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An understanding of the process of normal hair growth is necessary to comprehend and evaluate hair disorders. Each follicle progresses quite independently through regular cycles of growth and shedding (see FIG. 126.1).
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The three phases of follicular activity are:3
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Anagen phase—the active growth phase of hair production.
The dermal papilla stimulates division of epithelial cells that produce the hair shaft.
The hair shaft grows 1 cm per month.
It lasts for about 2.5–5 years on the scalp (average 1000 days).
It lasts 1–2 months on eyebrows and eyelashes and 6–9 months in the axilla and pubis.
It varies between individuals.
Catagen phase—a short transition phase from active growth to inactivity (the involutional stage).
Telogen phase—the resting (dormant) phase of the cycle at the end of which the club hair with its non-pigmented bulb is shed.
This lasts 2–4 months (average 100 days).
The percentage of hairs in telogen varies from site to site—10% in scalp to 60–80% in pubic hair.1
The hair is anchored in the follicle but does not grow longer.
The follicle then re-enters anagen.
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Thus every 3–5 years every hair on the scalp is shed and replaced.
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Some facts on hair numbers3
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Hair growth is asynchronous (i.e. continuous production and shedding).
Humans produce 1 km of hair a month.
About 50–100 hairs are shed daily without a reduction in density.
The scalp contains, on average, 100 000 hair follicles.
The hair follicle is subject to melanocytic activity.
At least 25% of hair must be shed before a noticeable loss of density occurs.
Hair loss counts consistently above 100 per day indicate excessive hair loss.
Significant hair loss tends to block the shower drain or be visible all over the pillow.
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Onset, duration, quantity and rate of loss
Localised or generalised loss
Associated symptoms (e.g. pruritus, scaling, pustules)
Systems review including fever, acute illness, surgery, stressors
Symptoms of hyperandrogenism in women (e.g. hirsutism, acne)
Endocrine features
Past history including skin disorders, cancer, thyroid disorders
Family history of hair loss
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General review with emphasis on endocrine system and examination of scalp
Look for exclamation mark hair, ‘white bulb’ hair, state of bald patch (clean, scaly, scarred or inflamed) and the unusual pattern of trichotillomania
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Alopecia areata, alopecia totalis and alopecia universalis
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Alopecia areata is a disorder of the hair follicle causing a sudden onset of localised or diffuse hair loss. It is thought to be an autoimmune disorder that has a genetic susceptibility (20% have a positive family history). Men and women are affected equally, with the disorder most commonly occurring in the first two decades of life.4 The hairs are affected during the growth phase, resulting in cessation of anagen.
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DxT patch of complete hair loss + clean scalp + exclamation-mark hairs ➜ alopecia areata
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Complete hair loss (small patch or diffuse)
Pigmented hairs often lost first
Clean normal scalp
No or minimal inflammation
Exclamation-mark hairs, especially around the periphery (see FIG. 126.2)
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An unpredictable pattern of remission and relapse is characteristic. Patches may:
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regrow hair spontaneously (up to 50% within 12 months if a single patch)
stay the same for many months
enlarge and coalesce with other patches
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The prognosis is poorer with more widespread involvement and younger age of onset (<5 years of age).
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Treatment options include:
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topical potent corticosteroid (especially in children), e.g. betamethasone dipropionate 0.05% cream or lotion, once or twice daily for 3–4 months
intralesional steroids—triamcinolone 10 mg/mL or betamethasone acetate/phosphate 5.7 mg/mL bd (caution needed on face—risk of cutaneous atrophy). Multiple injections required.
topical minoxidil 5% bd (for 4 or more months) only when hair growing
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Extensive area (>50% loss)
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Treatment options include:
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Counselling
Alopecia areata support group
Use of cosmetic aids (e.g. eyebrow tattoos, wigs, hair pieces, scarves) and camouflage
Topical steroids not recommended—ineffective
Topical immunotherapy or systemic immunosuppresion under specialist care may help
Systemic steroids only for active and progressive cases: prednisolone 0.75 mg/kg (o) daily for 3–4 weeks, then taper off over 2 months
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This is where the alopecia extends over the total scalp.
There is, at best, a 50% chance of hair recovery in a fit adult but only a very small chance in childhood.
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In this condition, the hair follicles are damaged and if the follicular openings cannot be seen with a magnifying lens, regrowth of hair cannot be expected. Thus, the process is irreversible and a scalp biopsy is essential to determine the diagnosis. Apart from obvious causes such as trauma, severe burns, a carbuncle and scalp ringworm with kerion, the causes of scarring alopecia are as follows.
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Lichen planopilaris—this is a variant of lichen planus that produces small follicular papules in the scalp that tend to heal with scarring and destruction of hair follicles; treatment, which is difficult, includes corticosteroids, antimalarials and etretinate3
Discoid lupus erythematosus—this gives a similar picture to the former and tends to be treated in a similar manner
Folliculitis decalvans—a chronic folliculitis of the scalp, probably as a response to staphylococci on the scalp; treated with long-term tetracyclines
Pseudopelade—a slowly progressive, non-inflammatory, scarring condition causing patchy areas of hair loss without any obvious preceding skin disease
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Telogen effluvium, which is increased shedding of hairs in the telogen phase, is one of the most common causes of diffuse hair loss and can be triggered by a variety of stressors.
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It is worth noting that follicular matrix cells have a high metabolic rate second only to haematological tissue and stress can result in shunting into premature telogen with cessation of anagen.3
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An obligatory delay occurs between the ‘insult’ or precipitating event and the onset of hair shedding because the hair follicle cycles through catagen and telogen—approximately 2–3 months when the club hairs with white bulbs of telogen are shed.
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Greater than 25% of hair must be lost before there is a perceptible thinning and in this disorder up to 50% loss is common.
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DxT stressful event + 2–3 month gap to diffuse hair loss + ‘white bulbs’ ➜ telogen effluvium
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Patients usually complain of large clumps of hairs with white bulbs coming out with gentle tugging on combing or shampooing (this can exceed 150 hairs per day compared with the normal average of 50–100 hairs).
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Stress precipitants of acute telogen effluvium
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Any severe stress
Childbirth (common)
High fever
Weight loss, especially crash dieting
Trauma—surgical or accidental
Oral contraceptive pill (OCP) cessation
Perimenopause
Malnutrition
Haemorrhage
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Course of telogen effluvium
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If uncomplicated, spontaneous recovery can be expected in 6–9 months so reassurance with explanation is usually all that is required. If it persists longer than 6 months, consider the chronic idiopathic form or an unmasked androgenetic alopecia. However, if there is concern about non-recovery and the stress factors are corrected, topical minoxidil 5% lotion (2% if too irritant) twice daily for a minimum of 4 months is an option.2 Referral to a specialist is advised for relapsing episodes or incomplete recovery.
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Chronic telogen effluvium6
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This occurs usually in perimenopausal and postmenopausal women. It may be primary and idiopathic or secondary to hypothyroidism, hyperthyroidism, malnutrition or cancer. The feature is episodes of dramatic hair shedding that recover but recur weeks to months later and last up to several days. It does not result in obvious balding—it is self-limiting and does not usually need treatment.
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This is hair loss during the anagen phase and is typically seen in association with cancer chemotherapy and radiotherapy to the scalp, which results in immediate metabolic arrest. Hair loss is diffuse, involving the whole scalp. Anagen hair shafts are identified by their long and pigmented hair bulb. The follicle may remain in anagen, leading to a quick recovery, or move into telogen, thus delaying growth by about 3 months.
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Drug-induced alopecia
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Drugs are a very important cause of alopecia (see TABLE 126.3). They may cause telogen effluvium, anagen effluvium or accelerate androgenetic alopecia.
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Drugs tend to cause telogen effluvium but cancer chemotherapy, radiation to the scalp, thallium/mercury/arsenic and colchicine in high dosage cause anagen effluvium. Acceleration of androgenetic alopecia is caused by hormone therapy, namely the OCP, danazol, testosterone and anabolic steroids.
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Androgenetic alopecia (male pattern baldness)
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This is the most common form of alopecia, which is age related and is genetically determined in addition to being androgen dependent. The key androgen is dihydrotestosterone, which is produced from testosterone by 5α reductase. The typical pattern of hair loss is recession of the frontotemporal hair with progression to the crown, with some men losing hair quickly and others more slowly. In others the pattern is unpredictable. The typical male pattern is shown in FIGURE 126.3.
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Alopecia affects 30% of men by age 30 and 50% by age 50.
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Androgenetic alopecia in women
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In women, the pattern of hair loss is different from men.
Diffuse thinning occurs, usually on the top of the head (the crown). The front hairline usually remains but in some women this can recede with bitemporal loss (see FIG. 126.4).
Although hair loss can appear in men and women as early as the 20s, it may not appear before the age of 50 in women.
Some women notice a short period of considerable hair loss but this may be followed by a long stable period of no loss. Total loss of hair rarely occurs in women.
It may be unmasked after an episode of diffuse hair loss such as after childbirth or an acute illness.
Hair loss may be accelerated by conditions associated with androgen excess (e.g. polycystic ovarian syndrome), however, fewer than 5% of women with androgenic alopecia will have elevated serum androgens.2
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It is appropriate to counsel men to accept their balding as part of a natural ageing process. This includes cutting the hair short to make it look better cosmetically. If baldness is not acceptable, some options include wearing a toupee, a wig or other hair substitute or having a hair transplant operation. However, with hair transplantation, the new hair is often just as likely to disappear as the original hair.
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Medical treatments are generally expensive and improvements are only sustained for the duration of treatment, so it is important to explore the patient’s expectations when discussing treatment options.
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Available medications2
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Minoxidil 5%, 1 mL applied once or twice daily to the scalp for at least 6–12 months. The results vary from good to no change. Reassure the patient that it is normal for hair shedding to increase in the first 4–6 weeks of minoxidil treatment.
Finasteride 1 mg tablet taken daily for a minimum of 2 years. There is a risk of sexual dysfunction (e.g. erectile dysfunction, reduced libido) and gynaecomastia (rare), which tend to resolve with time or cessation. Rare reports of persistent sexual dysfunction after stopping finasteride have been published. Mental health problems have also been noted.
For severe cases, use topical minoxidil and oral finasteride as combination therapy.
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Physical treatments/hair styling
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This includes the use of wigs, hair transplantation and camouflage. Wigs can be worn on the whole head or on the bald spot, or fibres can be interwoven into the remaining hairs.
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Camouflage can be used either by having the existing hair bleached by a skilled hairdresser or by colouring the scalp the same colour as the hair. Mascara can be lightly brushed into the roots of the hair at receding hairlines or along gaps.
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minoxidil 5% topical application bd for at least 6–12 months (to assess efficacy) although one large trial has approved its effectiveness generally in women7
or
spironolactone 50 to 100 mg daily, increasing to 200 mg daily if no apparent benefit after 6 months; monitor blood pressure, kidney function and liver biochemistry
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Spironolactone is contraindicated in pregnancy and side effects include postural hypotension, polyuria and irregular menses. Concurrent use with the combined oral contraceptive pill is appropriate to control menses and for contraception in women of reproductive age.
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As for men, these drugs tend to prevent further loss and, if effective, need long-term use.
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Trichotillomania (hair pulling)
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This is patchy hair loss caused by deliberate plucking or twisting of hair shafts. It is reasonably common in young children, where it may be of little significance, simply being a ‘habit’. In older children and adults it may be an obsessive compulsive disorder often associated with stress.3
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Incomplete patchy alopecia
Hairs of different length
Hairs broken and twisted
Strange pattern of loss
Tends to occur on side of dominant hand
Eyelashes or eyebrows may be involved