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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Alopecia is loss of hair. It comes in a variety of patterns with a variety of causes, although often it is idiopathic.

Each follicle produces a number of hairs during a lifetime. There are three phases:

  • Anagen or growth phase on the scalp lasts between three and five years and the hair grows at approximately 1 cm a month. The duration of the anagen phase varies from person to person and it determines how long hair will grow if not cut. Usually about 85% is in anagen phase.
  • Catagen phase follows the anagen phase and is an involutional stage that lasts around two weeks.
  • Telogen, or dormant, phase lasts about three months. The hair remains in the follicle but does not grow.

At the end of the telogen phase the follicle starts production of new anagen hair which displaces the old one from the follicle, with the old one being shed. In some animals this is synchronised to produce moults but in humans it is unsynchronised and around 50 to 100 hairs drop out each day, mostly unnoticed. Sometimes people go through a period of more predominantly telogen phase and they lose a lot of hair in brushes and combs, causing much anxiety; however, baldness does not develop.

In all forms of acquired baldness, skin that has previously been protected may be subjected to strong sunlight. Hats should be worn to prevent burning and possibly later malignant change.

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  • Prevalence varies with cause. Male pattern baldness occurs to some extent in over half of men over the age of 50. Women aged over 40 may have the same prevalence. One study found that up to 13% of premenopausal women reported some male pattern (androgenetic) hair loss. Another study reported that it affected 75% of women older than 65.[2]
  • Alopecia areata has a prevalence of about 0.1 to 0.2%, with a lifetime risk of 1.7%. There is no racial or sexual difference in incidence.[3]
  • Late-onset alopecia areata is characterised by marked female predominance and milder disease activity with increasing age.[4]
  • Some forms of cancer therapy almost invariably cause alopecia but hair regrows after treatment has stopped.[5]

It is essential to determine the type of hair loss, as this is fundamental to treatment and prognosis.

This condition is of unknown aetiology, although there is much support for an autoimmune component. It is more common in acquired thyroid disease, vitiligo, diabetes and collagen diseases. Stress is sometimes given as a factor but it may be that the disease is the cause rather than the result of stress. There is a tendency to run in families, especially the more severe cases and it is linked to some HLA antigens.

The circular pattern of hair loss is characteristic. There are usually smooth round or oval patches with normal skin devoid of hair. Exclamation mark hairs taper towards the proximal end and are said to be pathognomonic but not invariable. Differential diagnosis is with tinea capitis and trichotillomania.

Involvement of nails, usually fingernails, is reported to a variable extent. Studies suggests a figure of 10-15%.[6] Nail changes may come before or after the alopecia. The most common lesions are thimble pitting, usually suggestive of psoriasis with psoriatic arthropathy of the local distal interphalangeal (DIP) joint. Beau's lines are also reported. They usually represent loss of growth during serious illness.

The condition can strike at any age, including in childhood but the peak incidence is between 15 and 30 years of age. There may be a burning sensation or pruritus in some cases. Around 4 patients in 5 have a single lesion, 1 in 8 has two lesions and the rest have multiple lesions. There is no correlation between number and severity. Alopecia areata can affect any area, although the scalp is the most common. The beard is affected in about a quarter of men and, more rarely, eyebrows or extremities may be involved. Loss of 40% of the hair or more occurs in only about 1 in 10. More extensive forms occur in 7%. They are called alopecia totalis if all scalp hair is lost and alopecia universalis if all body hair, including eyebrows, is lost.

Alopecia areata showing fairly extensive, well-demarcated areas of hair loss.

Alopecia areata on the beard area. It can occur off the scalp but is less obvious

Spontaneous recovery can be expected within a few months to a year in minor disease and it is unlikely to be affected by treatment. Fewer than 10% of patients experience extensive alopecia and alopecia universalis occurs in less than 1%. The prognosis for more extensive lesions affecting at least 50% of the scalp, including alopecia totalis, is less favourable. Significant long-lasting growth is less likely to occur in extensive chronic disease.

As well as severe disease, factors associated with a poorer prognosis include nail abnormalities, atopy, onset at a young age, associated autoimmune disease and extensive alopecia.

Traditional wisdom is that no form of treatment is effective and, in mild forms where spontaneous resolution is to be expected, only reassurance should be offered. Nevertheless, if the condition causes distress and no conventional medicine is offered, alternative therapies are likely to be tried and lauded when spontaneous recovery occurs. In more severe cases, where the prognosis is much less favourable, controlled studies have shown some benefit from a number of treatments. However, the overall picture in the literature is of many different types of therapy that have been tried and have failed.

  • The psychological impact of the condition should not be underestimated and counselling may be appropriate.
  • GPs are in a good position to empower patients to make informed choices about treatment. Desperate patients may be vulnerable to reckless therapies offered by unscrupulous commercial providers. Likewise, patients should be forewarned that an initial response to conventional treatments can be followed by a relapse.
  • Intralesional steroid injections are first-line in patients with less than 50% hair loss. They do not invariably work but may produce some improvement for several months. They generally need to be repeated every 4-6 weeks.
  • Topical steroid creams may work but need to be used for at least three months. They are first-line for children under the age of 10. Skin atrophy and telangiectasia can result and maintenance therapy is required.
  • Oral steroids are reserved for cases which are rapidly progressive and severe.
  • Topical immunotherapy and phototherapy are first-line treatments for patients with more than 50% hair loss.
  • Psoralen combined with ultraviolet A (UVA) treatment (PUVA) has been investigated. Although there may be an initial response, the relapse rate is high and the treatment is not considered effective in the long term.
  • Oral ciclosporin is not effective.
  • Topical tacrolimus has no effect.
  • Minoxidil produces a variable response and is better in a stronger formulation such as 5% solution. It must be used under controlled conditions and does not seem to benefit mild disease. It is helpful in extensive alopecia areata but not alopecia totalis or alopecia universalis.
  • There is some evidence that better results are obtained with a combination of topical minoxidil and topical corticosteroids.[6]
  • Surgical intervention is ineffective but hairpieces may be acceptable.

In those aged under 16 and if hair loss exceeds 50% of the scalp, referral for specialist help is advised.[6]

Androgenetic alopecia is male pattern baldness. It shows a strong familial trait and tends to affect men from their late teens onwards, becoming progressively more common with advancing age. The two patterns are bitemporal recession and a central recession to produce a characteristic horse-shoe shape of remaining hair.

Women also suffer from it to a less obvious extent. There is a diffuse thinning of hair over the crown (the Ludwig pattern).[9] The thinning of hair in women may become rather more pronounced after the menopause when there are fewer oestrogens to counteract the androgens. Men tend to have baldness whilst women have thinning of hair and preservation of the frontal area. The condition is a matter of end-organ sensitivity to androgens and men who are deficient on their head characteristically have an abundance of hair over the rest of their bodies.

If a woman presents with male pattern baldness it is worth considering if she has abnormal levels of androgens, especially if hirsute too. One study found that androgenic alopecia was associated with metabolic syndrome in women but not in men.[10] Polycystic ovarian syndrome (PCOS) gives high levels of androgens but alopecia is an uncommon presentation (1.7% in one study).[11] Arrhenoblastoma is an uncommon androgen-secreting tumour of the ovary. Testosterone and dihydroepiandrosterone (DHEA) levels should be measured.[12]


This is a very common condition, especially in men; however, many find it very embarrassing and adopt various techniques to disguise it. Letting the lateral hair grow and combing it over the bald patch is an old and ineffective ruse. Women may wear wigs. A toupée is a small wig for men that may require an adhesive.

In recent years, two pharmacological agents have become available to treat male pattern baldness. Neither is effective in all cases. Both need long-term administration or there will be recurrence. Both must be prescribed on private prescription. Minoxidil comes in 2% and 5% solution that is applied to the scalp twice daily. The 5% solution is for men only. One study found that the 5% solution was 45% more effective than the weaker strength after a 48-week trial and was the preferred treatment for men. It may well be months before any improvement is seen and it should be discontinued if there is none after a year. Any improvement will wane after stopping.

A 5% cutaneous foam is now also available: half a capful should be applied twice a day but the treatment should be stopped if there is no improvement after four months.

Finasteride 1 mg tablets are for men only. The dose is 1 mg daily, compared with 5 mg for benign prostatic hyperplasia but it may be up to six months before benefit is seen and it reverts on cessation.

Various surgical techniques of implanting hair have varied success but are not available on the NHS.

Other options[3] Treatments which have been reported to have some benefit but which are currently unlicensed or in the research phase include:

  • Spironolactone, finasteride and cyproterone (in the contraceptive Dianette®.) in women.
  • Dutasteride.
  • Low-level laser light therapy.
  • Bio-engineered, nonrecombinant, human cell-derived formulation containing follistatin, keratinocyte growth factor and vascular endothelial growth factor.

This is when a physiological or hormonal stress triggers many hairs to move into telogen phase. When new hairs appear in anagen phase they push out the telogen hairs and this is between one and six months, on average three months, after the initial insult. This can be an acute or chronic condition but the chronic condition may go unnoticed. The acute condition may be precipitated by a variety of factors:

Management is the correction of any matters that require attention, such as poor diet and reassurance that hair will return in a matter of months. Minoxidil is occasionally prescribed for this condition.

This is when hair production is arrested in the anagen phase. This mainly happens when cancer chemotherapy, immunosuppression or radiotherapy causes rapid hair loss. Doxorubicin and cyclophosphamide are especially notorious but most antimitotics can have this effect.

Rarely, anagen effluvium can be a feature of pemphigus vulgaris, or be caused by trauma, pressure or exposure to chemicals such as thallium, boron and arsenic.

Within a few months of stopping chemotherapy the hair will return. Patients undergoing cancer chemotherapy are, however, entitled to free NHS wigs. If the treatment includes hormonal manipulation that may induce hot flushes, a wig may be very uncomfortable to wear. Minoxidil shortens the alopecia by about 50 days. Local cooling of the scalp may also be helpful.

Trichotillomania is a behavioural disorder which can be associated with obsessive-compulsive disorder but not invariably. In children it is more common in boys but in adolescence it is more common in girls. Hair loss is asymmetrical and has an unusual shape, with broken hairs across the bald patch which are not easily removed. Single or multiple areas can be affected, including eyebrows and eyelashes. There is minimal or no inflammation.

Genetic and environmental factors have been implicated. Lack of close physical contact with the mother has been identified in some cases. It may be possible to see that the individual wraps the hair around a finger and pulls on it, perhaps when concentrating on something such as when studying. Management involves behavioural modification.

This is really a form of traumatic alopecia. Traction alopecia can also occur with hairstyles that pull tightly on the hair, usually in girls, and it may lead to frontal recession.

Trichobezoar (swallowing hair which forms a ball in the intestines) can be a complication.

Behavioural therapy is the best initial treatment. Cropping the hair close to the scalp may be helpful. Cognitive behavioural therapy is the second-line option.
Unlicensed medications occasionally found to be helpful include:

There are a number of other conditions that can lead to loss of hair. Is the bald skin normal? Is there scarring?

  • Seborrhoeic dermatitis produces large amounts of dandruff and is often associated with thinning of hair.
  • Lichen planus and discoid lupus erythematosis can cause patches of hair loss.
  • Tinea capitis, especially animal ringworm, can cause local hair loss, as can impetigo.
  • Secondary syphilis causes a typical pattern of hair loss called glades in the wood.
  • Check thyroid function as overactivity or underactivity can affect hair. Check iron status too.

Further reading & references

  1. Kimura-Ueki M, Oda Y, Oki J, et al; Hair Cycle Resting Phase Is Regulated by Cyclic Epithelial FGF18 Signaling. J Invest Dermatol. 2012 May;132(5):1338-45. doi: 10.1038/jid.2011.490. Epub 2012
  2. Fenstein RP; Androgenetic Alopecia, Medscape, Mar 2013
  3. Bolduc C et al, Alopecia Areata, Medscape, Apr 2012
  4. Wu MC, Yang CC, Tsai RY, et al; Late-onset alopecia areata: A retrospective study of 73 patients from Taiwan. J Eur Acad Dermatol Venereol. 2012 Feb 20. doi: 10.1111/j.1468-3083.2012.04467.x.
  5. Zannini L, Verderame F, Cucchiara G, et al; 'My wig has been my journey's companion': perceived effects of an aesthetic care Eur J Cancer Care (Engl). 2012 Feb 20. doi: 10.1111/j.1365-2354.2012.01337.x.
  6. Alopecia areata; NICE CKS, June 2009
  7. Harries MJ, Sun J, Paus R, et al; Management of alopecia areata. BMJ. 2010 Jul 23;341:c3671. doi: 10.1136/bmj.c3671.
  8. Guidelines for the management of alopecia areata, British Association of Dermatologists (2012)
  9. Dinh QQ, Sinclair R; Female pattern hair loss: current treatment concepts. Clin Interv Aging. 2007;2(2):189-99.
  10. Yi SM, Son SW, Lee KG, et al; Gender-specific association of androgenetic alopecia with metabolic syndrome in Br J Dermatol. 2012 Apr 5. doi: 10.1111/j.1365-2133.2012.10978.x.
  11. Sanchon R, Gambineri A, Alpanes M, et al; Prevalence of functional disorders of androgen excess in unselected premenopausal Hum Reprod. 2012 Apr;27(4):1209-16. Epub 2012 Feb 17.
  12. Reddy P et al; An Unusual Case of Virilizing Ovarian Tumor Associated With Carcinoma Insitu of Cervix International Journal of Endocrinology and Metabolism 2009;7(4):255-258
  13. Hughes E, Telogen Effluvium, Medscape, Mar 2012
  14. Schwartz R, Anagen Effluvium, Medscape, Mar 2012
  15. Elston C et al, Trichotillomania, Medscape, Aug 2011

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Richard Draper
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Peer Reviewer:
Dr Helen Huins
Document ID:
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