Hair Disorders

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Introduction

This article will explore the characteristic features of various hair disorders, which can be broadly categorised into two main types:

  • Hair loss (alopecia): describes hair loss from an area where hair usually grows.1 It encompasses several hair loss variants and patterns, including diffuse and localised types. Alopecia can be subdivided into non-scarring and scarring alopecia.
  • Excessive hair growth

The hair cycle

Hair growth follows a four-stage cycle, however, these are not synchronised among all hair follicles.2 These four stages include:1-3

Anagen

The anagen phase is a period of active growth that may last several years. Normally, around 80-90% of hair follicles are in the anagen phase at one time.

Catagen

Epithelial cell division will decline and eventually stop, and the hair follicle starts to shrink. This period of follicular regression is known as the catagen phase and typically lasts around two weeks.

Telogen

Telogen involves the period between follicular regression and the onset of the next anagen phase. During this phase, hair does not grow and is shed before new hair is grown in the next anagen phase. The telogen phase usually lasts 1-4 months.

Kenogen

Some hair follicles may stay latent for a prolonged time after the hair is shed, known as kenogen.

Hair cycle
Hair cycle Figure 1. The hair cycle

Non-scarring alopecia

Androgenic alopecia

Androgenic alopecia (pattern hair loss) is the most common form of non-scarring alopecia.1 

Aetiology 

Androgenic alopecia in men (male pattern hair loss) becomes increasingly common with age. It is physiological after the age of 20 but can start during adolescence. There are significant ethnic variations, with Caucasian men being four times more affected than those of Afro-Caribbean origin.1 

Androgenic alopecia is also found in women (female-pattern hair loss).4 Onset is typically later than in men (age 50-60 years) and typically occurs after menopause. Female-pattern hair loss may also be accompanied by higher levels of androgens (e.g. PCOS).1 

Both male and female-pattern hair loss is often due to a combination of hormonal and genetic factors. Hair is gradually replaced by smaller, thinner, and lighter-coloured hairs. This results in hairs that are more easily shed in the telogen phase and fewer hairs in the anagen phase.

Clinical features

In men, there is bitemporal recession of hair before the involvement of the crown, producing a characteristic horseshoe shape of the remaining hair.1

In women, the pattern is more diffuse, with widespread thinning of the hair mainly centred on the crown of the scalp.5 The scalp usually looks normal, with no associated symptoms.

Male androgenetic alopecia
Female androgenetic alopecia

Investigations

Androgenic alopecia is usually a clinical diagnosis. However, further investigation is needed if an autoimmune cause is suspected.

Hyperandrogenism (e.g. ovarian or adrenal source) should be excluded in women with signs of virilisation (e.g. acne, deepened voice, clitoromegaly, breast atrophy, increased muscle mass).6-7

Investigations may include:

  • Serum prolactin
  • Serum follicle-stimulating hormone (FSH) and luteinising hormone (LH) 
  • Serum testosterone (total and free): raised in hyperandrogenism/PCOS
  • Sex hormone-binding globulin
  • Thyroid-stimulating hormone (TSH)
  • Serum 17-hydroxyprogesterone
  • Dehydroepiandrosterone sulfate (DHEAS): elevated levels would suggest an adrenal source 
  • Pelvic ultrasound: to identify ovarian cysts 
Causes of hyperandrogenism

Elevated testosterone signifies an ovarian source as the cause of hyperandrogenism. If mildly elevated, this may suggest polycystic ovarian syndrome (PCOS). However, consider an ovarian tumour if significantly elevated.

Elevated DHEAS would suggest an adrenal source as the cause of hyperandrogenism. If 17-hydroxyprogesterone is elevated, consider congenital adrenal hyperplasia.

Management

Usually, no treatment is needed, but consider specialist referral in cases of extensive hair loss (over 50%).1, 5

Management options include:

  • Aesthetic options: include wigs, hairpieces and surgical hair transplantation (unavailable on the NHS).
  • Topical minoxidil: used for at least six months to be effective and then used indefinitely to maintain any effect. Minoxidil is usually more effective in the early stages of balding than once established.
  • Oral finasteride: taken for at least 3-6 months to be effective. It is not used in women.

Alopecia areata

Alopecia areata is a chronic autoimmune condition affecting the hair follicles and is the second most common form of alopecia.8

Aetiology

There is an association with atopy and other autoimmune conditions such as vitiligo, thyroid disease and Down’s syndrome.4, 6

The estimated prevalence in the UK is 15 per 10,000. It can occur at any age but is more common in childhood and adolescence; incidence peaks between 15 and 29 years old.1 Males and females are affected equally. Around 20% have a positive family history.

Clinical features

Alopecia areata is characterised by well-circumscribed, non-inflammatory patches of hair loss, typically on the scalp or beard area.1 Pathognomonic broken hairs tapering towards the scalp, known as ‘exclamation mark’ hairs, are seen during active hair loss, particularly at the periphery of bald patches.4

Eyebrows, eyelashes, beard and body hair can also be affected. Nail changes, such as pitting or ridging, may occur and are associated with more severe disease.8

Severe forms of alopecia areata can lead to the total loss of scalp hair (alopecia totalis) and the total loss of body hair (alopecia universalis).

Patch of alopecia areata
Pathognomonic exclamation marks seen in alopecia aerate

Investigations

Alopecia areata is usually a clinical diagnosis, however, investigations are usually prompted if a coexisting disease is suggested.

Typical investigations for diffuse alopecia include:4 

  • Full blood count: for anaemia and inflammation, both of which are linked to hair loss
  • Urea and electrolytes: renal disease, such as chronic kidney disease or dehydration, can impair delivery of nutrients to hair follicles 
  • Liver function tests: chronic liver disease can result in nutritional deficiencies that lead to hair loss
  • Thyroid function tests: both hyperthyroidism and hypothyroidism are linked with diffuse hair shedding 
  • Ferritin/iron: deficiency is associated with hair loss (particularly linked with telogen effluvium) 
  • Vitamin D: important in hair growth
  • Zinc: structural component of hair follicles and deficiency can cause follicles to be weakened and more susceptible to shedding 

Other investigations are dependent on the history and examination (e.g. ANA for suspected lupus, scrapings of scale and plucked hairs for suspected tinea), however, dermoscopy can be used to aid in diagnosing the type of alopecia as it reduces the need for scalp biopsies.

Management

There is currently no cure for alopecia areata.8 Treatment is usually not needed in mild alopecia due to high levels of spontaneous remission.4 Patient education is important, and psychological support should be offered. Topical potent steroids (e.g. betamethasone valerate 0.1%) can be used.

Specialist treatments include:

  • Wigs and hair pieces
  • Dermatography (tattooing)
  • Intralesional corticosteroids
  • Topical immunotherapy
  • Topical minoxidil
  • PUVA light therapy

Prognosis

Spontaneous remission occurs in up to 80% of affected individuals, however, recurrence is common. Spontaneous regrowth is usual for smaller patches of alopecia and usually starts at the centre of the bald patch with fine white hairs; these thicken and regain their natural pigment over time.4, 8

The prognosis is worse for larger patches, more extensive involvement, early onset loss and when associated with atopy.

Telogen effluvium

Telogen effluvium occurs when hair follicles are moved into the telogen phase due to physiological or hormonal stress triggers.1

Aetiology

Common causes include:

  • Post-partum: known as telogen gravidarum and is estimated to affect 1/3 of women following childbirth
  • Post-fever
  • Severe chronic illness or infection
  • Severe trauma
  • Post-surgical
  • Thyroid disorders
  • Profound iron deficiency anaemia
  • Zinc deficiency (e.g. long-standing parenteral nutrition)
  • Sudden weight loss, anorexia nervosa and malnutrition
  • Chronic telogen effluvium: no obvious cause or preceding illness
  • Drugs (e.g. lithium, retinoids, contraceptives, anticonvulsants, antithyroid, beta-blockers)

Clinical features

Telogen effluvium is often preceded by a precipitating event around three months before diffuse shedding.6 This results in reduced hair density on the entire scalp and may involve other areas of body hair. Individuals often notice their hair shedding more than usual (e.g. handfuls of hair seen on the pillow or hairbrush).1

Investigations

Telogen effluvium is usually a clinical diagnosis based on the patient’s presenting history and appearance of their hair.9 A hair pull test may be done to assess for increased hair shedding or individual hair strands may be plucked and examined under a microscope. 

Management

Management involves identifying and managing underlying causes (e.g. stopping offending medications) and reassurance that hair will grow back.6 Complete hair regrowth often occurs after months or even years. 

Trichotillomania

Trichotillomania is a behavioural disorder that includes self-induced twirling, pulling, and/or breaking of the hair.6

Aetiology

This may be related to an underlying psychological disorder or stress and is often associated with mood and anxiety disorders.1 It can occur at any age but is most often seen in adolescence.

Clinical features

Plucking scalp hair results in asymmetrical hair loss with broken hairs across the area involved. Single or multiple areas, including eyebrows, eyelashes, and pubic hair, can be affected.

Trichotillomania can be distinguished from alopecia areata by shaving a defined area of involvement and observing for regrowth.6

Trichotillomania
Black dots suggesting hairs broken at the scalp level in trichotillomania

Management

Management typically involves counselling and treating any underlying psychiatric illness alongside behavioural modification (e.g. CBT, psychotherapy).


Scarring alopecia

Conditions resulting in alopecia associated with skin scarring are collectively known as cicatricial (or scarring) alopecia.1 Management typically involves managing the underlying condition. These are generally rare, but examples include:1, 6

  • Infections (e.g. folliculitis, tinea capitis, syphilis)
  • Discoid lupus erythematosus: a form of chronic cutaneous lupus erythematosus resulting in circular erythematous lesions with dilated follicles, atrophy and scaling
  • Lichen planopilaris: results in numerous alopecia patches with hair follicle loss and central scarring; 30% of affected individuals may have associated lichen planus involving skin, nails or mucous membranes.6 Women are more commonly affected than men.
  • Central centrifugal cicatricial alopecia: most commonly seen in black women and often related to thermal or chemical hair relaxers.6 Alopecia is slowly progressive and is centred on the crown and midline of the scalp. Secondary changes include crusting or pustules.
  • Traction alopecia: occurs after years of hair styling that causes traction; typically seen in black women and develops on the frontal scalp line
  • Secondary causes (e.g. burns, radiation dermatitis, pemphigoid, sarcoidosis)
  • Scleroderma
  • Dissecting cellulitis

Discoid lupus erythematosus
Tinea capitis
Traction alopecia
Central centrifugal cicatricial alopecia
Lichen planopilaris

 


Excessive hair growth

Hirsutism

Hirsutism refers to excessive hair growth in women or children in a pattern typically seen in adult men.5 

Aetiology 

Hirsutism occurs primarily due to hyperandrogenism or increased sensitivity of hair follicles to normal androgen levels. It affects around 5-10% of females of reproductive age but can also affect post-menopausal women.

Common causes include:

Clinical features

Single or multiple sites can be affected, typically in a male distribution pattern, such as facial hair, chest, abdomen, upper back and inner thighs.10 While hirsutism can cause excess hair, it can also cause hair thinning and loss, particularly on the scalp in a ‘male-pattern’ appearance (as seen in androgenic alopecia).

A diagnosis of hirsutism is made clinically. General history and examination may show signs of potential causes of hirsutism, such as:

  • Acanthosis nigricans: suggests insulin resistance
  • Purple striae, thin skin, bruising, facial plethora: suggests Cushing’s syndrome
  • Signs of virilisation (e.g. acne, deepened voice, clitoromegaly, breast atrophy, increased muscle mass): suggests hyperandrogenism
  • Oligo/anovulation with clinical signs of hyperandrogenism: suggests PCOS

Facial hirsutism
Facial hirsutism

Investigations

Investigations include general blood tests (e.g. FBC, U&Es, LFTs, TFTs, ferritin, etc.), however, additional tests may be required to exclude hyperandrogenism (i.e. in PCOS).

Typical investigations for suspected PCOS include:12 

  • Serum testosterone (total and free): raised in hyperandrogenism/PCOS
  • Sex hormone-binding globulin (SHBG): normal to low 
  • Testosterone to SHBG ratio: may be raised 
  • LH:FSH ratio: often raised
  • Oral glucose tolerance test: identify insulin resistance 

Management

Medical treatment of hirsutism usually involves addressing the underlying cause (e.g. PCOS). Weight loss and dietary control can manage insulin resistance associated with obesity. Otherwise, physical hair removal methods, such as shaving, waxing, electrolysis, or laser hair removal, are typically used.

Hypertrichosis

Hypertrichosis is defined as excessive hair growth occurring in any area of the body beyond what is normal for an individual’s age, sex and race.5 This is in contrast to hirsutism, which involves excessive hair growth in androgen-dependent sites in women, typically following a male distribution pattern.11

Aetiology 

Hypertrichosis can develop all over the body or in smaller patches. It can be congenital or be acquired later in life; congenital hypertrichosis is generally the result of rare genetic disorders, while acquired hypertrichosis is typically associated with drugs, malignancy and malnutrition.

Hypertrichosis
Hypertrichosis due to ciclosporin

Management

Treatment of hypertrichosis is primarily physical hair removal, such as shaving, waxing, laser, and electrolysis. However, these methods often need to be repeated regularly as hair continues to grow back. Potential complications include dermatitis, scarring, folliculitis or hypersensitivity reactions.


Final summary

  • There are various hair disorders ranging from different types of hair loss (alopecia) to excessive hair growth
  • Early identification and intervention of cicatricial (scarring) alopecia is integral to preventing irreversible damage and hair loss
  • Many hair disorders have an underlying hormonal influence (e.g. the role of testosterone in hirsutism and androgenic alopecia)
  • Hair disorders can have a significant impact on an individual’s mental health and can result in anxiety, depression and low self-esteem
  • Treatment depends on the diagnosis but generally aims to identify and treat the underlying cause (e.g. treat infections/underlying conditions, resolve any deficiencies or hormonal irregularities, stop causative drugs, psychological support)

Reviewer

Dr Farishta Khan

Dermatology Registrar


Editor

Dr Jamie Scriven


References

  1. Patient.info. Alopecia. 2020. Available from: [LINK]
  2. DermnetNZ. Alopecia areata. 2022. Available from: [LINK]
  3. The Primary Care Dermatology Society. Alopecia – an overview. 2024. Available from: [LINK] 
  4. Ibbotson SH. Dermatology, in Davidson’s Principles and Practice of Medicine. 2023. Elsevier. Available from: [LINK] 
  5. British Association of Dermatologists. Female pattern hair loss (androgenetic alopecia). 2016. Available from: [LINK] 
  6. Bolognia JL, Schaffer, JV, Duncan KO, et al. Alopecias, in Dermatology Essentials. 2022. Elsevier. Available from: [LINK] 
  7. DermnetNZ. Hyperandrogenism. 2014. Available from: [LINK] 
  8. British Association of Dermatologists. Alopecia areata. 2024. Available from: [LINK] 
  9. British Association of Dermatologists. Telogen Effluvium. 2020. Available from: [LINK]
  10. DermnetNZ. Excessive hair. 2016. Available from: [LINK] 
  11. DermnetNZ. Hypertrichosis. 2016. Available from: [LINK] 
  12. Geeky Medics. Polycystic Ovary Syndrome (PCOS). 2024. [LINK]
  13. Bolognia JL, Schaffer, JV, Duncan KO, et al. Hypertrichosis and Hirsutism, in Dermatology Essentials. 2022. Elsevier. Available from: [LINK]
  14. DermnetNZ. Hair Loss. 2023. Available from: [LINK]
  15. Pratt CH, King Jr LE, Messenger AG, et al. Alopecia areata. Nature Reviews Disease Primers. 2017. Available from: [LINK]

Image references

  1. Maral Hair. Hair Cycle. Licence: [CC BY 3.0 US]
  2. DermnetNZ. Male-pattern balding. License: [CC BY-NC-ND]
  3. DermnetNZ. Female pattern alopecia. License: [CC BY-NC-ND]
  4. Thirunavukkarasye-Raveendran. Single patch of alopecia areata. License: [CC BY 4.0]
  5. DermnetNZ. Pathognomonic exclamation mark seen in alopecia areata. License: [CC BY-NC-ND]
  6. DermnetNZ. Trichotillomania. License: [CC BY-NC-ND]
  7. DermnetNZ. Broken hairs in trichotillomania. License: [CC BY-NC-ND]
  8. DermnetNZ. Scarring alopecia due to discoid lupus erythematosus. License: [CC BY-NC-ND]
  9. DermnetNZ. Scarring alopecia due to tinea capitis. License: [CC BY-NC-ND]
  10. DermnetNZ. Traction alopecia. License: [CC BY-NC-ND]
  11. DermnetNZ. Central centrifugal cicatricial alopecia. License: [CC BY-NC-ND]
  12. DermnetNZ. Lichen planopilaris. License: [CC BY-NC-ND]
  13. DermnetNZ. Facial hirsutism. License: [CC BY-NC-ND]
  14. DermnetNZ. Facial hirsutism. License: [CC BY-NC-ND]
  15. DermnetNZ. Hypertrichosis. License: [CC BY-NC-ND]

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