Lecture by Dr. Patrick Treacy from Ailesbury Hair Clinics to ICAD 2014 Brazil on the reasons and treatments for female hair loss. Courtesy given at lecture to some other doctors and clinics for some images used. Images related to Ailesbury Hair Clinics were added at a alter time.
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Female hair loss (causes and management)
1. Hair Loss in Women
Preventing Female Hair Loss IACD Brazil 2014 Dr Patrick Treacy
Ailesbury Clinics
2. Female Hair Loss
Although alopecia can occur anywhere on the body, it is
most distressing when it affects the scalp. Hair loss can
range from a small bare patch that is easily masked by
hairstyling to a more diffuse and obvious pattern. Alopecia
in women has been found to have significant effects on
self-esteem, psychological well-being, and body image
3. Factors Causing Hair Loss
Hair loss can be divided into
disorders where
(1) hair follicle is normal but
hair growth cycle is
abnormal
(2) hair follicle is damaged.
Androgenetic alopecia is the
most common cause of hair
loss in women.
Other disorders include alopecia areata, telogen effluvium,
cicatricial alopecia, and traumatic alopecias
4. Factors Causing Hair Loss
We will look at the causes of each and how they can be managed
(1) Andogenetic Alopecia (AGA)
(2) Diffuse Hair Loss (DHL)
(3) Telogen Effluvium (TE)
(4) Chronic Telogen Effluvium (CTE)
5. Diagnosis
A careful history often suggests
the underlying cause of alopecia.
Crucial factors include the
duration and pattern of hair loss,
whether the hair is broken or
shed at the roots, and whether
shedding or thinning has
increased. The patient's diet,
medications, present and past
medical conditions, and family
history of alopecia are other
important factors.
6. Diagnosis
The physical examination has
three parts. First, the scalp is
examined for evidence of
erythema, scaling, or
inflammation. Follicular units are
apparent in nonscarring
alopecias but absent in scarring
types. Second, the density and
distribution of hair are assessed.
Third, the hair shaft is examined
for calibre, length, shape, and
fragility
7. Diagnosis
The “pull test” is an easy
technique for assessing hair loss.
Approximately 60 hairs are
grasped between the thumb and
the index and middle fingers. The
hairs are then gently but firmly
pulled. A negative test (six or
fewer hairs obtained) indicates
normal shedding, whereas a
positive test (more than six hairs
obtained) indicates a process of
active hair shedding. Patients
should not shampoo their hair 24
hours before the test is
performed
8. Androgenetic alopecia
Androgenic alopecia is the most common cause of
hair loss in women. Its aetiology in females is
multifactorial and polygenetic.
9. Female pattern, Ludwig
The so-called female pattern is characterized by a diffuse
thinning of the centroparietal region with preserving the frontal
hair line
10. Androgenetic alopecia
Only affects the top of the scalp. If your losing hair at back and sides
Probably another cause other than genetics
11. Androgenetic alopecia
• Testosterone is converted by the body into DHT
• This interferes with the hair follicles if they are
genetically susceptible
• Environmental factors do not seem to affect this
type of baldness greatly
• There is a 4 in 7 chance of receiving the baldness
gene
• Visible hair loss occurs in approximately one half of
all females by 50 years
12. Androgenetic alopecia
Women with androgenetic alopecia do not have higher levels of
circulating androgens.
They have higher levels of 5α-reductase (converts testosterone to
dihydrotestosterone), more androgen receptors, and lower levels
of cytochrome P450 (which converts testosterone to oestrogen).
13. Treatment Androgenetic Alopecia
Treatment is usually surgically by FUE or FUT
transplant. Medical treatments include Minoxidil
and products. LLLT and PRP are becoming
increasingly popular alone or with FUE
14. AGA Medical
Clinical Evidence The following slides summarize the
evidence-based efficacy assessment of the different medical
therapeutic options in the treatment of androgenetic alopecia
in women by literature search.
1.Minoxidil
2.5-alpha-reductase-inhibitors
3.Hormones
4.LLLT
5.Products
15. Minoxidil
Minoxidil was originally developed as an oral drug (trade
name Loniten®) to treat high blood pressure. Its possible use
in androgenetic alopecia was discovered when its side effect
of increasing hair growth was observed.
16. Minoxidil
Minoxidil
Chemically, minoxidil is a pyrimidine derivate. It was the first
product to be approved for the treatment of AGA in both men
and women. The 2 % topical solution was first approved by
the U.S. Food and Drug Administration (FDA) in1988 for the
treatment of androgenetic alopecia in men and in 1991 in
women. The 5 % solution was approved in 1997 for the
treatment of androgenetic alopecia in men followed by
approval of the 5 % foam in 2006 also for the treatment of
androgenetic alopecia in men.
.
17. Minoxidil
Mechanism of action
To exert its effect minoxidil needs to be transformed to its
active metabolite, minoxidil sulphate by the enzyme sul-photranspherase,
which is present in the outer root sheath of
anagen follicles. The exact mechanism by which minoxidil
promotes hair growth is still unclear. Its active metabolite,
minoxidil sulphate opens ATP-sensitive potassium channels in
cell membranes, which conveys vasodilatory effect.
Vasodilatation, however, does not appear to be responsible
for minoxidil-induced hair growth. Studies on skin blood flow
after topical minoxidil application produced inconsistent
results.
18. Minoxidil
Efficacy – females
11 studies that investigated the efficacy of topical minoxidil in
female patients suffering from androgenetic alopecia could be
included in the evidence-based evaluation. 3 studies treated
male and female patients. 7 studies obtained grade B
evidence, 4 studies grade A2 evidence, resulting in
an evidence level 1.
Outcomes
Minoxidil 1 % solution, applied twice daily led to mean changes
from baseline total hair count at 6 months from 15.2
hairs/cm2 (8.0 %) Minoxidil 2 % solution showed mean changes
from baseline non vellus hair count at 6 months between 21.0
hairs/cm2 and 50.1 hairs/cm2 (12.4–31.3 %). All studies showed
significant different mean changes from baseline hair counts in
comparison to placebo (p between 0.02 and < 0.001).
19. Minoxidil
Dosage
Concentration. The mean changes in non vellus hair counts
between minoxidil 5 % and 2 % in female patients were not
statistically significant (p = 0.129). At 12 months the mean
change from non-vellus hair count was 20.7 hairs/cm2 (13.8
%) for minoxidil 2 %, twice daily, 24.5 hairs/cm2 (17.3 %) for
minoxidil 5 %, twice daily and 9.4 hairs/cm2 (6.8 %) for
placebo, twice daily (p < 0.001 vs. placebo).
Therapeutic recommendation – Female
• Topical minoxidil 2 % solution 1 ml twice daily is
recommended to improve or to prevent progression of AGA
in female patients above 18 years with AGA.
• There is not enough data to recommend the 5 % minoxidil
solution instead of the 2 % solution.
• The response to treatment should be assessed at 6
months. If successful, treatment needs to be continued to
maintain efficacy.
20. Minoxidil
Dosage
Concentration. The mean changes in non vellus hair counts
between minoxidil 5 % and 2 % in female patients were not
statistically significant (p = 0.129). At 12 months the mean
change from non-vellus hair count was 20.7 hairs/cm2 (13.8
%) for minoxidil 2 %, twice daily, 24.5 hairs/cm2 (17.3 %) for
minoxidil 5 %, twice daily and 9.4 hairs/cm2 (6.8 %) for
placebo, twice daily (p < 0.001 vs. placebo).
Therapeutic recommendation – Female
• Topical minoxidil 2 % solution 1 ml twice daily is
recommended to improve or to prevent progression of AGA
in female patients above 18 years with AGA.
• There is not enough data to recommend the 5 % minoxidil
solution instead of the 2 % solution.
• The response to treatment should be assessed at 6
months. If successful, treatment needs to be continued to
maintain efficacy.
21. Minoxidil
Dosage
Concentration. The mean changes in non vellus hair counts
between minoxidil 5 % and 2 % in female patients were not
statistically significant (p = 0.129). At 12 months the mean
change from non-vellus hair count was 20.7 hairs/cm2 (13.8
%) for minoxidil 2 %, twice daily, 24.5 hairs/cm2 (17.3 %) for
minoxidil 5 %, twice daily and 9.4 hairs/cm2 (6.8 %) for
placebo, twice daily (p < 0.001 vs. placebo).
Therapeutic recommendation – Female
• Topical minoxidil 2 % solution 1 ml twice daily is
recommended to improve or to prevent progression of AGA
in female patients above 18 years with AGA.
• There is not enough data to recommend the 5 % minoxidil
solution instead of the 2 % solution.
• The response to treatment should be assessed at 6
months. If successful, treatment needs to be continued to
maintain efficacy.
23. Finesteride
Two types of 5-alpha-reductase-inhibitors exist in humans.
Type I predominates in liver, skin and scalp. Type II
predominates in prostate and genitourinary tract, but also in
the human hair follicle. Initially, pharmaceutical 5-alpha-reductase-
inhibitors were developed for the treatment of
benign prostatic hyperplasia. Two drugs inhibiting the 5-alpha-reductase
are available on the market: finasteride registered
in Europe in 1992, and dutasteride registered in 2003.
Mechanism of action
A single oral administration of finasteride 1 mg decreases
serum DHT as well as scalp DHT up to 70 % compared to
baseline. Tachyphylaxis is not observed with long-term
administration.
24. Finesteride
Efficacy – females
2 studies assessing the efficacy of finasteride 1 mg daily in
female patients were included in the evidence-based
evaluation. The grades of evidence were A2 and B, resulting
in an evidence level 2.
.
Outcomes
Both studies showed a further progression of hair loss. The
mean change from baseline hair count at 12 months was –
14.6 hairs/cm2 (–5.9 %) and –8.7 hairs/cm2 (–5.8 %).
Moreover, the mean decrease from baseline hair count in the
finasteride group outvalued the placebo group (0 hairs/cm2[0
%] resp. –6.6 hairs/cm2[–4.0 %]).
25. Finesteride
In postmenopausal female patients finasteride 1 mg failed to
show efficacy (evidence level 2). Additional research is
required at higher dosages and in different subgroups of
female patients with androgenetic alopecia. If finasteride is
used in women its use is off-label and at own responsibility; in
particular in women of childbearing age, a safe contraceptive
method is essential as finasteride may lead to feminisation of
the male foetus.
Therapeutic recommendation Female
Oral finasteride 1 mg daily is not suggested in the treatment of
postmenopausal women with female pattern hair loss.
High quality controlled clinical trials with finasteride at different
dosages on female patients are required.
27. Hormones
Introduction
The role of androgens in the aetiology of androgenetic
alopecia has led to the widespread use of hormonal agents in
its treatment. They fall into two broad groups: antiandrogens
and oestrogenic (or anti-oestrogenic) drugs, although
evidence of efficacy for any of these treatments is limited or
absent.
Peereboom-Wynia et al. compared a group of women treated
for one year with Diane® (50 μg estradiol + 2 mg cyproterone
acetate) + 20 mg cyproterone acetate days 1–14 with an
untreated control group. Trichogram data showed a mean
change in anagen percentage from 49.7 at baseline to 74.4
after one year in the treated group compared to a fall from
60.4 to 48.8 in the controls.
28. Hormones
Vexiau et al. reported a mean change in total hair count of –
2.8 hairs/cm2(–1,4) at 6 months and –7,8 % hairs/cm2 (– 3;9
%) at 12 months in subjects receiving oral contraceptive + 50
mg cyproterone acetate
Therapeutic recommendation – Female
• There is no or insufficient evidence to support the use of
oral antiandrogens (chlormadinone acetate, cyproterone
acetate (CPA), drosperinone, spironolactone, flutamide) to
improve or prevent progression of AGA in female patients
• Oral CPA can be considered in women with clinical or
biochemical evidence of hyperandrogenism.
• There is insufficient evidence to support the use of topical
alfatradiol to improve or prevent progression of AGA in
female patients.
• There is no evidence to support the use of topical natural
oestrogens or progesterones to improve or prevent
progression of AGA in female patients.
29. AGA Surgical
Only few of the 77
assessed publications
concerning hair surgery
studied efficacy in
female patients. None
of them fulfilled the
inclusion criteria, due to
high variation in
techniques, multiple
steps in the surgical
process, problems in
measuring hair growth.
Surgery, especially follicular unit transplantation (FUT) can be
considered in female patients with sufficient donor hair.
31. FUE Treatment
Donor Area must be
Trimmed to 1mm
Unless patient requests to a
non shaven procedure
32. FUE Implants
In FUE hair transplantation individual hair follicles are
extracted without causing damage to the scalp. This is done
by very small punches that hardly leaves visible scars.
As every single follicle is extracted individually this is a time
consuming procedure.
33. FUE PRP and 633
The technique uses wavelengths with red light therapy in
the range of 630 to 670 nanometers (nm) immediately post
FUE procedure. Red light is absorbed is because of an
intracellular enzyme called cytochrome c, responsible for
stimulating the hair follicle by sending it certain signals.
34. AHI Implanter assists to place the
Follicle at the correct angle,
direction and depth. Both are vital
factors in creating a natural
looking result
AHI Follicle Implanter
is used in to place the
follicles
35. FPHL Treatment
•Follicular units are
identified and removed
randomly.
•Up to 35% of donor
follicles can be extracted
without causing aesthetic
thinning
36. The hair line is important. The eye should
never be drawn to a hair line
38. The main difference between FUE hair transplantation and
older strip-surgery is in the way donor-hair is obtained. FUE
generally leads to higher patient satisfaction,quicker recovery,
and less scarring of the donor area.
39. 2. Telogen Effluvium (TE)
• A second condition, which can come as rather a
shock to most women is Telogen Effluvium
• Loss of hair up to three months after a severe stress
such as childbirth, pregnancy termination, or drug
therapy.
• Another possible cause is changes to the hormone
balance such as new birth control pills or drugs for
weight loss.
41. 2. Telogen Effluvium
• Similar condition to Diffuse Hair Loss
• Caused by shock to biological system
• Accident, injury or stressful event
• Number of hairs pass from growth phase to
resting phase prematurely
• Resting phase lasts three months
• Hair falls out three months later
43. 2. Telogen Effluvium
• Temporary Condition
• As long as cause isn’t ongoing hair should grow
back after a short period of time.
44. 3. Diffuse Hair Loss
• This requires a holistic approach, starting
with blood checks for hormone levels and
gland function and followed by lifestyle
adjustments where necessary and possible.
45. 3. Diffuse Hair Loss
A third condition is Diffuse Hair Loss Involves the back and sides
46. 3. Diffuse Hair Loss
• Diffuse Hair Loss is caused by illness or lack
of certain nutrients.
47. 3. Diffuse Hair Loss
• Important to identify what is causing it
• Fixing this solves the problem
• Iron deficiency disorders
• Thyroid hormone disorders
48. 4. Chronic Telogen Effluvium (CTE)
• TE is self limited and resolves in 3-6 months if the
trigger is removed or treated, while the prognosis of
CTE is less certain and may take 3-10 years for
spontaneous resolution
• This condition can trigger Genetic Hair Loss, which
is permanent if not treated
49. 4. Chronic Telogen Effluvium (CTE)
• This condition can trigger Genetic Hair Loss,
which is permanent if not treated.
50. Differences TE and GHL
• Abrupt, rapid, generalized shedding of normal club
hairs, 2-3 months after a triggering event like
parturition, high fever, major surgery, etc. indicates
TE
• Gradual diffuse hair loss with thinning of central
scalp/widening of central parting line/frontotemporal
recession indicates FPHL
51. Differences TE and GHL
• CTE is often confused with FPHL and can be
reliably differentiated from it through biopsy which
shows a normal histology in CTE and miniaturization
with significant reduction of terminal to vellus hair
ratio (T:V < 4:1) in FPHL.
52. Female Hair Loss treatments
• How do you know which products work and
which don’t
• Many manufacturers make claims
• FDA overlooks clinical trials
• Marketing licence only given after trials
• In US/UK/IRL only Minoxidil licenced
• Most others food supplements
• Not sufficient evidence of these
54. Products
The range of products is wide and reaches from topical to
systemic modalities; it includes cosmetic to pharmaceutical
products, natural products, functional food and even
electrostatic/-magnetic or laser treatment..
Mechanisms of action in androgenetic alopecia are as
various as the number of products. Though it remains unclear
how these products mediate their effects, most of them claim
at least one of the following mechanisms:
a) Promotion of hair regrowth by activation of the dermal papillae and
consequently induction of anagen hair re-growth.
b) Comparable to minoxidil promoting hair regrowth by improving the
perifollicular vascularisation.
c) Hormonal effects, mainly inhibition of 5-alpha-reductase and reducing
the activity of dihydrotestosterone (DHT).
d) Anti-inflammatory activity.
e) Improvement of hair follicle nutrition
55. Products
• Amino acids
• Iron supplements in absence of iron deficiency
• Vitamines (biotin, niacin derivates)
• Proanthocyanidines
• Millet seed (silic acid, aminoacids, vitamines, minerals)
• Marine extract and silicea component
• Chinese herbals
• Ginkgo biloboa
• Aloe vera
• Ginseng
• Bergamot
• Hibiscus
• Sorphora
• Caffeine
• Melatonin
• Retinoids
• Ciclosporine
58. FPHL treatment
• Topical minoxidil 2%
with or without
antiandrogens, hair
prosthesis, hair
cosmetics, and hair
surgery are the
therapeutically
available options for
FPHL management.
59. Low level laser therapy (LLLT)
• Low level laser
therapy (LLLT) has
been used to
promote hair growth
• Many controlled trials
show the safety and
physiologic effects of
LLLT on males and
females with
androgenic alopecia
60. Low level laser therapy (LLLT)
• (LLLT) is believed
to increase blood
flow in the scalp
and stimulate
metabolism in
catagen or telogen
follicles, resulting in
the production of
anagen hair.
61. Low level laser therapy (LLLT)
• The photons of light act on cytochrome C oxidase
leading to the production of adenosine triphosphate
(ATP). This is converted to cyclic AMP in the hair
follicle cells, releasing energy and stimulating
metabolic processes necessary for hair growth
62. Low level laser therapy (LLLT)
• The photons of light act on cytochrome C oxidase
leading to the production of adenosine triphosphate
(ATP). This is converted to cyclic AMP in the hair
follicle cells, releasing energy and stimulating
metabolic processes necessary for hair growth
• Release of nitric oxide from cells leads to increased
vascularisation to the scalp distributing nutrients and
oxygen to the hair roots
• Excessive build-up of DHT is prevented.