypersensitivity to low levels of systemic
absorption.
Women with hyperandrogenism
 <40% of women with FPHL have hyperandrogenism
(androgen hypersensitivity or overproduction)
 Efficacy of this drugs in women with FPHL who do not
have overt H.A have not specifically shown proven efficacy.
 Since all antiandrogens or 5aR inhibitors may cause
feminization of the mal fetus, all women of childbearing =
OCP.
Spironolactone
 Act by blocking cytoplasmic receptors for DHT. Also
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weakly inhibits androgen biosynthesis.
Spironolactone 100-300mg /d.(usually 200mg), check K at
baseline & 1 mo after beginning treatment (hyperkalemia).
Pts should keep well hydrated.
Spironolactone 200mg/d or cyproterone acetate 100mg
(days 5-15), will prevent further hair loss in up to 90% of
women. Regrowth may be seen in up to 40% after 1-2 yr of
treatment.
Contraindication: in pregnancy: risk of feminization in
male fetus & hypospadias.
(In childbearing: OCP is choice)
..Spironolactone
 Side eff.: are dose related, mense irregularity,
postmenopausal bleeding, breast tenderness or enlargement,
fatigue
 Concomitant use of OCP: reduced side eff.
 Rare cases of hepatocellular carcinoma & hepatitis (with
higher dose)
 Contraindication: in pregnancy: risk of feminization in male
fetus & hypospadias.
Finasteride
 1-1.25 mg/d. not useful in post-menopausal with FPHL.
 Some positive reports in women with HA treated with 1.25
mg /d have emerged.
 There are no anticipated side effects and no blood tests are
necessary.
Cyproterone acetate
 Androgen receptor blocker, potent progestin,
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antigonadotrophic effect.
May use for over 40 yr. For postmenopause, androcor with
or without estrogens may be used continuously.
100 mg days 5-15 with Diane 5-26, appears most useful.
Diane only , less effective in hair loss.
Side eff.: wieght gain, breast tenderness, loss of libido,
lassitude, depression, nausea, feminization of male fetus
No specific blood tests are necessary.
Flutamide
 A non-steroidal antiandrogen: inhibiting androgen uptake,
inhibiting nuclear binding of andogen within the target
tissue.
 In one study: F. is superior to androcor & finasteride
 Side eff.: rare but potentially fatal hepatotoxicity
Low-level light therapy
 Most are packaged like a hairbrush or comb which shines
red light directly on the scalp while it is used to comb
through the hair.
 Only on such device, called the HairMax LaserComb, has
obtained 510k FDA approval for use as a medical device
 Should be explain to patients: this device has safety
rather than actual efficacy.
Cosmetic aids & ….
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Not all treatment work for all people
Tinted powders, lotions, hair sprays
Shampoo ketoconazol,Sawpalmetto, palminex
Vitamins, supplements?
Wigs, hair pieces, Camouflages,…
Hair transplantation