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When a patient presents with the words, ‘I’m losing my hair’, this is almost invariably accompanied by a high level of anxiety, so remain calm: there is no point in two of you panicking. It is good to have a small road map in your head to help you deal with this distressing problem. This article will use the ‘no frills’ approach. Alopecia is a broad topic, which we will try to keep as simple as possible.
Before getting into the realm of alopecia, it is useful to know how hair grows: it does so in a cycle. It grows within, and from the hair follicle; at any one time, some hair is in a growth phase (anagen), which can last up to five years. Telogen is the resting phase, at the end of which the hair will be shed. The brief transitional period between anagen and telogen is called catagen.
Telogen effluvium (Figure 1) is the term used for a generalised fall of hair.
Figure 1: Telogen effluvium
Scarring or non-scarring?
The thing to establish first is whether or not the alopecia is scarring or non-scarring. Why is this so important? Because once a hair follicle scars, it can never again produce a hair. If the process is progressive, and involves many follicles, a bald patch will be evident, from which hair will never again grow. By and large, scarring alopecia of almost any sort, whether or not associated with a systemic disease, will need referral to a dermatologist.
Of course, the patient may consider it to be of very little comfort that his/her alopecia is non-scarring once the follicle is not producing hair. The most common type of alopecia is androgenetic, but, although not scarred, without hormonal intervention, the hair follicle in the affected area will produce at most only vellus or ‘baby’ hair.
How to tell scarring from non-scarring
Examine the area in a good light, preferably with a hand lens. Scarring alopecia begins with inflammation around the hair follicle. There may also be some scale.
In the case of discoid lupus erythematosus (DLE), there will be obvious plugging of the hair follicle with keratin. The inflammation will disappear when the follicle is destroyed. It may be hard to make out when single follicles are involved, but when they are several, adjacent to each other, the smooth, featureless appearance will confirm scarring. Another interesting feature of scarring alopecia is that some of the remaining follicles, in an effort to compensate for the lack of hair from neighbouring follicles, produce two or more hairs (tufted alopecia).
Now we have an idea about how the follicles may appear in alopecia — either destroyed due to an inflammatory process, or not scarred but prevented from producing hair from internal or external influences.
Now it is time to delve a little further. Let us take a look at some common examples of alopecia, beginning with non-scarring, which has the commonest examples.
Diffuse, non-scarring alopecia
Androgenetic — Male-pattern (Figure 2), and female-pattern (more diffuse than the well recognised male variant) (Figure 3).
Perhaps it is not strictly correct to call it ‘diffuse’ because it has a distinctive pattern, particularly in men, with bitemporal recession and a thinning area on the crown.
Figure 2: Male pattern alopecia
Figure 3: Female pattern alopecia
- Drive by androgens and genetics.
- Medical treatment, eg, minoxidil topically; finasteride (orally) gives mixed results.
- Surgical treatment may be helpful in some cases, but the patient should be aware that the outcome is not always what is hoped for, and is very expensive.
Drug-induced — The best known example is the swift and total hair loss with chemotherapy, a form of telogen effluvium. The hair regrows fully some months later.
Iron deficiency — Check iron parameters in a case of telogen effluvium; do not just rely on the haemoglobin level. If the iron deficiency is severe and prolonged, the fingernails may be spoon-shaped (koilonychia).
- Consider high levels of androstenedione in female pattern hair loss (request a sex hormone profile); cyproterone acetate, an anti-androgen (Dianette) may be effective.
- Is the young woman on an oral contraceptive pill, the progesterone component of which has androgenic actions? Dianette may be of help in such a case.
- Similarly, some progesterones in HRT with an androgenic action may have a similar adverse effect on hair growth.
- Did the patient have a baby five-to-six months ago? The two events may not be linked in the patient’s mind because of the time lag. A telogen effluvium is not uncommon after childbirth.
Thyroid activity — Both an over- and an underactive thyroid gland can cause hair loss. And so, check TSH and thyroxine levels in cases of unexplained hair loss.
- Telogen effluvium occurs with hyperthyroidism.
- Sparse, brittle hair is found in myxoedema.
After major surgery, or serious illness, telogen effluvium may occur several months later.
As part of systemic lupus erythematosus (SLE), the patient will be unwell with other signs and symptoms, eg, a butterfly rash.
Diffuse alopecia areata (AA). This is less common than AA presenting in patches. Eyebrows and lashes may also fall out (alopecia totalis); there may be nail pitting, all of which carry a poor prognosis for regrowth. When all body hair is also lost, the condition is called alopecia universalis.
Localised (patches or plaques) of non-scarring of alopecia
AA — an area of alopecia, anywhere on the scalp (Figure 4); may be multiple:
- Not inflamed.
- Exclamation hairs present (hair apparently broken 1mm or so from the scalp, Figure 5).
- Good prognosis, hair regrowing spontaneously in four-to-six months.
- Poor prognostic signs include involvement of hairline, loss of eyebrows or eyelashes, and nail pitting.
- Potent topical steroids or intralesional triamcinolone may speed this process up, as may the application of irritant ointments such as dithranol.
Tinea — a fungal or dermatophyte — infection
- Person-to-person spread.
- Scaly patches with alopecia in the scalp.
- May not itch.
- Not inflamed.
- T.mentagrophytes and T.tonsurans often responsible.
- Has been a problem in recent years in children of Afro-Caribbean origin, possibly related to hair fashions.
- Clinical diagnosis may be confirmed by sending scales and plucked hair for mycology.
Figure 4: Alopecia areata
Figure 5: AA with exclamation mark hairs
- Microsporum canis (M.canis, Figure 6) is cat and dog ringworm, which may be transmitted to humans. The most common source is a new kitten. The fungus can be seen to fluoresce under a Wood’s lamp.
Figure 6: Tinea of scalp, M canis
- Tinea verrucosum (cattle ringworm); cattle-to-human. It is an inflammatory process. If a boggy mass or tumour occurs, the term kerion (Figure 7) is used. If the diagnosis is delayed and the condition left untreated for too long, scarring may occur.
Figure 7: Kerion
Treatment for scalp ringworm
An oral antifungal (terbinafine; itraconazole) is given for six weeks. Remove the scales in tinea and microsporum with a toothbrush and apply a topical antifungal cream. Local remedies are only necessary initially. In the case of a kerion, an oral antibiotic such as flucloxacillin or erythromycin should be given concurrently with the oral antifungal treatment, as secondary staph and strep infection is usually present. A topical, potent steroid will help to reduce the inflammatory component and the risk of resulting scarring.
- Trichotillomania (hair-pulling; Figure 8) — may be a form of habit tic, as in hair-twisting and pulling, but may be seen in upset or attention-seeking teenagers.
Figure 8: Trichotillomania
However, it may represent a more serious underlying psychiatric disorder.
- Corkscrew hairs (from twisting) are evident.
- The scalp skin is otherwise normal.
- Psychological therapy may be needed.
Trauma – a physical blow, a surgical incision, or localised radiotherapy can all result in patch alopecia.
There are many weird and wonderful forms of scarring alopecia, but I am only going to mention the ones most frequently encountered.
Scaly, inflamed patches/plaques
In discoid lupus erythematosus (DLE, Figure 9), small plugs of keratin are present in the hair follicles.
Figure 9: DLE
- Whilst the scalp may be affected in isolation, it is more common for it to accompany facial plaques of DLE (photosensitive).
- Check the nail folds for periungual erythema and for ragged cuticles.
Investigation includes biopsy to confirm the diagnosis, and blood work to ensure that the problem is localised to the skin and that the problem is not systemic (SLE).
Pustular, inflamed alopecia
- Usually a single patch, gradually expanding (folliculitis decalvans (Figure 10); sore rather than itchy.
Figure 10: Folliculitis decalvans
- Pustules are seen around the hair follicles. When these resolve, scarring occurs.
- Two or three hairs may be seen emerging from one follicle in the scalp’s vain effort to compensate for the loss of hair from scarred follicles (tufted; Figure 11).
Figure 10: Folliculitis decalvans with tufting
Investigation and treatment
A biopsy is taken to confirm the diagnosis. Treatment with a potent topical steroid is given. In most cases, dapsone is given as oral medication, as the problem is neutrophilic.
Frontal fibrosing alopecia (Figure 12)
- The diagnosis is confirmed by histology (biopsy).
- This is a condition that presents in postmenopausal females.
- The hair loss is insidious with a frontal and bitemporal distribution.
- The cause is unknown.
- Inflammation around individual hair follicles is evident.
Figure 12: Frontal fibrosing alopecia
This is administered with potent topical steroids; use with caution, as there is a real risk of atrophy with the terrain involved. The oral drug of choice is the antimalarial drug hydroxychloroquine.
The histology of frontal fibrosing alopecia has some features in common with DLE, where hydroxychloroquine is the drug of choice.
This has been rather a gallop through many types of alopecia, but it may provide you with some confidence in approaching the problem when next it presents in your surgery.