Female hair loss

Abstract

Hair loss in female patients is a distressing condition. Patients can present to GPs for assessment, advice and consideration of onward referral. A wide range of disorders can lead to hair loss in females. This article will outline common disorders and their clinical features, including investigation and management strategies for primary and secondary care. A sound understanding of the course and prognosis of diseases allows open discussion with patients during healthcare consultations, and is important given the distressing nature of hair loss.

Assessing and categorising hair loss

History and examination are initial steps in determining the cause of hair loss in females. Assessing the timeframe of onset and the distribution of hair loss helps identify different causes. Basic examination of the scalp can help subdivide hair loss into scarring (cicatricial) and non-scarring alopecias. Examination of the scalp during consultation may reveal inflammation, or obvious scaring, which is indicative of a scarring alopecia. A detailed examination of the skin, nails and mucous membranes may reveal other features to help guide diagnosis and provide useful information for onward referral to dermatology.

A wide spectrum of conditions can cause scarring alopecia. Scarring alopecia may occur as secondary to a host of genetic and congenital disorders. These patients are unlikely to present primarily complaining of hair loss in primary care. However, hair loss may be a feature of the underlying syndrome.

Hair loss can also be associated with congenital and systemic illness, so knowledge of past medical history is important in assessment. A thorough drug history should be sought, as hair loss can be related to medication, for example, cytotoxic drugs, anti-thyroid medication, colchicine, levodopa, propanolol and retinoids.

Referral to dermatology is useful when there is diagnostic uncertainty, when scarring alopecia is suspected, and for counselling on the suitability and limitations of available treatments. Prior to referral, an initial assessment in primary care to screen for co-morbid issues such as thyroid disease, nutritional deficiencies, offending medications and personal stress factors is useful and may prompt early interventions. Treatments are often prescribed on an off-licence basis, and so prior consultation with a dermatologist is often necessary. Minoxidil is available over-the-counter, and can be tried in cases of androgenic alopecia. However, it is important for patients to be aware of the significant cost and that regrowth may not be to an acceptable cosmetic level. In cases of trichotillomania, psychological interventions are paramount and additional referral may be useful. Often hair appliances are required; however, provision of hair appliances on the NHS varies within the UK.

Hair loss can be divided into three broad categories: scarring, non-scarring and structural hair abnormalities. For the purposes of this review we will focus solely on the former categories.

Non-scarring hair loss

Female pattern hair loss (female androgenic alopecia)

Female pattern hair loss is common, it is estimated to affect up to one half of women, to some degree, over the age of 65 years. The clinical spectrum of the condition is diverse: ranging from mild generalised thinning to more extensive hair loss. A combination of genetic and hormonal factors probably contributes to the development of androgenic hair loss. Hair follicle exposure to dihydrotestoseterone results in regression and shrinkage of follicles leading to non-scarring hair loss.

Typically, the condition presents in post-menopausal women. In younger females, an association with androgen excess such as polycystic ovary syndrome may be causative. Investigations may be required in these patients if other features of androgen excess are present, for example hirsutism or other signs of virilisation. However, the majority of woman will have a normal androgen profile.

Patients may present complaining of gradual thinning of hair in the central and crown areas of the scalp extending frontally. Temporal recession is typically absent, reflecting preservation of non-androgen-sensitive hair follicles in the temporal and posterior scalp. In cases of androgen excess, temporal recession may indeed be present, thus acting as a prompt for further investigation (see Box 1 for suggested investigations). There may be retention of a normal frontal hairline with a thin fringe of hair.

Box 1.

Suggested investigations for suspected hyperandrogenism.

• Follicle-stimulating hormone

• Oestradiol

• Lluteinising hormone

• Prolactin

• Testosterone

• Sex-hormone-binding globulin

• 17-hydroxyprogesterone

• Dehydroepiandrosterone sulphate

• Thyroid function tests

• Pelvic ultrasound

Topical minoxidil may slow the progression and partially improve hair coverage. However, over-the-counter preparations are expensive. Patients should be advised that a response is only sustained as long as treatment is continued. Trials of minoxidil should be continued for at least 4 months, but optimally for up to a year, to assess for clinically apparent benefit. Patients should be counselled that an initial increase in hair shedding may be noticed over the first few weeks, related to impact on hair cycle.

Additionally, minoxidil can cause local scalp irritation, such as erythema and scaling. The 5% foam preparation (once-a-day) can be less irritating than the 2% lotion preparation (twice-a-day) as the foam does not contain propylene glycol. Other therapeutic strategies include finasteride and spironolactone. These are assessed on an individual basis for patient suitability and depend on tolerance of side effects. Hair shedding is often episodic in these patients, but female pattern hair loss is unfortunately a progressive condition. The rate of progression is variable, but rarely progresses to complete baldness. Good supportive measures and referral for a hair appliance is often necessary.

Alopecia areata

Alopecia areata (AA) is a non-scarring alopecia that typically appears as oval featureless, well-demarcated patches of hair loss (see Fig. 1). Patients may give a history of an abrupt and rapid onset. On examination, short tapered hairs may be visible at the edge of areas of hair loss; these are known as exclamation point hairs. There is usually no associated inflammation or scale within the discrete patches. The condition can also affect eyebrows and eyelashes. There is a predilection for pigmented hair, so retained white hairs may be seen within the patches of hair loss. In approximately 10% of patients, there may be associated nail pitting. About 1-in-5 patients with AA have a positive family history. In cases where hair loss affects the entire scalp, the term alopecia totalis applies. Alopecia universalis applies when there is loss of hair from both the scalp and body.

Figure 1.

Alopecia areata.

Reports have shown an association between hair loss and iron depletion, and with autoimmune conditions such as thyroid disease, diabetes and vitiligo. Guidance from the British Association of Dermatologists does not recommend any routine testing in assessment of AA (Messenger et al., 2012). However, if clinical suspicion of autoimmune disease or indeed fungal infection exists, further investigation prior to onward referral can include blood tests (thyroid function, B12, iron profile, antinuclear antibodies, erythrocyte sedimentation rate (ESR)) skin scrapings or cultures.

AA results from the loss of the normal immune privilege that protects hair follicles from autoimmune destruction. The retention of the follicle in AA permits the potential for hair regrowth. Prediction of the clinical course is extremely difficult, and the 1-year complete regrowth rate ranges between 34 and 80% in the reported literature. Poor prognostic features include the extent and duration of hair loss, ‘ophiasis’ subtype of AA (in which hair loss appears in bands in the parietal, temporal or occipital areas), history of atopy, and presence of nail disease. Those who have lost more than half of hair coverage have a 10% chance of complete regrowth of hair. Approximately 1-in-4 patients will progress to alopecia totalis.

It is important to counsel patients that treatments aim to control, not cure the condition. No treatment has been shown to alter the long term course of the disease. Topical and intra-lesional corticosteroids can be used to treat smaller patches of hair loss or in affected eyebrows. Tapered systemic steroids may lead to modest hair regrowth (up to 25% improvement), but treatment cessation leads to recurrence of hair loss. The potential benefit of steroid treatment should be balanced with the side effects of steroids. Minoxidil has been shown to promote hair regrowth in up to 45% of patients but, unfortunately, not to a cosmetically suitable level. Second line treatments include contact immunotherapy and ultraviolet light, but with limited evidence of sustained benefit. There is little evidence for the role of immunosuppressant therapies. More recent reports of clinical benefit from ongoing studies with oral Janus Kinase inhibitors are of interest (Crispen et al., 2016). Coverage with hair appliances is often required alongside appropriate support and open discussion about prognosis.

Telogen effluvium

Sustained hair regrowth is dependent on the balance between the number of hairs shed and the number of follicles entering the growth phase (anagen) of hair shaft development (see Fig. 2). Typically, 50 to 150 hairs are shed daily. In telogen effluvium, the balance is disrupted, causing increased hair shedding as an increased number of follicles enter the resting, telogen phase. In normal hair growth, 10% of follicles are in the shedding phase, but this increases to approximately 30% in telogen effluvium. Patients may complain of increased hair shedding while brushing or washing their hair. The typical history of hair loss usually follows around 3 months after physical stress or a traumatic trigger (see Box 2). In one third of patients, no obvious precipitating cause can be identified. On examination there may be diffuse non-scarring hair loss and reduction of hair volume throughout the scalp (see Fig. 3).

Figure 2.

The normal hair cycle.

Figure 3.

Telogen effluvium.

Box 2.

Triggers for telogen effluvium.

• Child birth

• Trauma

• Severe physical illness

• Bereavement

• Psychological stress

• Weight loss

• Nutritional deficiency

• New medications

Patients should be reassured that telogen effluvium typically resolves within 12 months without the need for intervention, as medication or treatments do not expedite hair regrowth. Hair regrowth occurs as follicles eventually re-enter the anagen growth phase. Cases lasting longer than 6 months can be classified as chronic telogen effluvium.

Scarring hair loss

Frontal fibrosing alopecia

Frontal fibrosing alopecia is thought to be a variant of lichen planopilaris (LPP) and typically affects post-menopausal woman. The condition results from inflammation and destruction of the hair follicle by lymphocytic infiltrate. Similarly to LPP, the breakdown and destruction of the normal immune barrier is not fully understood. Scarring hair loss is present at the fronto-temporal scalp with retention of a small volume of hairs at the frontal hair line, the so called ‘lonely hair sign’. The affected underlying skin may appear pale and smooth in comparison with the surrounding skin of the forehead (see Fig. 4). Eyebrow involvement is common and may precede the scalp hair loss. Perifollicular changes similar to LPP may be seen at the periphery of the area of hair loss.

Figure 4.

Frontal fibrosing alopecia.

Therapeutic strategies are aimed at halting progression in active disease. Strategies include topical steroids and tetracycline antibiotics to reduce inflammation. Systemic agents such as hydroxychloroquine or mycophenolate mofetil can be tried, with the aim of halting further progression of hair loss. Unfortunately, once hair loss has occurred, due to the scarring, the regrowth potential is limited. Referral for a hair piece may be required.

Lichen planopilaris

LPP is an uncommon scarring alopecia that is a form of lichen planus typically affecting the vertex and parietal areas of the scalp. The provoking cause for the inflammatory response and loss of follicular immune privilege is not fully understood.

Patients may present with symptoms of burning, pruritus or tenderness of the scalp with associated hair loss. On clinical examination, peri-follicular erythema and scaling are often noted at the periphery of the scarring patches in active disease. Clinical assessment may reveal evidence of lichen planus of skin, mouth, genitals and nails, aiding diagnosis and onward referral.

LPP is difficult to treat, but treatment strategies aim to reduce inflammation in active disease in order to prevent further progression. Treatments include topical or intralesional steroids, and tetracycline antibiotics. Systemic agents shown to be of benefit include: hydroxychloroquine, dapsone, ciclosporin and mycophenolate. Mycophenolate has been shown to be most effective, especially in refractory cases. Emerging evidence suggests that targeting peroxisome proliferator-activated receptors with the agent pioglitazone may be of therapeutic benefit (Mesinkovska et al., 2015).

Traction (or cosmetic) alopecia

Hair loss is caused by tension on the hair shaft generated by hairstyling techniques. Patients affected typically have non-scarring hair loss distributed in the frontal scalp with a ‘fringe sign’, where there is retention of hair at the frontal and temporal areas. There may be associated scale with minor inflammation. Multiple short broken hairs may be seen on examination.

Clinical assessment should explore hair styling techniques, as the condition may be due to braiding, ponytails, or use of rollers or straightening devices. The mainstay of treatment is cessation of techniques causing traction. Traction alopecia does not cause scarring, but excessive and chronic traction can disrupt the normal hair follicle, which prevents potential hair regeneration.

Trichotillomania

Trichotillomania is an under-reported cause of hair loss that is characterised by compulsive repetitive hair pulling. It is more common in adult women, and equally common in male and female children. It commonly affects the frontal and parietal scalp, but can occur anywhere including eyelashes, eyebrows and body hair. On examination, short broken hair of varying length may be evident. Patients often describe a feeling of relief and gratification with hair pulling.

Trichotillomania is a disorder within the obsessive–compulsive spectrum. Anxiety and stress are commonly associated with trichotillomania and should be explored during clinical consultation. In children, it is often associated with changes in household dynamics such as sibling rivalry, family illness or altered parent–child relationships.

Referral to a holistic multidisciplinary psycho-dermatology service is advocated to treat the condition. Psychological interventions, such as habit reversal training (HRT) are employed to treat the hair pulling compulsion. Additional psychological approaches include acceptance and commitment therapy and dialectical behaviour therapy. The literature reports N-acetylcysteine and selective serotonin re-uptake inhibitors as possible therapeutic agents. However, HRT is more effective than any of the pharmacological strategies.

Pseudopelade of Brocq

Pseudopelade of Brocq is a clinical entity that typically affects young to middle-aged women. The pathophysiology of pseudopelade of Brocq is not fully understood. There has been contentious discussion in the literature as to whether the disorder represents the end-stage of other forms of scarring alopecias or a separate non-inflammatory process where there is atrophy of hair follicles as opposed to scar formation. Typically, patients will report a prolonged history of asymptomatic hair loss that may have occurred over years to decades. Hair loss is centred on the crown of the head, but can also occur in the parietal area. Early lesions appear as round or ovoid areas of hair loss, with an erythematous rim of skin surrounding individual hairs follicles and no scale. Over time, areas merge to form a larger, irregular area of hair loss, sometimes described as a ‘foot prints in the snow’ appearance. Hairs can be easily plucked from edges of patches when activity is present.

No treatment has been shown to reduce progression or promote hair re-growth. Cases of spontaneous remission are, however, possible. If extensive, hair appliance referral may be appropriate.

Discoid lupus erythematosus

Discoid lupus erythematosus (DLE) appears as discrete, often well-demarcated patches of hair loss. Early in the disease process, the areas may closely resemble the appearance of LPP. Well-established areas are more obvious with diffuse scaling, erythema, telangiectasia and hyperpigmentation. On examining the scalp there may be follicular plugging evident, so called ‘carpet tack scale’. Later in the disease process, areas are smooth and atrophic with diffuse scarring. Other commonly affected areas include the conchal bowls of the ears and face. DLE may present independently of systemic lupus erythematous (SLE). In patients with no systemic features of SLE at presentation, the risk of development of SLE in localised disease is much lower compared with generalised DLE.

Treatments aim to reduce the inflammatory process and halt the extent of disease and scarring. Therapeutic agents include steroids (topical, intralesional or systemic), antimalarial medications such as hydroxychloroquine and mepacrine, and systemic immunosuppression with agents including methotrexate and mycophenolate mofetil, alone or combined with hydroxychloroquine.

Central centrifugal cicatricial alopecia

Central centrifugal cicatricial alopecia commonly occurs in relation to use of heated hairstyling devices. The pathophysiology is not fully understood, but causation is thought to be related to a combination of traumatic traction and chronic inflammation from superimposed bacterial infection. There is some evidence to suggest a relationship to metabolic disorders such as Type 2 diabetes. It most often affects women of African descent. On examination, hair loss is typically noted on the crown or vertex with associated inflammation and scaling. The extent of inflammation can be variable with the highly inflammatory subtype thought to overlap with folliculitis decalvans. There is a pseudopelade pattern variant in which there is absence of a significant follicular inflammatory process.

Treatment is primarily aimed at reduction of inflammation. Topical steroids can be utilised, as well as a prolonged course of tetracycline antibiotics such as doxycycline as an anti-inflammatory agent. As with all scarring alopecias, the potential for hair regrowth is absent in the presence of follicular destruction. In cases where there is extensive hair loss, hair appliances may be necessary.

Folliculitis decalvans, acne keloidalis, and dissecting cellulitis

Folliculitis decalvans, acne keloidalis and dissecting cellulitis are inflammatory conditions that more commonly affect young men, but can also affect women. Common to all processes is a significant inflammatory response resulting in destruction of hair follicles and scarring.

Folliculitis decalvans presents as a pustular eruption, which progresses to scarred areas of hair loss with peripheral pustules. It is thought to be caused by an abnormal inflammatory response to Staphylococcus aureus, which is often present as a commensal microbe. Patients will typically complain of an itchy and irritated scalp. A variant of the condition is tufted folliculitis, in which the characteristic ‘tufted’ feature is seen where several hairs emerge from the same follicle.

Treatment aims are to reduce inflammation and reduce further hair loss: these include antimicrobials (topical and systemic) and topical steroids. Antibiotic agents aim to alter the carriage and burden of S.aureus on the skin.

Dissecting cellulitis is a rare scarring alopecia that most commonly affects black males. It has been described as part of the follicular occlusion disorders, which includes dissecting folliculitis, acne and hidradenitis suppurativa. It appears as inter-connecting inflammatory nodules which merge to form boggy fluctuant areas with sinus tracts, purulent discharge and patchy hair loss. Early cases may respond to antibiotics and the anti-inflammatory action of dapsone. Extensive cases may require surgical intervention. Similar to the other follicular occlusive disorders, other treatment strategies include isotretinoin, acitretin or biologic agents such as adalimumab.

Acne keloidalis appears as an inflammatory acneiform eruption of papules and pustules at the nape of the neck and posterior scalp. There is subsequent, often extensive, keloid scarring. Therapeutic strategies include oral antibiotics to reduce inflammation, prevent keloid scarring and ultimately reduce follicular destruction and hair loss. In advanced cases surgery may be necessary.

KEY POINTS

Hair loss in females is caused by a variety of disorders, with differing clinical features

Hair loss is typically divided into scarring and non-scarring alopecias

Assessment of the scalp, nails and mucous membranes helps diagnosis, onward referral and counselling of patients

Hair loss is often difficult to treat; when scarring is present there is no potential for regrowth and treatment is aimed at halting progression of hair loss

Counselling and hair appliances may be appropriate supportive measures for patients with extensive disease

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