Disorders of hairDisorders of hair

Less hairExcessive hair

The hair can be divided into three parts

(1) The bulbA swelling at the base which

originates from the dermis (2) The root

The hair lying beneath the skin surface(3) The shaft

Which lies above the skin surface.

In cross-section,

(1) The medullaAn area in the core which contains

loose cells and airspaces (2) The cortex

Which contains densely packed keratin and (3) The cuticle

Which is a single layer of cells arranged like roof shingles.

ClassificationClassification

Hairs are classified into three main types◦Lanugo hair◦Vellus hair◦Terminal hair

Terminal hairs convert to vellus hairs in male pattern alopecia

Vellus hairs convert to terminal hairs in hirsutism.

Lanugo hair Fine long hair

covering the foetus

Shed about 1 month before birth unless born prematurely.

May reappear sometimes in severe malnutrition and anorexia nervosa.

Vellus hair Fine, short

unmedullated hair covering much of the body surface.

They replace the lanugo hair just before birth.

Terminal hair Fully developed Long coarse

medullated hair in the scalp or pubic regions.

Their growth is influenced by circulating androgen levels.

The hair cycleThe hair cycleEach follicle passes through regular

cycles of growth and shedding. There are three phases of follicular

activity◦Anagen

The active phase of hair production.◦Catagen

A short phase of conversion from active growth to the resting phase.

Growth stops, and the end of the hair becomes club-shaped.

◦Telogen A resting phase at the end of which the club

hair is shed.

The duration of each of these stages varies from region to region.

On the scalp it is said to contain an average of 100,000 hairs◦Anagen lasts for upto 5 years◦Catagen for about 2 weeks◦Telogen for about 3 months

As many as 100 hairs may be shed from the normal scalp every day as a normal consequence of cycling.

AlopeciaAlopecia

The term alopecia means loss of hair

Alopecia has many causes and patterns.

One convenient division is into◦ Localized◦ Diffused

It is also important to decide if the hair follicles are replaced by scar tissue; if they have, regrowth cannot occur.

CLASSIFICATION OF CLASSIFICATION OF ALOPECIAALOPECIA Localised Non-scarring Tinea capitis Alopecia areata Androgenetic alopecia Traumatic (trichotillomania,

traction, cosmetic) Syphilis

Scarring Idiopathic Developmental defects Discoid lupus erythematosus Herpes zoster Pseudopelade Tinea capitis/kerion

Diffuse Androgenetic alopecia Telogen effluvium Metabolic Hypothyroidism Hyperthyroidism Hypopituitarism Diabetes mellitus HIV disease Nutritional deficiency Liver disease Post-partum Alopecia areata Syphilis

Discoid lupus erythematosus Radiotherapy Folliculitis decalvans Lichen planus pilaris

Localized alopeciaLocalized alopecia

Alopecia areata

EtiologyEtiology

An immunological basis is suspected because of an association with ◦ Autoimmune thyroid disease◦ Pernicious anemia◦ Vitiligo◦ Atopy

Histologically, T lymphocytes cluster like a swarm of bees around affected hair bulbs because cytokines produced by the dermal papillae in lesions not only attract lymphocytes to perifollicular region but also stimulate them to multiply

Alopecia areata is probably inherited as a complex genetic trait

Sometimes HLA-DQ3, -DR11 or -DR4 act as susceptibility factors◦ With an increased occurrence in the first-

degree relatives of affected subjects and twin concordance.

It affects some 10% of patients with Down’s syndrome, suggesting the involvement of genes on chromosome 21.

Environmental factors as well as emotional factors may trigger alopecia areata in the genetically predisposed.

EpidemiologyEpidemiologyAA is the common typeBoth gender affectedCan start at any age

PresentationPresentation

A typical patch of hair loss area is uninflamed, with no scaling, but with empty hair follicles

Pathognomonic ‘exclamation-mark’ hairs may be seen around the edge of enlarging areas.

They are broken off about 4 mm from the scalp

Are narrowed and less pigmented proximally

Incidence is most common in the scalp and beard but other areas, especially the eyelashes and eyebrows, can be affected too.

An uncommon diffuse pattern is recognized, with exclamation-mark hairs scattered widely over a diffusely thinned scalp.

Up to 50% of patients show fine pitting or wrinkling of the nails.

The characteristic uninflamed patches ofalopecia areata.

Exclamation-mark hairs: Pathognomonic ofalopecia areata.

CourseCourseThe outcome is unpredictable. In a first attack, regrowth is usual within a

few months. New hairs appear in the centre of patches

as fine pale down, and gradually regain their normal colour

The new hair may remain white in older patients.

Fifty percent of cases resolve spontaneously without treatment within 1 year

Only 10% have severe chronic diseaseSubsequent episodes tend to be more

extensiveRegrowth is slower.

Hair loss in some areas may coexist with regrowth in others.

A few of those who go on to have chronic disease loose all the hair from their heads (alopecia totalis) or from the whole skin surface (alopecia universalis).

other variant is ophiasis which is lose of hair in a band like patternat the periphery of scalp

Regrowth is tiresomely erratic but the following suggest a poor prognosis:

1. Onset before puberty2. Association with Atopy or Down’s

syndrome3. Unusually widespread alopecia and4. Involvement of the scalp margin

(ophiasiform type)

Alopecia totalis

Alopecia universalis

Differential diagnosisDifferential diagnosis

Ringworm infectionLupus erythematosusLichen planusHair-pulling habit of childrenTraction alopeciaSecondary Pseudopelade

InvestigationsInvestigations

None are usually needed.

The histology of bald skin shows lymphocytes around and in the hair matrix.

Syphilis can be excluded with serological tests

Organ-specific autoantibody screens

TreatmentTreatmentA patient with a first or minor attack

can be reassured about the prospects for regrowth.

Topical corticosteroid creams of high potency can be prescribed

The use of systemic steroids should be avoided in most cases

Intradermal injection of 0.2 ml intralesional triamcinolone acetonide (5–10 mg/ml), raising a small bleb within an affected patch, leads to localized tufts of regrowth.

Side effects dermal atrophy evident as depressed areas at the sites of injections.

Regrowth within a patch of alopecia areata aftera triamcinolone injection.

Ultraviolet radiation or even psoralen with ultraviolet A (PUVA) therapy may help in extensive cases, but hair fall often returns when treatment is stopped.

Contact sensitizers (e.g. diphencyprone) seemed promising but the long-term effect of persistent antigen stimulation is worrying; they are still being used only in a few centres under trial conditions.

Wigs are necessary for extensive cases.

A trial of diphencyprone to one side of the scalpcaused some regrowth

Androgenetic alopecia Androgenetic alopecia (male-pattern baldness)(male-pattern baldness)

CauseIt is because of miniaturization of hair

follicles

Although clearly familial, the exact mode of inheritance has not yet been clarified.

Male-pattern baldness is androgen dependent

In females, androgenetic alopecia (female-pattern hair loss), with circulating levels of androgen within normal limits, is seen only in those who are strongly predisposed genetically.

PresentationPresentation

The common pattern in men is the loss of hair first from the temples, and then from the crown

However, in women the hair loss may be much more diffuse, particularly over the crown

In bald areas, terminal hairs are replaced by finer vellus ones.

Androgenetic alopecia beginning in the frontal area

ComplicationsComplications

AnxietyBald scalps burn easily in the sunIt has been suggested recently

that bald men are more likely to have a heart attack and prostate cancer than those with a full head of hair

Differential diagnosisDifferential diagnosis

The diagnosis is usually obvious in men, but other causes of diffuse hair loss have to be considered in women

TreatmentTreatment

Scalp surgeryHair transplantsWigsTopical application of minoxidil lotion may slow

early hair loss and even stimulate new growth of hair but the results are not dramatic◦ Small and recently acquired patches respond

best. ◦ When minoxidil treatment stops, the new hairs

fall out after about 3 months.Antiandrogens help some women with the

diffuse type of androgenetic alopecia.

TreatmentTreatmentFinasteride (Propecia), an inhibitor of

human type II 5α-reductase, reduces serum and scalp skin levels of dihydrotestosterone in balding men and at the dosage of 1 mg/day, it may increase hair counts ◦ Lead to a noticeable improvement in both

frontal and vertex hair thinning. ◦ However, the beneficial effects slowly

reverse once treatment has stopped. ◦ This treatment is not indicated in women

or children. Side-effects are rare, but include

◦ Decreased libido, erectile dysfunction and altered prostate-specific antigen levels

Telogen effluviumTelogen effluviumAll the hair follicle are not

synchronous in their cycle If anagen phase of several

adjoining hair follicles is aborted and these follicles enter telogen phase at the same time and several hair are shed simultaneously this is called telogen effluvium

Etiology:Infections: typhoid, malaria,

dengueChildbirth:prolongedSurgical traumaHaemorrhageEmotional stress

Clinical features: hair loss occurs after 2-3mths after the precipitating factor

Severe cases associated with anemia and beau’s lines of the nails.

Treatment: stops spontaneously after2-3mths

Excessive hairExcessive hair

HypertrichosisHirsutism

Hirsutism and Hirsutism and hypertrichosishypertrichosis

Hirsutism is the growth of terminal hair in a woman which is distributed in a pattern normally seen in a man (for example, mustache, beard, central chest, shoulders, lower abdomen, back, and inner thighs).

Hypertrichosis is an excessive growth of terminal hair in either sex that does not follow an androgen-induced pattern

Types of hypertrichosisTypes of hypertrichosisCongenital Hypertrichosis is very

rare. ◦A fetus is covered with lanugo and it

does not fall off but continues to grow.

Acquired Hypertrichosis◦Occurs after birth. ◦Unpigmented vellus hair or pigmented

terminal hair. ◦The excessive hair may cover the entire

body (Generalized), or it could be localized to one area.

Congenital Localized forms:Hypertrichosis cubiti (Congenital

hairs on elbows)Hairy pinna (Congenital hairs on

the external ears)

Acquired hypertrichosisAcquired hypertrichosis

Causes of hypertrichosisCauses of hypertrichosis

Localized◦ Melanocytic naevi◦ Becker’s naevi◦ Satyr’s tuft in sacral area- in patients with spina

bifida ◦ Chronically inflamed joints◦ Under plaster casts◦ Carrying weights over shoulder

Causes of hypertrichosisCauses of hypertrichosis

Generalized

Anorexia nervosa, starving, malnutrition Drug induced- minoxidil, diazoxide, ciclosporin

anabolic steroids. porphyrias Fetal alcohol syndrome Fetal phenytoin syndrome Hypertrichosis lanuginosa(congenital or acpuired) General systemic illness (such as advanced HIV infection) Hypothyroidism or other endocrine disorders

HirsutismHirsutism

CauseIncreased level of androgens or an oversensitivity of hair follicles

to androgens Racial or familial trait (Mediterranean, Caucasians and Asians) Idiopathic hirsutism Hormonal: Polycystic Ovarian Syndrome Cushing's disease Tumors in the ovaries or adrenal gland Congenital adrenal hyperplasia postmenopausal women Itragenic: Drugs- androgens or progesterones, anabolic steroids.

PresentationPresentationAn excessive growth of

hair in◦ Beard area and side burn◦ Chest ◦ Shoulder-tips◦ Around the nipples◦ Abdomen◦ Male pattern of pubic hair ◦ Androgenetic alopecia

Signs of virilization◦ Temporal hair recession◦ Acne◦ Deep voice, increased size of Adam's

apple◦ Oily perspiration◦ Breast atrophy◦ Muscle hypertrophy◦ Loss of female body contour◦ Clitoral enlargement

InvestigationsInvestigations

Significant hormonal abnormalities are not usually found in patients with a normal menstrual cycle.

Investigations are needed if:◦ Hirsutism occurs in childhood◦ There are features of virilization ◦ Hirsutism is of sudden or recent onset ◦ There is menstrual irregularity or cessation

The tests sent areThe tests sent are Total and free testosterone Sex hormone binding globulin Free androgen index Dihydroxyepiandrosterone sulfate Androstenedione (drawn after 10 a.m.) If there is also menstrual disorder, additional tests may

be requested. ◦ Luteinizing hormone (LH) and follicle stimulating

hormone (FSH) ◦ Oestradiol, 17-hydroxy progesterone ◦ Prolactin

Tests may be requested to evaluate other related aspects of health, for example: ◦ Thyroid function ◦ Cortisol or overnight dexamethasone test ◦ Glucose ◦ Lipids (cholesterol and triglyceride)

Pelvic ultrasounds

TreatmentTreatment

Treat underlying disorderHome remedies for minor hirsutism include

commercial, waxing or shaving, or making its appearance less obvious by bleaching

Plucking should be avoided as it can stimulate hair roots into Anagen.

The abnormally active follicles can be destroyed by electrolysis.

If numerous, by laser Topical therapy with eflornithine, an inhibitor

of ornithine decarboxylase, can slow regrowth.

Oral antiandrogens ◦Oral contraceptive pills with oestrogen

and cyproterone- antiandrogenic activity

◦Cyproterone acetate 50-200 mg for 10 days each cycle

◦Spironolactone 50-200 mg daily can slowly reduce excessive hair growth-long term.

Pregnancy must be avoided during such treatment as it carries the risk of feminizing a male fetus.