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Causes of alopecia

Alopecia «hair loss» is due to a disorder of the hair follicle in which the scalp skin looks normal (nonscarring alopecia) or due to a disorder within the scalp skin that causes permanent loss of the follicle (scarring or cicatricial alopecia). This latter form causes shiny atrophic bald areas in the scalp which are devoid of follicular openings.

 

 

Non-scarring alopecia

• Androgenic alopecia

• Telogen effluvium

• Alopecia areata

• Trichotillomania (selfinduced hair-pulling)

• Tinea capitis

• Metabolic (iron deficiency, hypothyroidism)

• Drug (e.g. Heparin, isotretinoin, chemotherapy)

   

Androgenic alopecia (male pattern baldness) is the most common type of non-scarring hair loss and depends on genetic factors and an abnormal sensitivity to androgens. It presents in young men with frontal receding followed by thinning of the crown and there is often a positive family history. It also occurs in females but tends to occur at a later age, be milder and show little in the way of frontal recession. If acne and menstrual disturbance are also present, polycystic ovary syndrome and other endocrine disorders of androgens can be present. Treatment required is topical 5% minoxidil lotion or oral finasteride (1 mg daily) help to arrest disease progression and may cause a small amount of regrowth, providing it is used early in disease but the treatment needs to be continued possibly lifelong. Approximately one-third of patients will not respond to either therapy. Finasteride is a selective inhibitor of  5-alpha-reductase type II and it can cause side-effects in 1% of patients such as loss of libido. It should not be used in females as it can affect the sexual development of a male fetus. However, antiandrogen therapy (e.g. cyproterone acetate or spironolactone) helps some women.

 

 

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Telogen effluvium: diffuse hair loss that occurs some 3 months after pregnancy or a severe illness. It occurs because ‘stress’ puts all the hairs into the telogen phase of hair shedding at the same time. The hair fully recovers and the normal staggered hair growth/hair shedding cycle resumes within a few months. Telogen effluvium is a transitory (2–4 months), generalised, diffuse hair loss over the scalp and an increased number of hairs in the resting phase of the growth cycle. It is associated with high fever, stress, malnutrition, surgery, oral contraceptives and following childbirth.

 

 

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Alopecia areata is defined as a loss of hair that leaves single or multiple, discrete, often round, areas of shiny baldness on the scalp (most common), in the beard area or any hair-bearing part of the body. A sign of disease activity is the presence of broken hairs at the advancing edge of the lesion that look like exclamation marks. These are very short hairs that taper and become depigmented when approaching the scalp – they are in the telogen (resting) phase. Nail dystrophy should always be looked for, which takes the form of very fine pitting and is much finer than psoriatic nail pitting. Alopecia areata is considered to be an autoimmune disease, mainly due to its association with other autoimmune diseases such as vitiligo, thyroid disease, pernicious anaemia, rheumatoid arthritis and diabetes, but no specific antibody has yet been identified. Approximately one-third of patients have a positive family history, implying that a genetic component is involved. Many patients experience hair regrowth within 9–12 months.  Alopecia areata is an immune-mediated type of hair loss. It is associated with other autoimmune diseases. It presents in childhood or young adults with patches of baldness. These may regrow to be followed by new patches of hair loss. The presence of broken exclamation mark hairs (narrow at the scalp/wider and more pigmented at the tip) at the edge of a bald area is diagnostic. Regrowth may initially be with white hairs and often occurs slowly over months. Occasionally all of the scalp hair is lost (alopecia totalis) and rarely all body hair is lost (alopecia universalis). The nails may be pitted or roughened. Treating the associated underlying autoimmune disease appears to have no positive effect on the alopecia. Steroids, 5% minoxidil, PUVA (psoralen–ultraviolet A) and contact allergen therapy may be useful and patient support groups are often beneficial. No scarring occurs with this form of hair loss.

 

 

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Trichotillomania is the self-inflicted pulling out of one’s hair. It is differentiated from alopecia areata by the patterns of irregular hair loss and the fact that growing hairs are always present: hairs cannot be extracted until they are long enough to be seen or caught hold of. Patches of hair loss tend to be unilateral and on the same side as the dominant hand. 

 

 

Scarring alopecia

• Discoid lupus erythematosus

• Kerion (tinea capitis)

• Lichen planus

• Dissecting cellulitis

• X-irradiation

• Idiopathic (‘pseudopelade’)

 

Discoid lupus erythematosus (DLE), lichen planus, scleroderma and radiodermatitis, in which the hair follicle is destroyed and signs of inflammation are present. The scalp is atrophic with absent hair follicles in the patches of hair loss and regrowth never occurs. DLE lesions comprise well-defined plaques of erythema with scaling, atrophy and follicular plugging, which affect light-exposed areas of the body and are exacerbated by sunlight.

 

 

 

 

Tinea capitis: both scaling and broken hairs are present in patients with fungal infections (tinea capitis). Fungal spores or hyphae are visible on microscopic examination of hair specimens.

Dissecting cellulitis: is a chronic folliculitis affecting predominantly young black males. It presents with papules and pustules over the occipital region of the scalp with hair loss. If severe, the back of the scalp becomes a boggy swelling (discharging pus) with areas of scarring alopecia. It can be complicated by keloid scar formation (‘acne keloidalis nuchae’). Treatment with prolonged courses of low-dose antibiotics, prolonged courses of isotretinoin and deep surgical excision can be used in recalcitrant cases.