Diseases of the hair and nails

Both hair and nails are composed of keratin and are derived principally from the epidermal layer. Each may be affected by the same type of disease process, e.g. lichen planus, or altered by conditions that affect primarily the epidermis.


The extent and distribution of body hair is largely determined genetically. At the time of puberty, terminal hair growth occurs in males on the beard area, over the upper lip, chest, abdomen and thighs. Androgens determine the extent of secondary sexual patterns of hair growth during adolescence in both sexes. In females any marked alteration in the extent of hair growth or hair loss at times other than at puberty or the menopause may reflect serious endocrine disturbance.


Hirsuties is defined as an excessive growth of hair of male type and distribution in females. In many parts of the world an excess of body hair is accepted as a racial characteristic or may, in addition, be seen as a family trait. In the Western World, excess body hair in females is considered less acceptable and women may become selfconscious about the extent of their hair growth. Most hirsute females do not have recognizable clinical or biochemical evidence of endocrine disease, though this must be excluded by a careful history, examination and hormone profile where appropriate. Some drugs alter the texture and extent of hair growth; these include cortisone, minoxidil, diazoxide, hydantoins and cyclosporin. Here the hair growth is non-androgenic in pattern and the term hypertrichosis is used. Methods of hair removal include abrasion with mittens that have a roughened surface, shaving and plucking, but these give short-term relief. Depilatory creams and waxing should not be used frequently on facial hair but may be used elsewhere, such as on the legs. Bleaching facial hair with peroxides will produce an acceptable appearance for fine hair. Coarse hairs are best dealt with by electrolysis but this needs to be performed by skilled personnel and may produce scarring, especially if acne is a concurrent problem on the chin. With severe hirsutism, antiandrogens (e.g. cyproterone acetate) or prednisolone (5 mg at night and 2.5 mg in the morning) may be used to produce a slowing of hair growth so that mechanical removal need not be so frequent or vigorous.

Hair loss

Hair loss that occurs to the extent that scalp skin becomes  abnormally visible is termed alopecia. It may be permanent, when the hair follicles are damaged by scarring (e.g. in lichen planus or discoid lupus erythematosus), or may recover if the follicles are left intact (e.g. in some endocrine diseases or alopecia areata).

Diffuse hair loss

Hairs are lost in the telogen phase. Normally about 100 hairs are shed each day. In severe illness or following pregnancy there is an increase in the number of hairs entering the telogen phase (telogen effluvium). Hair loss is seen 3-4 months after the event when the new anagen hair pushes out the old telogen hair. Nail growth may be affected in the same way.
Other causes of diffuse hair loss include endocrine disease such as hyperthyroidism or hypothyroidism and androgen overactivity in both males and females. Iron deficiency, rapid weight loss associated with dieting, and drugs such as lithium or vitamin A and its derivatives also produce diffuse and treatable hair loss.

Androgenetic alopecia

This is premature hair loss in both males and females over the vertex of the scalp. Increased Sa-reduction of testosterone to dihydrotestosterone (DHT) occurs in frontal, but not occipital, hair follicles. DHT is responsible for miniaturization of follicles, fine hair growth ensues and there is a shortening of the anagen phase of hair growth.

Alopecia areata

This occurs in both sexes and all races and is usually seen in young adults or children as a well-defined patch of hair loss. Only 25% of cases are seen over the age of 40 years and 25% of patients give a family history of the condition.

AETIOLOGY. There is often a personal or family history of atopy. Alopecia areata occurs in association with autoimmune diseases such as thyrotoxicosis, Addison’s disease, pernicious anaemia and vitiligo. The association of alopecia areata with such diseases suggests that immune changes are important in the pathogenesis. It is also seen in association with Down’s syndrome and hypogammaglobulinaemia. CLINICAL FEATURES. Patches of hair loss can occur over any part of the body, e.g. the beard area or eyebrows, but the scalp is most frequently affected. Asymptomatic loss may first be noticed by a relative or hairdresser. Patches tend to regrow over the course of several months within the scalp margin in adults. An extension into the actual hair margin (ophiasis) is often less quick to recover. Children with an atopic background may lose all their scalp hair (alopecia totalis) and the prognosis in such patients should be guarded; alopecia totalis is seen· less frequently in adults. Loss of hair from all body sites(alopecia universalis) may occur by extension from other  sites but can also occur acutely. The extension of hair loss occurs in a peripheral fashion; at the advancing edge, broken hairs (exclamation mark hairs) provide evidence of disease activity. Diffuse loss of hairs in alopecia areata is an infrequent occurrence and may be difficult to differentiate from other causes of hair loss. Regrowing hair appears as a fine, depigmented downy growth. Areas of alopecia principally affect pigmented hair and premature greying is seen after diffuse hair loss.


 Large doses of corticosteroids will produce a regrowth of hair, but relapse often occurs after treatment is stopped. Topical corticosteroids may also help to speed the rate of regrowth of hair. Other treatment modalities, effective in small numbers of patients, include PUV A therapy and topical minoxidil. This is available as a 2% solution. It will induce hair growth in about onethird of individuals but this tends to fall out on cessation of treatment.

Premature male-pattern baldness

Recession of the hair margin is an ageing characteristic of primates. This may appear early in males but such a pattern of loss in young females may indicate serious androgenicity. Vertical thinning is seen in association with margin recession in both sexes. In young women there is often evidence of androgen excess, which may be treated by antiandrogen therapy over an interval of a year with some recovery. The primary defect is atrophy of the hair follicle. It is due to a number of factors other than excess androgen activity, for antiandrogen therapy is not always effective in stimulating strong terminal hair growth in females.

Abnormalities of the hair shaft

The hair shaft may become twisted, beaded or broken, leading to hair loss. Short, unruly or broken hair is then the primary complaint. Similar patterns of loss will be seen with drying of the hair or the effect of weathering, cosmetics, bleaching agents or grooming.Traction Traction associated with fashion, traditional or ethnic  practices, such as hot combing, braiding or plaiting, may also cause a localized hair fall, especially over the temporal region. Straightening or relaxing the hair, undertaken by those with naturally curly hair may, in addition, produce permanent root damage.


The nail plate grows continuously, although the rate slows with advancing years, and with some generalized diseases. Growth of finger-nails is normally at a rate of about 1 cm every 3 months, so that renewal of a fingernail may take 6 months, and toe-nails, which grow moreslowly, may take from 18 months to 2 years. An increase in the rate of growth of the nail plate occurs in psoriasis and other skin diseases.
The nail plate arises from the matrix and lies on the nail bed that also contributes to its growth. The hard outer layer is formed from the proximal matrix and the bulk of the nail, composed of soft keratin, is produced by the distal matrix.
The nail matrix lies within a fold of epidermis, so that dermatoses or infections that involve the posterior nail  fold may also cause abnormalities of the  nail plate; these include chronic paronychia, fungal disease, eczema and psoriasis. These nail changes have been discussed in the appropriate sections.
Congenital defects of the nail occur in conjunction with abnormalities of the epidermis, teeth or skeleton. Nail disorders in generalized diseases


Connective tissue diseases

Short and brittle nails occur in severe circulatory disorders, e.g. Raynaud’s phenomenon, especially in association with systemic sclerosis. Pterygium formation also occurs when a thin skin-fold merges with the cuticle, widening it by several millimetres. Chronic paronychia may persist despite all therapeutic manoeuvres in patients with severe digital ischaemia. Nail fold capillary dilatation and distortion or the absence of capilla ries, usually with severe Raynaud’sphenomenon, is seen in systemic sclerosis. Ragged cuticles  containing haemorrhages are often most pronounced in patients with dermatomyositis.

YeIIow nail syndrome

The nail plate is thickened, yellow in colour, smooth and with an increased lateral curvature. The rate of growth the nail is reduced. Such nails are seen in association with chronic oedema of the hands, feet, ankles or face, congenital lymphoedema, pleural effusions, chronic sinus
infection and thyroid disease.

 White bands

Distal white bands that are parallel to the lunula and separated from this and each other by a normal pinkcoloured portion are seen in patients with hypoalbuminaemia. The nails return to normal when the level of protein is restored.

Half-and-half nails

This is the name given to nails in which the proximal nail is pale or white and the distal portion is red or brown in colour; these nails occur in renal failure.

Brown streaks

Longitudinal brown streaks are commonly seen in black patients when pigment cells are incorporated into the nail matrix. Alteration of pigment beneath the nails that is localized and not related to obvious trauma in whiteskinned patients may require a biopsy of the nail to exclude subungual melanoma.


Onycholysis or separation of the distal edge of the nail from the vascular nail bed will cause whiteness of the free edge and this most commonly follows trauma or faulty or excessive manicure. Psoriasis is another common cause and similar changes may be seen in thyrotoxicosis or following photo-onycholysis produced by photoactive drugs such as tetracycline or psoralens, as well as in porphyria. Splinter haemorrhages
These are most frequently caused by trauma to the nail;
infective endocarditis, SLE and psoriasis are less common causes.


Spoon-shaped nails or koilonychia is seen in association with iron deficiency anaemia but it may also follow trauma, e.g. in garage mechanics who regularly fit tyres.

Chronic paronychia

This is due to chronic infection from Candida albicans. It is rarely a manifestation of an underlying systemic disease such as hypoparathyroidism, multiple endocrine disease or chronic iron deficiency.

Transverse lines

Transverse lines (Beau’s lines) related to acute physical or psychiatric illness or the use of cytotoxic drugs represent a temporary arrest of growth. They may be associated with an arrest of hair growth and subsequent fall (telogen effluvium).

Blue discoloration of the nail

This may be seen in hepatolenticular degeneration (Wilson’s disease) as blue lanulae.

Effects of drugs

A number of drugs, including antimalarials such as chloroquine, may cause a blue/black discoloration of the nail plate. Mepacrine may stain the nail plate blue and fluoresces green on examination by Wood’s light. Argyria occurring as an occupational disease or following, for . example, the use of silver-containing nose drops will stain the nails a grey/blue colour. Phenothiazine produces a blue/black coloration that is often accentuated in summertime.

Cytotoxic drugs

Diffuse, longitudinal or horizontal melanonychia affecting the nail base or nail plate may occur in association with pigmentary changes of the surrounding skin with doxorubicin, busulphan, cyclophosphamide and daunorubicin therapy.

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