HAIR DISORDERS

(Alopecia, Scarring
Alopecia & Excess Hair
Growth)

Mohammad Azeem
Normal Hair Anatomy
Hair Growth Cycle
Anagen Growth phase; lasts variable periods of
time depending on body site. Duration: 16 years;
average 3 years; varies with age; determines the
ultimate length
of hair at a site. Scalp, beard: long anagen.
Eyebrows,
eyelashes, axillary/pubic hair: anagen is
short; telogen prolonged.

Catagen Apoptosis-driven phase between

telogen and anagen phase. Duration: few weeks.

Telogen Period of relative quiescence, last

variable periods of body site.

Exogen Active process of hair shaft shedding.

Effluvium Process of increased daily hair shaft

shedding (normal scalp 25100 hairs).
Endocrinology of Hair
Follicle
Hair follicles can vary in size under the influence
of androgens
Hair follicles response towards testosterone and
dihydrotestosterone under genetic control.

1) Dihydrotestosterone causes growth of the

prostate, growth of terminal hair, androgenetic
alopecia, and acne.

2) Testosterone causes growth of axillary hair and

lower pubic hair, as well as sex drive, growth of the
phallus and scrotum, and spermatogenesis.
Laboratory Examinations
Hair Pull
-Scalp is gently pulled. Normally, three to five hairs are
dislodged; shedding more hair suggests pathology.

Trichogram
-Determines the number of anagen and telogen hairs and
is made by epilating (plucking) 50 hairs or more from the
scalp.
-Normally, 8090% of hairs are in anagen

Scalp Biopsy
-Offers insight into pathogenesis of alopecia.
Alopecia
Pattern Hair Loss
Alopecia Areata
Telogen Effluvium
Anagen Effluvium
Pattern Hair Loss
Is the most common type of progressive balding.

Occurs through the combined effect of:

-Genetic predisposition

-Action of androgen on scalp hair follicles

Age of Onset

-Males : May begin any time after puberty, often fully

expressed in 40s.

-Females : Later in about 40% occurs in the sixth decade.

More common in males
Pathophysiology
Testosterone is converted to DHT by 5-reductase.
DHT causes hair loss by shorten anagen and longer
telogen and also miniaturizing hair follicle.
In genetically predisposed individuals, DHT causes
terminal follicles to transform into vellus-like follicles,
which in turn undergo atrophy.
During successive follicular cycles, hairs produced are of
shorter length and of decreasing diameter.
DHT
Clinical Manifestation
Most patients present with complaints of gradually thinning
hair or baldness.
Males:
- There is a receding anterior hairline, especially in the
parietal regions, which results in an M-shaped recession
- If AGA progresses rapidly, some patients also complain of
increased falling out of hair.
Females :
- Parietal and temporal recession is not usually a major
feature, severe thinning is not common.
- In young women, manifestations of androgen excess should
be sought as significant:
Acne
Hirsutism
Irregular menses
Virilization.
CLASSIFICATION
MALE (HAMILTONS) FEMALE (LUDWIGS)
Type I: Loss of hair along frontal margin. Grade I : Visible hair thinning on the
crown, situated 1 to 3 cm behind the
frontal hairline
Type II: Increasing frontal hair loss as well Grade II: Pronounced reduction of hair on
as the crown seen within the area seen in
onset of loss of occipital (vertex or Grade I
crown).
Types III, IV, and V: Increasing hair loss in Grade III: Full baldness within the areas
both seen in Grades I and II.
regions with eventual confluent and
complete
balding
DIAGNOSISof top of scalp with sparing of
Clinical, based on :-
sides
- History
- Pattern of alopecia
- Family history.
Skin biopsy may be necessary in
some cases.
Hair loss Pattern

Hamilton and Ludwig Classification

 Investigations
Trichogram

- In pattern hair loss, the earliest changes are an increase in the

percentage of telogen hairs.
Dermatopathology

- Abundance of telogen stage follicles is noted, associated with hair

follicles of decreasing size and eventually nearly complete atrophy.
Hormone Studies

In women with hair loss and evidence of increased androgens

- Testosterone: total and free

- Dehydroepiandrosterone sulfate (DHEAS)

- Prolactin

Diagnosis = History + Pattern of Alopecia + Family history

AGA
Management
Oral Finasteride - 1 mg PO daily

- Effects can be seen 3months to 1 year

Topical Minoxidil 2% and 5% solution

Antiandrogens
- In women with AGA who have elevated adrenal androgens
can give, spironolactone, cyproterone acetate, flutamide,
and cimetidine
Hairpiece
- Wigs, toupees, prosthetics; hairweaves.

Surgical Treatment
- Hair transplantation

- Scalp reduction/rotation flaps

Alopecia Areata
A localized loss of hair in round or oval areas with
no apparent inflammation of the skin. Most
common on scalp.
Etiology Unknown. Association with other
autoimmune diseases and immunophenotyping of
lymphocytic infiltrate around hair bulbs suggests
an antihair bulb autoimmune process
Age of Onset : Any age but common in young
adults (<25 years)
 Pathogenesis
Chronic organ-specific autoimmune disease, mediated by
autoreactive T cells affecting hair follicles and nails
Follicular damage occurs in anagen followed by rapid
transformation to catagen and to telogen.
While the disease is active, follicles unable to progress
beyond early anagen and do not develop normal hair.
Follicular stem cell is spared; hair follicles are not
destroyed.
Clinical Manifestation.
Gradual over weeks to months. Patches of AA can be
stable and often show spontaneous regrowth.
Associated Findings
- Autoimmune thyroiditis.
- Down syndrome.
- Autoimmune polyendocrinopathy
- Candidiasis
- Ectodermal dysplasia syndrome.
Nail
- Fine pitting (hammered brass) of dorsal nail plate.
- Mottled lunula,
- Trachyonychia (rough nails),
- Onychomadesis
 Hair
- Round patches of hair loss. May combine(coalesce).
- Alopecia often sharply defined.
- Normal-appearing skin with follicular openings present
- Exclamation mark hairs.
- Scalp most commonly.
- Any hair-bearing area.
(Beard, eyebrows, eyelashes,pubic hair.)

Alopecia areata : Solitary or multiple

areas of hair loss.
AA totalis : Total loss of terminal scalp
hair.
AA universalis: Total loss of all terminal
body and scalp hair.
Ophiasis: Bandlike pattern of hair loss
overperiphery of scalp .
Investigations
Serology ANA (to rule out SLE);
Rapid plasma Reagen (RPR test) to rule out
secondary syphilis.
KOH Preparation rule out tinea capitis.
Dermatopathology
- Peribulbar, perivascular, and outer root sheath
mononuclear cell infiltrate of T cells and macrophages;
- Follicular dystrophy with abnormal pigmentation and
matrix degeneration.
Management
No curative treatment is currently available due to high
recurrence
Temporary treatment available.

Most important factor in management of the patient is

psychological support
With extensive scalp involvement may prefer to wear a
wig or hairpiece and apply make up to eyebrows.
 Topical Glucocorticoids
Intralesional Injection

Triamcinolone acetonide, 37mg/mL,can be very effective

temporarily.
Systemic Glucocorticoids

May induce regrowth but risk of long term use

Systemic Cyclosporine

Induces regrowth, but recurs when drug is discontinued.

Oral PUVA (Photochemotherapy) -

-Variably effective, as high as 30%,however cause

immuno supress
 Telogen Effluvium
Is the transient increased shedding of normal club
(telogen) hairs from resting scalp follicles.
Occur at any age and more common in women due to
hormonal changes.
2nd most common alopecia
Due to reaction pattern to a variety of physical or
mental stressors:
- Endocrine
- Nutritional
- Physical Stress
- Psycological Stress
- Intoxication
- Drugs
- Disease
- Idiopathic
Clinical Manifestation
Patient presents with complaint of increased hair
loss on the scalp that may be accompanied by
varying degrees of hair thinning.
Most individuals are anxious, fearing baldness.
The patient often presents a plastic bag
containing shed hair.
Nails
- The precipitating stimulus for TE may also affect
the growth of nails, resulting in Beau lines
 Hair
- Diffuse shedding of the scalp hair.
- Gentle hair pull gathers several to many club or
telogen hairs.
- Distribution:
Hair loss occurs diffusely throughout the scalp and
includes the sides
and back of the head.
Short regrowing new hairs are present close to the scalp;
these hairs are finer than older hairs and have tapered
ends.
Investigations
Hair Pull

- More hair shed with reduce anagen and more telogen

Blood investigations ( FBC , Serum Iron, TIBC)

- To rule out iron deficiency anemia

- Thyroid function test to rule out thyroid disease

- Serology (ANA and RPR) to rule out secondary causes

Histopathology

- No abnormality other than an increase in the

proportion of follicles in telogen.
Management
Telogen effluvium is self-correcting.
It is really not influenced by any treatment that
can be given.
However, gentle handling of the hair, avoiding
over-vigorous combing, brushing and any type of
scalp massage are important.
Anagen Effluvium
Refers to hair shedding that arises during the
anagen stage of the hair cycle.
Onset is usually rapid and extensive
Usually due to radiation therapy to head,
chemotherapy with alkylating agents, intoxication
or severe protein malnutrition.
Pathogenesis:
- Occurs after any insult to hair follicle that impairs
its mitotic/metabolic activity. Rapid growth arrest or
damage to anagen hairs that skip catagen and
telogen phases and are shed.
Clinical Manifestation
Normal Skin and Scalp
Nails
- Show transverse banding or ridging.
Hair
- Hair Scalp hair loss is diffuse, extensive.
- Hair breaks off at the level of the scalp.
- Eyebrows/lashes, beard, body hair may also be
lost.
Management
No effective preventive measures are available.
A wig is preferred by many persons.

Hair regrows after discontinuation of

chemotherapy
Regrowth after radiation depends on type, depth,
dose-fractionation.
Scarring Alopecia
Lichen Planus (Lichen Planopilaris)
Discoid Lupus Erythematus
Lichen Planopilaris
Lichen planus is a chronic inflammatory skin condition
affecting skin and/or mucosal surfaces. Characterized by flat-
topped pink to violaceous, shiny, pruritic polygonal papules.
One of the types of lichen planus is lichen planopilaris.

Lichen Planopilaris results in patchy progressive permanent

hair loss mainly on the scalp.

Three forms are recognized:

- Classic lichen planopilaris.

- Frontal fibrosing alopecia

- Graham Little syndrome

Very rare, and commonly affects middle-aged women.

Clinical Manifestation
Can present with scalp pain or itchiness
Scalp
- Perifollicular erythema
- Hyperkeratosis.
- Violaceous discoloration of scalp.
- Prolonged inflammation results in scarring
alopecia.
- Distribution: most common on parietal scalp
Investigations
Do careful examination of the mouth, nails
and skin for evidence of lichen planus
elsewhere.
Trichoscopy
- reveals absent follicles, white dots, tubular
perifollicular scale and perifollicular erythema.
Scalp biopsy
Management
Glucocorticoids
Topical high-potency and intralesional
glucocorticoids (e.g., triamcinolone) are the
mainstay of treatment, improving symptoms and
hair growth.
Hydroxicloroquine and Ciclosporin
Acts as anti inflammatory.
Hair piece
Surgery
- scalp reduction
- hair transplantation
Discoid Lupus
Erythematus
This chronic, indolent skin disease is
characterized by sharply marginated, scaly,
infiltrated, and later atrophic red (discoid)
plaques, usually occurring on habitually exposed
areas.
Age of Onset is between 2045 years.

More in female than male

The manifestations of DLE are due to

loss of regulation of the immune system

in the skin.
 Clinical Manifestation
Skin Lesion
- Precipitated by sunlight and can be pruritic
- Well-demarcated, erythematous, hyperkeratotic plaques
with atrophy, follicular plugging, and adherent scale
Mucous membrane involvement (<5%)
Nail dystrophy
Scalp
- Scarring alopecia with residual inflammation
and follicular plugging
Investigations
Trichoscopy and Scalp biopsy
- Hyperkeratosis, atrophy of the epidermis, follicular
plugging, liquefaction degeneration of the basal cell
layer.
- Edema, dilatation of small blood vessels, and
perifollicular and peri-appendageal lymphocytic
inflammatory infiltrate.
Other Investigations
Immunofluorescence

Lupus Band Test positive in 90% of active lesions at least

6 weeks old and not recently treated with topical
glucocorticoids.
Blood investigations

- Full blood count - leukopenia

- Antinuclear antibody (ANA, ANF; if present, they are

usually in low titre)
- Anti-annexin 1 antibodiesthese may be a diagnostic
marker for discoid CLE
 Management
Prevention

- Topical sunscreens (SPF > 30) routinely.

- Vitamin D supplement

- Stop Smoking

Local Glucocorticoids and Calcineurin Inhibitors

Antimalarials

- Hydroxychloroqine , 6.5 mg/kg body weight per day.

Retinoids

- acitretin0.5 mg/kg body weight

Thalidomide

- 100300 mg/d
Excess Hair Growth
Hirsutism
Hypertrichosis
 Hirsutism
Excessive hair growth (women) in androgen dependent
hair patterns, secondary to increased androgenic activity.
Risk Factors

-Familial, ethnic, and racial influences.

-Hirsuteness: white > black > Asian .

Etiology

- Androgen secreting tumour

- Functional androgen excess

- Medication or drug induced

- Idiopathic
Pathogenesis
Androgens promote conversion of vellus to
terminal hairs in androgen-sensitive hair follicles:
Beard area, face, chest, areolae, linea alba, lower
back, buttocks, abdomen, external genitalia and
inner thighs.
In hyperandrogenic women, a greater percentage
of androgens may be secreted directly by by
andrenal glands and ovary which promotes the
conversion.
 Clinical Manifestation
History

- Family history

- Drug history

- Virilization symptoms

- Menstual changes or irregularity

Skin Findings

- Acne, acanthosis nigricans, striae.

Cushing Syndrome

- Centripetal obesity, muscle wasting (especially peripheral

muscle weakness), violaceous striae.
Pelvic Examination

- If polycystic ovary (PCO) syndrome is suspected.

 Hirsutism scale

8
 Investigation
Serum Testosterone

- If > 200 ng/mL, have to exclude androgen-secreting tumor

Serum Free Testosterone and Dehydroepiandrosterone

- Elevated in PCOS

17-Hydroxyprogesterone
- Raised level suggests congenital adrenal hyperplasia

Serum Prolactin and FSH

Urinary 17-Ketosteroid

- Helpful in evaluating the overall amount of androgen secretion.

Ultrasound
Management
Cosmetic Treatment
- Bleaching : Hydrogen peroxide
- Temporary removal : Waxing, shaving , chemical or cream
- LASER epilation
- Electrolysis

Weight Loss

Endrocrinology consultation
- If suspected tomour, CAH or Cushing.

Systemic Anti- Androgen Therapy

- Oral antiandrigen (Spironolactone)
- Oral Contraceptive
- Bromocriptine (for prolactinoma)
 Hypertrichosis
Is excessive hair growth (density, length) beyond
accepted limits of normal for age, race, sex in areas
that are not androgen sensitive
May be generalized/universal or localized .
May consist of lanugo, vellus, or terminal hair.

Can be congenital or aquired , localized or

generalized.
Management
Remove Known causes
Cosmetic Treatment

-Bleaching : Hydrogen peroxide

-Temporary removal : Waxing, shaving , chemical or

cream
-LASER epilation

-Electrolysis