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       Hair Loss

 
 

     Hair loss cause, investigation

 
 
 
Getting to the Root of the Problem

Hair is comprised of two distinct parts: the hair follicle, the point from which the hair grows, and the hair shaft, the visible hair

strands. Hair is composed mainly of dead cells that have turned into keratin and binding material, along with water. Keratin, a complex protein made up of amino acid chains, is found primarily in the cortex, the inner layer of the hair, and its strength allows it to withstand damage caused by daily manipulation from hair dryers, chemical treatments, brushes and combs.

The color of hair is due to the presence in the cortex of granules of pigment called melanin. Melanin is found in two forms. Eumelanin is the dark pigment that predominates in black and brunette hair. Phaeomelanin is a lighter pigment, found in red and blond hair. Most people have a unique mixture of the two, determined by genetics, with the mixtures also varying across one person’s head. he inner cortex is protected by the cuticle, the outer layer made 4-8 overlapping layers, arranged like shingles on a roof.
The “f-layer”, (or 18- methyleicosanoic acid) is covalently bound to the cuticle surface of virgin hair and is hydrophobic in nature. The hydrophobicity protects the hair shaft against water and friction.
When healthy, the cuticle reflects light on its surface, resulting in a visual shine band. However, environ- mental, chemical and mechanical manipulation can cause uplifting of the cuticle scale edges, which makes hair feel rough and look dull or, worse, can completely remove the entire cuticular layer, leading to breakage and splits in the shaft.

Damage to the hair cuticle due to repeated chemical treatments (left), backcombing or teasing (middle) and excessive heat and brushing (right).

Environmental damage occurs slowly over time through exposure to UV light, which works in a similar way to bleach, oxidizing the melanin pigments in hair, changing its color and breaking down the keratin protein in the cortex of the hair, making it significantly weaker. The most serious mechanical damage occurs from backcombing (“teasing”), where the hair is combed in a reverse direction, thus lifting the cuticle scale edges up and back, permanently damaging the cuticle. Chemical treatments, such as perms and color-reatments, have to alter the structure of the hair to produce their cosmetic effect and if done repeatedly can rough up the cuticle while also leaving it more fragile so that future heat styling can quickly tear off areas of cuticle, leaving the cortex exposed. If a high conditioning rinse-off conditioner is used after every shampoo, chemical treaters can help shield the fragile cuticle from the damaging effects of heat styling.

Normal Hair Density-How many hairs do we have

5 million follicles
100,000-150,000 on the scalp
Birth:  1135/cm2
1 year:  795/cm2
20-30:  615/cm2
30-50:  485/cm2
80-90:  435/cm2

 
What is follicular Unit

Normal follicular unit is composed of

1-4 terminal hairs
1-2 vellus hairs
Sebaceous glands
Erector pili muscles
Blood vessels
Nerves
Connective tissue
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)

Type of hair loss

1) Cicatricial: lichen planus, DLE, kerion, Favus, Morphea, Burning,….
2) Non cicatricial: male pattern alopecia, alopecia areata, psoriasis,

Androgenetic Alopecia

Male Pattern Balding
Female Pattern Balding
CAUSE: a combination of heredity, hormones and age causes progressive shrinking or
miniaturization of terminal hair, converting it to vellus hair
Known as male pattern baldness in men
Affects 40 million men in
Affects 20 million women .
Can begin as early as teens
Frequently seen by age 40
By age 35, almost 40 % of men & women show some degree of loss
Gene can be inherited from either side of family

Miniaturization of follicles
Decreased anagen/
increased telogen
Increased latency Autosomal dominant – variable penetrance
30% of white men by age 30
50% of white men by age 50
Site-specific action of androgens
  • Pubic/axillary/chest/beard:  vellusàterminal

  •     Scalp:  terminalàvellus

  •     Men—testosterone: 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)

  •     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.

  •     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

  •     In scalp biopsy: in men with MPHL: 5aR activity & DHT levels are increased

Androgenetic alopecia (horizontal). Even in the superficial subcutis, variability in the caliber of hair
follicles, with an increased number of miniaturized hairs, is apparent. Several fibrous streamers are
also seen
Women—adrenal androgens

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.

Alopecia Areata

Sudden loss of hair in round or irregular patches; may occur on scalp or anywhere else on body. It’s
highly unpredictable; affects almost 5 million people in the U.S.
Immune system attacks hair follicles
Begins with one or more small, bald patches
Can progress to the total scalp hair loss (alopecia totalis) or complete body hair loss (alopecia universa
Occurs in males and females of all ages and races
Can begin in childhood
Scalp shows no sign of inflammation
No obvious signs of skin disorder or disease

Cicatricial Alopecia
Traumatic Alopecia
Diffuse Alopecia
Post partum alopecia

Temporary hair loss at conclusion of pregnancy
Growth cycle generally returns to normal within one year after the baby is delivered

CLINICAL SIGNS-

Male Pattern Baldness: 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
Affected hair: miniaturization (finer, shorter) and decreased 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.

FEMALE PATTERN BALDNESS

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 hair-loss
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.

 
Why treat?
Emotional Impact

Men with severe hair loss
Negative social and emotional effects
More 

 
preoccupation with baldness
Make effort to conceal or compensate for hair loss
Lower self-esteem
Mental distress
Women with hair loss

Devastating- women try to hide it from everyone including their doctor
Causes anxiety – women feel helpless and less attractive

Stereotypes

Older
Weaker
Less productive
Less attractive
Less virile

First line therapies

Topical minoxidil           A
Finasteride                    A
Dutasteride                   C
Spironolactone             B
Cyproteron acetate       B
Camouflage                  D

Second line therapies:

Scalp surgery or transplantation         C

Patient evaluation for treatment

Donor Hair

Type I
Type II
Type III
Type IV

Patient evaluation for surgery

Age

NOT a contra-
indication for surgery
Established pattern
Hair color
Co-existing medical conditions
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,..)
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.

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, 21-hydroxylase def.
If prolactin or 17-OH progesterone is increased  = refer to endocrinologist
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
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 indepen        dent of MPHL or FPHL)
A punch biopsy (not less than 4 mm), into the subcutaneous fat. Many dermatopathologists         favor horizontal sectioning of biopsy.
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