Diseases of the HairHair Follicle: cycling

• Anagen (90%)Growth phase 3 years duration• Catagen(<1%)Involution

phase; 1-2 weeks duration• Telogen (10%)Resting/

shedding phase; Lasts 3-5 months

The types of hair are

•Lanugo hairs, fine long hair covering the fetus, but shed about 1 month before birth.•Vellus hairs, fine short unmedullated. They replace the lanugo hairs just before birth.•Terminal hairs, long coarse medullated hairs seen, for example, in the scalp or pubic regions

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Hair Loss (Alopecia)Shedding of hair is termed effluvium or defluvium, and the resulting condition is called alopecia (Gr. Alopecia, “baldness”). Alopecia classified into:• Noncicatricial alopecia: no clinical sign of tissue

inflammation, scarring, atrophy of skin.• Cicatricial alopecia: evidence of tissue destruction

such as inflammation, atrophy, and scarring.

Nonscarring Alopecia

Diffuse (global) hair loss• Telogen effluvium• Diffuse alopecia areata• Androgenetic alopecia• Systemic disease

(thyroid, iron deficiency, SLE, dermatomyositis).

focal (patchy, localized)•Alopecia areata •Tinea capitis •Traction alopecia ± scarring•Trichotillomania ± scarring •Syphilis

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Scarring Alopecia

• Discoid lupus erythematosus

• Lichen planopilaris (follicular lichen planus)

• Folliculitis decalvans• Dissecting cellulitis\

folliculitis • Acne keloid.

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Nonscarring AlopeciaAlopecia Areata

Alopecia areata is characterized by rapid and complete loss of hair in one or more round or oval patches, usually in the scalp, beard area, eyebrows, eyelashes and less commonly on other area. Often patches are from 1-5 cm in diameter. • Alopecia totalis: is complete loss of scalp hair• Alopecia universalis: is complete loss of all hairs from

skin surface. • Ophiasis: along the temporal and occipital scalp• Sisaipho: entire scalp except for this area

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Alopecia areata

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Clues to the correct diagnosis include a history of periodic regrowth, nail pitting, and the pathognomonic ‘exclamation point’ hairs may be seen around the edge of enlarging areas. They are broken off about 4 mm from the scalp, and area narrowed and less pigmented proximally.

Examination

Associated disease

• Usually occurs without associated disease• However, there is a higher incidence in

patients with atopic dermatitis, Down syndrome, LP, LE, thyroiditis, myasthenia gravis and vitiligo

• Nails may develop nail pitting that may form transverse or longitudinal lines – 10 %

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etiology

• Cause unknown• Most evidence points toward its being an

autoimmune disease mediated by the cellular arm and modified by genetic factors

• 25% report family history• Patients with early onset, severe, familial

clustering alopecia areata have a unique and highly significant association with HLA antigens DR4, DR11, and DQ7

• Stress is frequently cited. 9

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Include trichotillomania, telogen effluvium, tinea capitis, early lupus erythematosus, syphilis.-In trichotillomania there are short and broken hairs. -Hair loss occurs over the entire scalp with telogen effluvium. -The ‘moth-eaten’ appearance in syphilis. -KOH is positive in tinea capitis.

Differential diagnosis

TX• Some patches will regrow without any treatment• Intralesional injections of corticosteroid • High-strength topical steroid• Induction of contact sensitivity using topical anthralin• Topical Minoxidil alone or combined therapy• Topical or oral methoxsalen and UVA (PUVA).• Psychotherapy.Poor prognosis are; the presence of atopic dermatitis,

childhood onset, widespread involvement, ophiasis, duration of longer than 5 years, and onychodystrophy.

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Telogen effluvium

• Early and excessive loss of normal club hairs from normal resting follicles in the scalp

• Loss results from traumatization of the normal hair by some stimulus, such as surgery, parturition, fever, drugs, or traction which precipitates the anagen phase into catagen and telogen phases

• Follicle is not diseased and inflammation is absent

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Exam. {Normal telogen account is below 10%;100-150 hair lost daily; 150-400 hairs lost in TE.}

• Positive hair pull test-grasp 40 hairs firmly and pull slowly (>4-6 club hairs is positive).Other tests:

• Collect all hairs: the patient combs (from vertex to anterior hairline) for 1 minute prior to shampooing on 3 consecutive days (10-15 normal, >50 common in TE).

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• Clip test: 25 to 30 hairs are cut just above the scalp surface and mounted. Indeterminate and telogen hairs are short and of small diameter.

• Trichogram evaluation provide information on the anagen-to-telogen ratio. Plucking 50 to 100 hairs from different parts of the scalp, sticking them to a slide, and examining them under a microscope. 

Telogen effluvium

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Causes of telogen effluvium:• Endocrine: childbirth, miscarriage, abortion; hypo- and

hyperthyroidism.• Stressful events: febrile illnesses; catabolic illnesses

(malignancy, chronic infection); major surgery; major trauma; psychological stress.

• Nutritional: rapid weight loss; caloric or protein deprivation; iron deficiency; excessive vitamin A ingestion.

• Intoxication: mercury; arsenic.• Drugs: anticoagulants; β blockers; captopril; cholesterol

lowering drugs; cytotoxic agents; retinoids; interferon.• Inflammatory scalp disease: seborrheic dermatitis;

erythroderma.

TX

• No specific therapy• In the majority of cases it will stop

spontaneously within a few months and the hair will regrow

The prognosis is good if a specific event can be pinpointed as a possible cause.

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Anagen effluvium• Usually results from hair shaft fracture• Seen frequently following the administration of

cancer chemotherapeutic agents.• Only anagen hairs are involved• With cessation of the drug the follicle resumes

normal activity within a few weeks• Process being entirely reversible

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Pattern Hair Loss(androgenetic alopecia)• Pattern hair loss is by far the most common type of hair loss

in both sexes.• Female pattern hair loss has also been termed androgenetic

alopecia, in the belief that is the same entity as in men, but the requirement for androgens is less clearcut than in men and the distribution of hair loss is generally different.

• However, in both men and women, pattern hair loss is characterized by a progressive decline in the duration of anagen, an increase in the duration of telogen, and miniaturization of scalp hair follicles, indicating a final common pathway of follicular regression.

• Pattern hair loss is biologically normal trait.

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Androgenetic alopecia (male-pattern baldness)Baldness in men is not a disease, but rather a physiologic reaction induced by androgens in genetically predisposed men. The pattern of inheritance is probably polygenic.

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Skin androgen metabolism• Testosterone is converted to dihydrotestosterone by 5α-

reductase.• Skin cells contain 5α-reductase (type 1 and 11). The type

1 is found in sebaceous glands, and type 11 is found in hair follicles and the prostate gland.

• T and DHT increase the size of hair follicles in androgen-dependent area such as the beard during adolescence, but letter in life DHT binds to the follicle androgen receptor and activates transformation of large, terminal follicles to miniaturized follicles. The duration of anagen shortens and the follicles become smaller, producing shorter, fine hairs.

• Androgenitic alopecia does not develop in men with a congenital absence of 5α-reductase type 11.

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Clinical features.The progression and various patterns of hair loss are classified by the Hamilton male baldness classification system.Type 1: Triangular frontotemporal recession.Type 11: Increased frontotemporal recession + midfrontal recession.Type 111 through V11: Hair loss in a round area on the vertex, and the density of hair decreases, sometimes rapidly, over the top of the scalp.

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-Topical minoxidil promotes survival of dermal papilla cells, induces and prolongs anagen phase, and results in enlargement of shaft diameter .

-Finasteride (men aged 18-41): Type 2 5-alpha reductase inhibitor. Prolongs anagen phase.1 mg daily can prevent further hair loss -Hair transplantation

Treatment

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Androgenetic alopecia in women

• Scalp hair loss is a feature of hyperandrogenism in women, and when accompanied by other signs of androgen excess such as hirsutism, amenorrhea, and a raised circulating testosterone level, should prompt a search for an androgen-secreting tumor, polycystic ovaries.

• Many women with pattern hair loss do not exhibit other biochemical or clinical signs of androgen excess, however, and do not respond to anti-androgen treatment, suggesting that androgens do not play a role.

• No genetic loci associated with female pattern hair loss have yet been identified.

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Female. Ludwig described the hair loss, as following.Grade 1: rarefaction of the hair on the crown. Grade 11: result in further rarefaction of the crown, with preservation of the fringe.Grade 111: is near-complete baldness of the crown.

Clinical features.

• The midline part is an important clinical clue to the diagnosis, revealing this central thinning by the appearance of the “Christmas tree pattern”

Androgenetic alopecia in women

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Investigations are probably unnecessary in men and in most women with typical pattern hair loss.• Serum ferritin: there is some evidence that women with

serum ferritin less than 40 µg\L respond poorly to anti-androgen treatment.

• Thyroid stimulating hormone: hair loss is traditionally regarded as a feature of thyroid deficiency.

• Serum androgens: especially in women with concomitant evidence of hirsutism, severe acne, acanthosis nigricans, irregular menses, and\or galactorrhea. Screening should include free and\or total testosterone with or without dehydroepiandrosterone sulfate.

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Treatment :• Topical minoxidil• Oral antiandrogens spironolactone; cyproterone

acetate.• Finasteride • Hair transplantation.

Trichotillomania

• A neurotic practice of plucking or breaking hair from the scalp or eyelashes

• Usually localized but may be widespread• Areas of alopecia characteristically contain hairs of

various lengths• Seen mostly in girls under 10, may also be seen in

boys and adults• Shave 3 X 3 cm area and watch the hair regrow

normally. Hairs in this ‘skin window” will be too short for plucking

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Trichotillomania

• May be a manifestation of obsessive-compulsive disorder

• May be associated with depression or anxiety

• TX – psychotherapy.

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Other Forms of Noncicatricial Alopecia

• Alopecia syphilitica

• Vascular or neurologic alopecia

• Endocrinologic alopecia

• Congenital alopecia

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Scarring AlopeciasPrimary: Target of destruction is the hair follicle

Secondary: Nonfollicular disease indirectly causes follicular destruction e.g. sarcoid, morphea, leprosy

many scarring alopecias begin as nonscarring

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Cicatricial Alopecia•Lymphoid-mediated disorders: lupus

erythematosus, lichen planopilaris.•Neutrophil-mediated disorders: folliculitis

decalvans, dissecting cellulitis.•Mixed: acne keloidalis, acne necrotica

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Other forms of permanent alopecia: • Traction alopecia occurs from prolonged tension

on the hair. Most commonly involves the periphery of the scalp, especially the temples and the above the ears.

• Pressure alopecia occurs in adults after prolonged pressure on the scalp during general anesthesia, with the head fixed in one position and also appear in chronically ill persons.

• Tumor alopecia refers to hair loss in the immediate vicinity of either benign or malignant tumors of the scalp.

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Excessive Hair Growth

HirsutismHypertrichosis

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Hirsutism is an excess of terminal hair growth in women in a pattern more typical of men. Androgen-dependent growth areas affected include the upper lip, cheeks, chin, central chest, breasts, lower abdomen, and groin.

Hypertrichosis is an overgrowth of hair not localized to the androgen-dependent areas of the skin.

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• May or may not be associated with other signs of virilization (Virilization symptoms: female pattern hair loss to male pattern balding, acne, dependent voice, increased muscle mass, enlargement of the clitoris, increased libido, personality change.)

• When virilization accompanies hirsutism, especially when progression is rapid, a neoplastic cause is likely.

• Most medically significant hirsutism is related to the polycystic ovarian syndrome.

Hirsutism-pathogenesis

Hirsutism-pathogenesis• Racial variation: women of European have

facial, abdominal, and thigh hair; whereas Asian and Indian have little terminal hair growth in these areas.

• May result either from excessive of androgens from either the ovary or the adrenal gland, or from excessive stimulation by pituitary tumors

• Ovarian causes include polycystic ovarian disease and a variety of ovarian tumors, both benign and malignant

• Adrenal causes include congenital adrenal hyperplasia and adrenal tumors such as adrenal adenomas and carcinomas

Hirsutism-pathogenesis

• Pituitary causes include Cushing’s disease, acromegaly, and prolactin-secreting adenomas

• Other conditions in which prolactin levels may be elevated and that may lead to hirsutism include hypothyroidism, phenothiazine intake, and hepatorenal failure

• Other causes include the exogenous intake of androgens and certain high-progesterone.

• Idiopathic

Hirsutism-evaluation• History should focus on onset and progression,

virilization, menstrual history, and family/racial background

• Laboratory evaluation should include a total testosterone and a dehydroepiandrosterone sulfate level for relatively stable and mild hirsutism

• Dexamethasone suppression test to screen for Cushing’s disease

• In patients with menstrual dysfunction add prolactin level and an LH/FSH ratio to evaluate suspected polycystic ovarian disease

treatment

• Shaving, wax depilatories, chemical depilatories, bleaching of the hair, laser hair removal, and electrolysis

• Oral contraceptives and glucocorticoidsContraceptive helpful in 75% of hirsute women• Antiandrogens include, cimetidine, cyproterone

acetate, spironolactone, flutamide, and ketoconazole

• Finasteride• Gonadotropin-releasing hormone agonist such as

leuprolide

treatment

• Oral contraceptives and glucocorticoids• Contraceptive helpful in 75% of hirsute

women• Antiandrogens include, cimetidine,

cyproterone acetate, spironolactone, flutamide, and ketoconazole

• Finasteride• Gonadotropin-releasing hormone agonist such

as leuprolide and nafarelin

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Etiology and Pathogenesis May be congenital or acquired, generalized or localized Other causes – medications, malignancy

Hypertrichosis

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Causes of generalized hypertrichosis: 1)Congenital\hereditary: Congenital hypertrichosis lanuginosa 2) Acquired • Acquired hypertrichosis lanuginose (malignancy) • Drugs (minoxidil, diazoxide, phenytoin, cyclosporine,

psoralen, topical steroids)• Porphyria • POEMS (polyneuropathy, organomegaly, endocrinopathy, M

protein, and skin changes) syndrome• Juvenile dermatomyositis• Hypothyroidism• Malabsorption syndromes• Central nervous system (related problems) or trauma.

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Causes of localized hypertrichosis: 1)Congenital\hereditary 2) Acquired• Post Morphea• Reflex sympathetic dystrophy• Scrotal hair in male infants• Drugs (interferon, topical minoxidil)• Irritants (topical)• Repeated trauma• Stasis\lymphedema• Chronic osteomyelitis• Site of immunizations (smallpox)• Chicken pox; HIV