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Hair disorders

Hair disorders

The way a person looks is very much influenced by their hair and hairstyle. For many people self-esteem is closely linked to physical appearance and the loss of hair may have a profound affect on a person’s sense of wellbeing. The perceived loss of attractiveness in part explains the anxiety many patients, in particular female patients, feel when they lose their hair. Effective management of patients with a disorder of their hair requires an understanding of the social and cultural importance of hair as well as the anxiety the patient feels. There are numerous disorders that can affect the hair and the diagnosis and management of these conditions can be complex.

An understanding of the normal hair cycle is fundamental to understanding hair disorders. On the scalp, hair growth is cyclical with each follicle producing a number of different hairs during one’s lifetime. The anagen growth phase lasts for about 3 to 5 years on the scalp, and during this phase the hair grows at a rate of approximately 1cm per month. The duration of anagen varies from person to person and is the prime determinant of how long one’s hair will grow if not cut.

The anagen phase is followed by an involutional stage known as catagen, which lasts for 2 weeks and leads into a 3-month dormant phase known as telogen. During telogen, the hair remains anchored in the follicle but does not grow longer. At the end of telogen, the follicle is reactivated and production of the next anagen hair commences. As the new hair grows, it displaces the old telogen hair from the follicle. Thus, every 3 to 5 years every hair on the scalp is shed and replaced. Unlike animals, in which the growth cycle is synchronised leading to a scheduled moult, in humans the hair growth is unsynchronised, so rather than replacing all scalp hair at once at the end of the growth cycle, a few hairs are lost every day.

Alopecia areata, alopecia totalis, alopecia universalis

Alopecia is a generic term for hair loss. Areata refers to multiple areas. Alopecia areata is a descriptive term for a disorder characterised by one or more discrete circular areas of hair loss. These areas can occur anywhere on the body, but patients are more likely to present when they occur on the scalp, eyebrows or beard areas. Alopecia totalis and universalis are variants of alopecia areata, differentiated only by the extent of the hair loss.

Alopecia areata is a chronically relapsing autoimmune disease. The natural history is extremely variable. Patches may regrow spontaneously, remain unaltered or enlarge and coalesce into alopecia totalis (entire scalp) or alopecia universalis (entire body).

If a patient presents with a solitary patch of hair loss, there is a 33% chance of complete regrowth within 6 months and a 50% chance within 1 year. Unfortunately, most patients (86% in one study) will ultimately relapse. Poor prognostic factors for regrowth include: early age of onset (before the age of 10); alopecia totalis; peripheral rather than central hair loss (oophiasis pattern); associated nail pitting; coincidental atopy; and associated organ-specific autoimmune disease. In addition, if the hair loss has persisted for many years, the prospect of regrowth is diminished.

The aetiology of alopecia areata is unknown, but genetic factors are important, as evidenced by a positive family history in 20 % of cases, strong human leucocyte antigen (HLA) associations (relative risk 30.2), and linkage with other organ-specific autoimmune diseases. The pathogenesis involves inflammation of anagen hair bulbs that leads to cessation of hair growth but not destruction of the hair follicle. Hence, the potential for hair regrowth always remains. The specific trigger for the inflammation may be a febrile illness, severe emotional stress, pregnancy or childbirth. Usually no trigger is identified, and patients with multiple episodes of hair loss tend to have multiple triggers rather than a single trigger.

While severe stress such as a major car accident, death of a parent or divorce could precipitate alopecia areata, day-to-day stress is not considered to be a trigger. More commonly, stress is the product of alopecia rather than the cause of it.

Consider trichotillomania and tinea, see Fungal infections, as other possible causes of loss of hair in patches. In both of these conditions, the patch is not entirely bald but is covered by a short stubble of broken hairs. Discoid lupus erythematosus and lichen planus can produce scarring alopecia of the scalp.

The aim of treatment is to stimulate hair regrowth where possible, and to provide emotional and social support whilst awaiting regrowth or when hair regrowth cannot be achieved. Once regrowth has been achieved, it is important to warn patients that most will eventually relapse, although the period of remission is unpredictable and may last many years. Treatment is not always required but if treatment is deemed appropriate, the therapy chosen will depend on the extent and duration of the hair loss.

First-line therapy consists of topical therapy with corticosteroids, dithranol or minoxidil. In general, each of these treatments should be tried for 3 to 6 months in order to judge efficacy. Topical corticosteroids, dithranol and minoxidil are probably equally effective but are indicated in different circumstances.

Topical corticosteroids are most commonly used for new lesions or expanding lesions, especially when large areas are involved. Use

a very potent topical corticosteroid applied once or twice daily.

Topical corticosteroids are favoured by many dermatologists, even though there are no controlled trials to support their use. As they are often used for limited diseases with a good prognosis for spontaneous regrowth, it is often difficult to determine whether the treatment has altered the natural history of the disease.

Intralesional corticosteroids are more effective, but their use is limited by the practicalities of multiple injections. Use

triamcinolone acetonide 10mg/mL OR betamethasone acetate/sodium phosphate 5.7mg/mL, injected intradermally.

This treatment has a high probability of success. It is appropriate for the eyebrows and small areas on the scalp, but is not recommended for the eyelashes due to the risk of cataract, glaucoma and cutaneous atrophy. Caution is also required when injecting patches of hair loss on the face, due to the risk of cutaneous atrophy.

Topical dithranol is often used for chronic stable areas of hair loss that may have previously failed to respond to topical corticosteroids. Use

dithranol cream, commencing at 0.5% and increasing to 1% initially and subsequently 2%, applied once daily (see Dithranol - Difficult to use preparations).

The aim of this short-contact therapy is to produce mild skin irritation, although it is controversial whether skin irritation is required for regrowth. The exact basis for the effectiveness of dithranol is not clear and the treatment is only effective in a small proportion of cases.

Topical minoxidil is used for recalcitrant lesions or areas that regrow only a short stubble of hair that fails to grow longer. Use

minoxidil 5% lotion, 1mL topically, twice daily.

This is a nonspecific hair growth stimulant and probably acts to prolong the anagen phase of the hair cycle. Minoxidil 2% strength is not considered to be effective and minoxidil 5% is effective in only a small number of people.

If topical therapy is not successful, or the hair loss is extensive, management options include camouflage, oral corticosteroids or topical immunotherapy.

A wig can be used for camouflage if regrowth is deemed unlikely or the patient wishes to disguise the hair loss. The type, price and quality of wigs vary considerably [Note].

If regrowth is deemed likely, use

prednisolone 0.75mg/kg orally, daily for 3 to 4 weeks and then gradually taper the dose over 2 months.

A reduction in hair shedding may be apparent within 4 weeks, while regrowth tends to become evident after 6 to 8 weeks. Patients with multifocal alopecia areata do best, but regrowth can also occur in patients with oophiasis and alopecia totalis. Relapse often occurs on cessation of treatment and can occasionally occur with dose reduction. Adjunctive topical therapy may lessen the relapse rate.

Alternatively, the patient can be referred to a specialist for consideration of topical immunotherapy, using dinitrochlorobenzene or diphencyprone as the allergen, or alternatively psoralen and ultraviolet A photochemotherapy, see Points on phototherapy. Success rates of up to 50% have been reported with these modalities.

Telogen effluvium

Diffuse shedding of telogen hairs from the scalp is common. It occurs when anagen hair growth is interrupted, causing follicular hair production to cease and hairs to enter the telogen rest phase of the hair cycle. The telogen phase lasts 3 months before anagen hair growth is resumed. The new anagen hairs push out the old telogen hairs, which are shed en masse 3 months after the triggering event.

An acute telogen effluvium almost invariably occurs after pregnancy and may also follow an acute illness, a major surgical procedure, a crash diet or the discontinuation of an oral contraceptive pill. The shedding begins 3 months after the trigger and almost invariably resolves after 6 months.

Chronic telogen effluvium is far less common than acute telogen effluvium. It may be primary and idiopathic or secondary to iron or zinc deficiency, hypothyroidism, hyperthyroidism, malnutrition, cancer or tuberculosis. It may also occur as an adverse effect of a medication.

The effects of hypothyroidism and hyperthyroidism on hair growth are similar, although hair shedding occurs more diffusely with hyperthyroidism. The pattern of hair loss with hypothyroidism is more variable. It may occur diffusely or be confined to the vertex and mimic androgenetic alopecia. Hypothyroidism inhibits cell division in both the epidermis and skin appendages, but the mechanism by which hyperthyroidism affects hair growth is unknown.

Medications that have been reported to cause hair loss are listed in Table . The time frame is variable, but the hair loss usually begins within 12 months of commencing a new medication.

Primary chronic telogen effluvium is a newly described condition. It has been arbitrarily defined as diffuse scalp hair shedding for at least 6 months and may continue for a number of years before spontaneously resolving. The hair shedding is noticed particularly with combing and shampooing and may be sufficiently severe to block the shower drain. The onset is sudden and women characteristically complain of loss of hair volume, although to the casual observer the scalp looks normal. Bitemporal recession of the frontal hairline is a feature on examination. Clinically this condition may be difficult to distinguish from early androgenetic alopecia, where the pattern of hair loss over the vertex of the scalp has not yet been established. As chronic telogen effluvium does not progress to baldness and does not respond to antiandrogen therapy, it should be differentiated from androgenetic alopecia.

The aim of treatment is to reassure the patient with acute telogen effluvium that the condition is self-limiting and likely to correct itself within 6 months. It is important to highlight the relationship of the hair loss to the preceding trigger. Primary chronic telogen effluvium is also a self-limiting and self-correcting event that may last 3 to 7 years. Women in particular require reassurance that they are not going bald. Secondary chronic telogen effluvium requires correction of the underlying condition.

First-line therapy consists of:

           correction of identified triggers where possible

           reassurance whilst awaiting spontaneous cessation of hair shedding over 3 to 6 months for an acute telogen effluvium or longer for a chronic telogen effluvium.

If this is not successful, use

minoxidil 2 or 5% lotion, 1mL applied to the scalp twice daily for a minimum of 4 months.

Topical minoxidil has been used for this condition on the basis that it is a nonspecific hair stimulant, acting to prolong anagen; however, evidence of its success is not available.

If the hair shedding qualifies as chronic by continuing beyond 6 months, referral to a dermatologist for consideration of scalp biopsy for differentiation from androgenetic alopecia is recommended.

Anagen effluvium

Anagen effluvium is the dramatic and rapid hair loss most commonly seen in association with cancer chemotherapy and radiotherapy to the scalp. Other causes are listed in Table 1. The insult to the hair follicle is sufficiently severe to cause an immediate metabolic arrest with complete cessation of hair production. The hair may come out by the root or, if the insult is brief, the hair shaft will narrow, providing a point of weakness that subsequently snaps off. The follicle may remain in anagen, in which case recovery is quick, or move into telogen, in which case regrowth will be delayed by about 3 months.

Androgenetic alopecia

Androgenetic alopecia is a progressive patterned baldness that is sufficiently common among both men and women to be considered a secondary sexual phenomenon. It is also called common baldness, male patterned baldness or female patterned alopecia.

When it occurs prematurely in a man, it can be an unwanted and distressing event and patients may present for treatment. People are generally unaware that androgenetic alopecia also affects females. When this occurs in women, it is usually both unexpected and unwanted at any age, and female patients commonly present for both diagnosis and treatment.

Female androgenetic alopecia frequently has a prodrome of diffuse hair shedding from all over the scalp before the characteristic Ludwig pattern of diffuse thinning over the vertex is established. In such cases, the patient will require investigations to exclude iron deficiency, hyperthyroidism and hypothyroidism. A drug history looking for a potential cause of iatrogenic hair loss is important and a scalp biopsy may be required to exclude chronic telogen effluvium.

In women, androgenetic alopecia may be a manifestation of systemic virilisation. Routine investigation for this is not required unless the patient has other features of virilisation such as irregular menses, hirsutes or severe acne vulgaris. The aim of such investigation is to exclude an androgen-secreting tumour, and a serum testosterone and serum dehydroepiandrosterone sulfate should suffice for this purpose.

Prolactinomas may also present with virilisation, but galactorrhoea will usually also be present. Polycystic ovarian syndrome is probably the most common cause of virilisation in women. In this syndrome hirsutism accompanies oligomenorrhoea or amenorrhoea, acne and obesity. There is often an elevation of the ratio of luteinising hormone to follicle stimulating hormone. Investigations to further delineate this condition are only required if it is perceived that the results will alter the management of the condition.

Genetic factors are important in the aetiology of androgenetic alopecia. The inheritance is complex but appears to be either polygenic or autosomal dominant. The pathogenesis involves excess dihydrotestosterone binding to the androgen receptors. This produces both a progressive reduction of the duration of the anagen phase and a miniaturisation of the hair follicle. The shorter anagen duration means that with successive cycles the hair produced becomes shorter and shorter until ultimately it fails to emerge from the follicular pore. The progressive miniaturisation means that the hairs produced become finer and paler, before they ultimately disappear.

Dihydrotestosterone is produced by reduction of testosterone by the enzyme 5 alpha-reductase. Both testosterone and dihydrotestosterone bind to the same androgen receptor, but dihydrotestosterone binds five times more avidly. Thus, androgen receptor antagonists will block the effects of both dihydrotestosterone and testosterone, while 5-alpha-reductase antagonists will selectively block the production of dihydrotestosterone without impacting on testosterone levels or action.

The aim of treatment of androgenetic alopecia is to provide an accurate diagnosis, to prevent further hair loss and to stimulate hair regrowth where possible. In addition, the provision of emotional and social support is the cornerstone of treatment whilst awaiting regrowth or when hair regrowth cannot be achieved. The treatment of men and women is sufficiently different to warrant separate consideration.

First-line therapy for men consists of

minoxidil 2 or 5% lotion, 1mL applied to the scalp twice daily for a minimum of 12 months, to assess efficacy.

Both 2% and 5% formulations of minoxidil are available. The 5% solution has a more rapid onset of action and appears to be marginally more effective in the long term. If this is not successful, use a 5-alpha-reductase inhibitor

finasteride 1mg orally, daily for a minimum of 2 years, and continued indefinitely if successful.

Clinical trials conducted by the manufacturer have demonstrated that at 2 years one-third of men will have moderate or marked hair regrowth, one-third will have minimal regrowth and one-third will have remained unchanged, with no progression of the hair loss. Only 1% of men will show progression of their hair loss.

As testosterone and dihydrotestosterone share a common receptor, androgen receptor antagonists such as spironolactone and cyproterone acetate are unsuitable for men due to adverse effects such as impotence, gynaecomastia and feminisation.

Treatment alternatives for women consist of topical therapy with minoxidil, or antiandrogenic therapy with spironolactone or cyproterone acetate. The choice is often based on patient factors such as expense of treatment, preference for oral or topical medication, and co-existing illness and medications. Since hair regrowth in females is unlikely, treatment should be started as early as possible to prevent further hair loss. The patient also needs to understand that treatment will have to be continued indefinitely. Use

minoxidil 2 or 5% lotion, 1mL applied to the scalp twice daily for a minimum of 12 months, to assess efficacy

OR

spironolactone 200mg orally, daily for 6 months.

Good clinical trials documenting the efficacy of spironolactone treatment in androgenetic alopecia are not available. Its use is based on observations of efficacy in hirsutes and clinical observation. There seems to be a dose threshold for efficacy of 200mg daily and it should be continued for at least 6 months before being assessed. It will prevent further hair loss in up to 70% of women, as evidenced by a reduction or cessation of hair shedding. Hair regrowth is only seen in a small percentage of women and usually only becomes evident after 1 to 2 years.

Spironolactone should not be administered to patients with renal failure due to the potential for potassium retention. The patient’s potassium status should be checked prior to commencing therapy and on an annual basis thereafter. It is a peripheral androgen receptor antagonist and a weak inhibitor of testosterone biosynthesis. Adverse effects include menstrual irregularity, which may require concurrent use of an oestrogen/progesterone preparation for cycle control, premenstrual breast tenderness and occasionally polyuria and postural hypotension. Tolerance rapidly develops to these adverse effects in most cases over 3 to 4 months.

In menstruating women, use

cyproterone acetate 100mg orally, daily for 10 days of each menstrual cycle.

This seems to prevent further hair loss in up to 70% of women. Like spironolactone, most of the clinical studies have been conducted in hirsutes. Cyproterone acetate generally needs to be combined with a contraceptive pill to regulate the menstrual cycle, but even then menstrual irregularities and confusion over when to commence the next cyproterone acetate administration are common. In such cases timing the contraceptive and cyproterone acetate with the calendar month may be appropriate.

In postmenopausal women, use

cyproterone acetate 50mg orally, daily continuously.

Cyproterone acetate has a similar antiandrogen action to spironolactone, but its more pronounced progestogenic action usually leads to menstrual irregularities when used alone. Other adverse effects include fatigue, reduced libido and weight gain.

Preliminary trials of oral finasteride in postmenopausal women have shown no superiority over placebo.

Drug-induced alopecia (Table 1)

Hirsutes

While unwanted hair occurs in both men and women, traditionally men rarely present to doctors complaining of this. Unwanted hair in a female, or hirsutes, is difficult to define objectively due to racial, cultural and fashion norms. Superfluous hair on a woman in a distribution that mirrors the development of secondary sexual hair in a male is common. Most cases are due to hair follicle hypersensitivity to normal levels of circulating androgens, while a proportion will be due to elevated levels of circulating androgens. Such patients will usually have other features of systemic androgen excess such as menstrual irregularity, severe acne and premature androgenetic alopecia.

Routine investigation of these women is not required unless they have other features of virilisation. The aim of such investigation is to exclude an androgen-secreting tumour and a serum testosterone level alone should suffice for this purpose. In general, the serum testosterone is elevated to at least twice the upper limit of the normal range when an androgen-secreting tumour is present. A secondary aim of investigation is to detect those women in whom fertility troubles can be anticipated. Testing for this is often unsatisfactory and is not usually required.

Hirsutism should be distinguished from hypertrichosis, which is the widespread overgrowth of nonandrogen-dependent hair and which does not respond to antiandrogen therapy. Hypertrichosis may be primary, in which case it is usually apparent prior to puberty and the hair is evenly distributed over the back and limbs. Prepubertal hypertrichosis is commonly familial, but a positive family history is not always found. Causes of secondary hypertrichosis include drugs such as minoxidil, diazoxide, cyclosporin, phenytoin, local corticosteroids, and recurrent inflammatory change.

The aim of treatment is to effectively deal with the high level of anxiety this condition generates in some women, and to remove unwanted hairs as conveniently and safely as possible and for as long as possible.

The following physical measures may be used.

           Bleach can be used to make the hairs less noticeable.

           Waxing, plucking, shaving or depilatory creams are all suitable methods of hair removal.

           Electrolysis, in experienced hands, can achieve temporary hair removal. Regrowth of more than 40% of the treated hairs can be expected within 3 months.

           Ruby or Nd:YAG or alexandrite laser can be used for temporary hair removal lasting up to 6 months. Hair follicles seem to enter a prolonged telogen phase but are not destroyed, and hair regrowth occurs in 6 to 9 months. At present there is no laser treatment available that permanently removes hair.

If physical therapies are unsatisfactory or poorly tolerated, systemic antiandrogen therapy can be considered. See Androgenetic alopecia for precautions required with the use of spironolactone and cyproterone acetate. In general, the effects of spironolactone are not seen for at least 6 months.

spironolactone 50 to 200mg orally, daily

OR

cyproterone acetate 2mg with ethinyloestradiol 35 microgram orally, daily on days 1 to 21 of the menstrual cycle

OR

cyproterone acetate 10 to 100mg orally, daily for 10 days of each menstrual cycle, combined with an oral contraceptive pill.

While late-onset congenital adrenal hyperplasia is a rare cause of hirsutes for which adrenocortical suppressive therapy with prednisolone or dexamethasone has been advocated, the above agents can also be used in such patients with good effect.

Scaly scalp disorders

Dandruff, pityriasis capitis and seborrhoeic dermatitis are related conditions on a continuum of severity. They have a common pathogenesis and are all chronic recurring conditions that present with scaling on the scalp and with a varying degree of itch. They all respond to similar treatments. The pathogenesis of these disorders involves increased cell proliferation, with the rapid cell turnover limiting the opportunities for cell maturation. Most treatments used for the scaly scalp disorders are keratolytic and antiproliferative agents. The role of pityrosporum yeast is suggested by increased yeast numbers and response to antiyeast therapy [172-174].

Psoriasis may also produce a scaly scalp. While it is generally accepted that psoriasis is a distinct disease, for practical purposes when psoriasis occurs on the scalp it can be simply considered as the most severe of the scaly scalp disorders.

Seborrhoeic dermatitis may also affect the skin of the face and trunk. Psoriasis may also affect the skin on the trunk, the nails and the joints but tends not to affect the face. Manifestations of these conditions outside the scalp are considered elsewhere in these Guidelines.

The aim of treatment is to provide symptomatic relief and to deal with recurrences as they develop. Prophylactic therapy is advised for severe cases to prevent recurrences. First-line therapy consists of frequent washing with an antidandruff shampoo (zinc pyrithione, selenium sulfide, ketoconazole, coal tar) or even a normal shampoo. If control is not achieved with shampooing, topical therapy with corticosteroid lotions, coal tar pomades, dithranol washable ointment or sulfur cream can be tried. In cases where there is a large build up of scale and crust, this will need to be removed to allow the treatment to reach the target skin, using a keratolytic oil such as salicylic acid 30% in mineral oil. This treatment is discussed in detail in Scalp seborrhoeic dermatitis.

Pseudofolliculitis barbae

Pseudofolliculitis barbae is not a true folliculitis as the inflammation is adjacent to, rather than within, the hair follicle. It is seen on the beard area of men who shave. Short, freshly cut hairs retract back into the follicle and subsequently penetrate the side wall of the follicle. Naked hair shafts in the dermis act as a foreign body and produce inflammation. It is more common in men with curly hair.

The aim of treatment is to prevent hairs disrupting follicles and to alleviate dermal inflammation. First-line therapy consists of physical methods (alteration of shaving habits) and the use of topical antiseptics, if necessary. Permanent cessation of shaving (growing a beard) offers the only real cure, but is not always feasible. Alternatives include restricting shaving to work days, avoiding close shaving, shaving every second or third day, shaving only in the direction of hair growth and avoiding blunt blades that pull on hairs rather than cleanly cutting them.

Topical therapy is with

benzoyl peroxide 5% solution, used as a wash twice daily. It may take up to 6 weeks for any response to become apparent.

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