Dr Jennifer Martinick – Warning about Hair Disorders
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Transcript of Dr Jennifer Martinick – Warning about Hair Disorders
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.