Hair

Hair Disorders

By
Dr. Hala- Al- Salman
M.B.Ch.B., F.I.B.M.S.

Hair are classified in to 3 types:
Lanugo hairs: Fine long hairs covering the fetus, but shed about 1 month before birth.
Vellus hairs: Fine short unmedullated hairs covering much of the body surface, They replace the lanugo hairs just before birth.
Terminal hairs: Long coarse medullated hairs seen in the scalp and pubic area. Their growth is often influenced by circulating androgen levels.

Terminal hairs convert to vellus hairs in male pattern alopecia, and vellus hairs convert to terminal hairs in hirsutisim.

Hair cycle:

Each follicle pass, independently of its neighbors, through regular cycles of growth and shedding. There are three phases of follicular activity:
Anagen: The active phase of hair production, last 2-3 years.
Catagen: a short phase of conversion from active growth to the resting phase. Growth stops and the end of the hair become club- shaped, last about 3 weeks.
Telogen: a resting phase at the end of it the club hair is shed, last about 3 months.


* Average number of brown/black scalp hairs: 100,000. * 10% more on blondes.* 10% less on redheads. * Fastest Growth: between 15 and 30 years of age.* Slow growth in infants and elderly.* Average scalp hair growth: 0.35 mm/day or ~1 cm/month.
* cutting or shaving the hair have no effect on hair growth. * Hair grows faster in summer than in winter.* Percentage of hair in anagen phase: 85%-90%.
* 2%-3% in catagen.
*10%-15% in telogen. * Average daily numbers of hair shed: 50 to 100.* Female hair grows faster than male hair.

Hair loss

Non-scarring
(Non-cicatricial)Scarring
(cicatricial) Alopecia areata Burn, radiodermatitis Androgenetic alopecia Lichen planus Trichotilomania DLE Traction alopecia pseudopalade T.capitis kerion

Localized Alopecia:

Alopecia Areata (AA):
It affect about 2% of patients attending a dermatology clinic.
Cause:
Immunological basis is suspected because of the association with thyroid disease, vitiligo and atopy. An interaction between genetic and environmental factors may trigger the disease. Positive family history occurs between 10-30%. Psychological stress play important role in the pathogenesis of AA.

Clinical picture:

It characterized by sudden onset of hair loss in one or several patches 1-4 cm in diameter, mostly on the scalp, but it can affect any hairy area e.g. eyebrows, eyelashes, beard area. The skin is smooth and white or may have short stubs of hair. Some patients complain of itching, tenderness or burning sensation before the patch appears.
"exclamation- mark" hairs may be seen around the edge of enlarging area, which are broken off about 4mm from the scalp, and are narrowed and less pigmented proximally.
50% of the patients show nail changes in the form of pitting, longitudinal striation or wrinkling.




Course:
The outcome is unpredictable. In the first attack, regrowth is usual within a few months. New hairs appear in the centre of the patch as fine and white then change gradually to normal texture and color, but it may remain white, especially in older patients.
Subsequent episodes tend to be more extensive and regrowth is slow.
Few patients loss all the scalp hair (alopecia totalis), or from the whole skin surface (alopecia universalis).

Poor prognostic signs:

onset before puberty.
family history of AA.
other immune diseases.
nail changes.
association with atopy or Down's syndrome.
widespread alopecia.
involvement of scalp margin ( opasiform ), especially at the nape of the neck.

Differential Diagnoses:

tinea capitis.
DLE.
Lichen planus.
traction alopecia.
trichotilomania.
secondary syphilis.


Treatment:
Reassurance and tranqulizers.
Topical steroid.
Intralesional steroid.
Minoxidil 2-5% solution, spray.
Local Anthralin.
Topical immunosuppressive ( tacrolimus ).
Systemic steroid ???

Trichotillomania (hair-pulling habit):

Recurrent pulling out of hair, resulting in noticeable hair loss. It affect children, adolescents and women. Most children have mild form of hair pulling habit, but the severe degree occur in disturbed adolescents and those with underlying psychological problem.
The patches of hair loss are irregular in outline and hair loss is never complete, the hairs that remain are bent or broken and of variable length.

Traction (cosmetic) alopecia:

Hair can be pulled out by many methods; including hot combing, tight hairstyle and using hair rollers.
Hair being lost in area of maximal tug. Marginal alopecia is a commom pattern, in which hair loss occur around the edge of the scalp (at the sides or at the front). The bald area show short broken hairs, folliculitis and sometime scarring.
Malepattern alopecia(Androgenic alopecia in men):
Baldness in man is not a disease, but a physiological reaction induced by androgen in genetically predisposed men. Its inherited as polygenic. Thinning of the hair begin between the age of 12-40 years. About 50% of the population develop this condition before the age of 50. Its due to progressive shortening of successive anagen cycles.
Hamilton pattern:
I: Triangular fronto-temporal recession occurs normally in most young men.
II: First sign of balding are increased fronto-temporal recession with mid-frontal recession.
III VII: hair loss in round area on the vertex and the density of hair decrease over the top of the scalp.


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Treatment:

Topical minoxidil 2%, 5%.
Oral fenisteride 1mg, 5mg.
Hair transplant.
Scalp reduction and flap.

Female Pattern Baldness:

The most common form of hair loss in women is Androgenetic Alopecia or what is known as female pattern baldness. And like male pattern baldness it has a large genetic predisposition, and it involves androgen and DHT. Androgen is a male hormone that all men and women produce. Androgen in turn produces a chemical called dihydrotestosterone( DHT).
excess DHT causes hair follicles to make thinner and thinner hair until they eventually stop making hair altogether.
There is gradual loss of hair on the central scalp, with retention of the normal hair line without fronto-temporal recession. It affect females in their 20s or 30s.
The typical pattern of female pattern baldness is different from that of male pattern baldness. The hair thins all over the head, but the frontal hairline is maintained. There may be a moderate loss of hair on the crown, but this rarely progresses to total or near baldness as it may in men. Another difference is that male pattern baldness can begin at puberty whereas female pattern baldness usually begins around the age of thirty, and it often gets worse with the onset of menopause.
The hair loss of female pattern baldness or severe thinning may be permanent.
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Diffuse hair loss:

Telogen Effluvium:
A number of events prematurely terminate anagen and cause an abnormally high number of normal hairs to enter the resting telogen phase. Usually no more than 50% of the hair is affected.
The follicle is not diseased, scarring and inflammation are absent.
Resting hairs on the scalp remain about 100 days before they are lost, so telogen hair loss should occurs approximately 3 months after the event that terminate the normal hair growth.
The hair loss begins abruptly and last about 4 weeks. Full recovery can be expected.
Causes:


PhysiologicDrugs and toxins
1. Physiologic effluvium of the newborn
2. Postpartum effluvium
3. Injury or stress
4. High or prolonged fever
5. Severe infection
6. Severe chronic illness
7. Severe psychologic stress
8. Major surgery
9. Hypothyroidism & endocrinopathies
10. Severe dieting or malnutrition
1. aminosalicylic acid.
2. captopril,
3. propranolon,
4. lithium
5. Antikeratinizing agents [Tegison])
6.Anticoagulants (heparin)
7. Antithyroid agents
8. Alkylating agents
9. Anticonvulsants
10.Hormones


Anagen Effluvium:
There is abrupt loss of hair from follicles that are in their growing phase. The only hair left are those in the telogen phase. The rapidly dividing cells of the matrix and cortex are affected.
Since 90% of the scalp hairs are in anagen phase, a large number of hair can be affected.
Causes:
chemotherapy.
radiotherapy.
poisoning: arsenic, lithium.


Differences between telogen and anagen hair loss

Clinical presentationTelogenAnagen 1. Onset of shedding2-4 months1-4 weeks 2. Percent of hair loss20-50%80-90% 3. Type of hair lostNormal club (white)Anagen hair (pigmented)4. Hair shaftnormalNarrowed or fractured

Historical Clues and Possible Hair Loss Etiologies

If the patient has or had...
Consider...

Systemic/chronic illness (e.g., autoimmune disorder, cancer)

Alopecia areata, cicatricial alopecia, telogen effluvium

Infection (systemic or local)

Cicatricial alopecia, telogen effluvium, tinea capitis

Medication exposure (especially chemotherapy) or serious illness within previous three to four months
Telogen effluvium

Psychiatric disorder (e.g., psychosis, anxiety, obsessive compulsive disorder)

Trichotillomania

Physical stress (e.g., surgery, pregnancy, malnutrition) or life-threatening psychologic stress
Telogen effluvium


Tight braids or "pulled-back" hairstyle
Traction alopecia

Signs and symptoms of hormonal abnormalities

Hirsutism, amenorrhea, infertility
Androgenetic alopecia (women)

Hypothyroidism, other endocrinopathies

Alopecia areata, telogen effluvium



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Studies That May Be Helpful in Diagnosing Alopecia

Hair loss disorder
Studies
Findings


Female androgenetic alopecia
Prolactin, FSH, LH, DHEAS
Hyperandrogenism

Telogen effluvium

TSH, other endocrine tests
Metabolic disorder

Alopecia areata, telogen effluvium

ESR, ANA, RF
Autoimmune disease

Alopecia areata

CBC
Pernicious anemia

Tinea capitis

Culture swab, KOH examination, fluorescence with Wood's lamp*
Fungal infection

Telogen effluvium

Hair-pull test with microscopic evaluation
White bulb on shaft


Tinea capitis, environmental/external factor, systemic disease
Same as above
Mid-shaft, fractured hairs

Alopecia areata, alopecia totalis, alopecia universalis

Same as above
Exclamation-point hairs

Telogen effluvium

Hair-pluck test
Increased telogen:anagen ratio

Unclear etiology, mixed signs/symptoms, failure to improve with treatment

Scalp biopsy
Underlying pathology

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