Female hair loss (causes and management)
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Transcript of Female hair loss (causes and management)
Hair Loss in Women
Preventing Female Hair Loss IACD Brazil 2014 Dr Patrick Treacy Ailesbury Clinics
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
Factors Causing Hair Loss
Other disorders include alopecia areata, telogen effluvium, cicatricial alopecia, and traumatic alopecias
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.
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)
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.
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
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
Androgenetic alopecia
Androgenic alopecia is the most common cause of hair loss in women. Its aetiology in females is multifactorial and polygenetic.
Female pattern, Ludwig
The so-called female pattern is characterized by a diffuse thinning of the centroparietal region with preserving the frontal hair line
Androgenetic alopecia
Only affects the top of the scalp. If your losing hair at back and sides Probably another cause other than genetics
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
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).
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
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.Minoxidil2.5-alpha-reductase-inhibitors3.Hormones4.LLLT 5.Products
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.
Minoxidil
MinoxidilChemically, 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..
Minoxidil
Mechanism of actionTo 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.
Minoxidil
Efficacy – females11 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.
OutcomesMinoxidil 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).
Minoxidil
DosageConcentration. 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.
Minoxidil
DosageConcentration. 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.
Minoxidil
DosageConcentration. 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.
Finesteride
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 actionA 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.
Finesteride
Efficacy – females2 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..
OutcomesBoth 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 %]).
Finesteride
Therapeutic recommendation FemaleOral 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.
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.
Hormones
Hormones
IntroductionThe 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 cyproteroneacetate) + 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.
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, cyproteroneacetate (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.
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.
FUE Treatment
The Donor Area
which is not testosterone sensitive
FUE Treatment
Donor Area must be Trimmed to 1mm
Unless patient requests to a non shaven procedure
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.
FUE Implants
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.
FUE PRP and 633
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
FPHL Treatment
•Follicular units are
identified and removed
randomly.
•Up to 35% of donor
follicles can be extracted
without causing aesthetic
thinning
The hair line is important. The eye should never be drawn to a hair line
FPHL Treatments
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.
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.
2. Telogen Effluvium (TE)
• Usually loss seems totally unexpected
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
2. Telogen Effluvium
Hair falls out three months later
2. Telogen Effluvium
• Temporary Condition • As long as cause isn’t ongoing hair should grow
back after a short period of time.
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.
3. Diffuse Hair Loss
A third condition is Diffuse Hair Loss Involves the back and sides
3. Diffuse Hair Loss
• Diffuse Hair Loss is caused by illness or lack of certain nutrients.
3. Diffuse Hair Loss
• Important to identify what is causing it• Fixing this solves the problem • Iron deficiency disorders• Thyroid hormone disorders
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
4. Chronic Telogen Effluvium (CTE)
• This condition can trigger Genetic Hair Loss, which is permanent if not treated.
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
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.
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
Products
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
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
Products
Improved perifollicular vascularisation
• Prostaglandines (viprostol, latanoprost)
• Aminexil
• Glyceroloxyesters and silicium
• Minerals
• Niacin derivates
• Mesotherapy
DHT-inhibitory activity
• Saw palmetto
•ß-sitosterol
• Polysorbate 60
• Green tea
• Cimicifuga racemosa
Anti-inflammatory activity
• Ketoconazol
• Zinc pyrithione
• Corticosteroids
Products
Improved hair nutrition • Vitamines (biotin, niacin derivates)
• Trace elements (zinc, copper)
Others • Botulinum toxin
• Electromagnetic/-static field
• Low level laser
FPHL treatment
• Topical minoxidil 2% with or without antiandrogens, hair prosthesis, hair cosmetics, and hair surgery are the therapeutically available options for FPHL management.
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
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.
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
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.
Hair Supplements
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