Hair complaints

ALOPECIA
The two major forms of alopecia are
1. scarring and
2. nonscarring.

Scarring alopecia is associated with
1. fibrosis,
2. inflammation, and
3. loss of hair follicles.

A smooth scalp with a decreased number of follicular openings is usually observed clinically, but in some patients, the changes are seen only in biopsy specimens from affected areas.

In nonscarring alopecia, the hair shafts are absent or miniaturized, but the hair follicles are preserved, explaining the reversible nature of nonscarring alopecia.

In women with androgenetic alopecia, an elevation in circulating levels of androgens may be seen as a result of ovarian or adrenal gland dysfunction or neoplasm. When there are signs of virilization, such as a deepened voice and enlarged clitoris, the possibility of an ovarian or adrenal gland tumor should be considered.

Exposure to various drugs can also cause diffuse hair loss, usually by inducing a telogen effluvium. An exception is the anagen effluvium observed with antimitotic agents such as daunorubicin.

Alopecia is a side effect of the following drugs: warfarin, heparin, propylthiouracil, carbimazole, isotretinoin, acitretin, lithium, beta blockers, interferons, colchicine, and amphetamines.
Less commonly, nonscarring alopecia is associated with lupus erythematosus and secondary syphilis.

In systemic lupus there are two forms of alopecia
1. scarring secondary to discoid lesions
2. nonscarring.

The latter form coincides with flares of systemic disease and may involve the entire scalp or just the frontal scalp, with the appearance of multiple short hairs (“lupus hairs”) as a sign of initial regrowth. Scattered, poorly circumscribed patches of alopecia with a “moth-eaten” appearance are a manifestation of the secondary stage of syphilis. Diffuse thinning of the hair is also associated with hypothyroidism and hyperthyroidism.

Scarring alopecia is more frequently the result of a primary cutaneous
disorder such as lichen planus, folliculitis decalvans, chronic cutaneous (discoid) lupus, or linear scleroderma (morphea) than it is a sign of systemic disease. Although the scarring lesions of discoid lupus can be seen in patients with systemic lupus, in the majority of patients, the disease process is limited to the skin. Less common causes of scarring alopecia include sarcoidosis (see “Papulonodular Skin Lesions,” below) and cutaneous metastases.

In the early phases of discoid lupus, lichen planus, and folliculitis
decalvans, there are circumscribed areas of alopecia. Fibrosis and
subsequent loss of hair follicles are observed primarily in the center
of these alopecic patches, whereas the inflammatory process is most
prominent at the periphery. The areas of active inflammation in discoid lupus are erythematous with scale, whereas the areas of previous inflammation are often hypopigmented with a rim of hyperpigmentation.

Different Non-scarring Alopecia
1. Telogen effluvium
Diffuse shedding of normal hairs. Follows major stress (high fever, severe infection) or change in hormone levels (postpartum). Reversible without treatment. Stress causes more of the asynchronous growth cycles of individual hairs to become synchronous; therefore, larger numbers of growing (anagen) hairs simultaneously enter the dying (telogen) phase. Observation; discontinue any drugs that have alopecia as a side effect; must exclude underlying metabolic causes, e.g., hypothyroidism, hyperthyroidism.

2. Androgenetic alopecia (male pattern; female pattern)
Miniaturization of hairs along the midline of the scalp. Recession of the anterior scalp line in men and some women. Increased sensitivity of affected hairs to the effects of androgens. Increased levels of circulating androgens (ovarian or adrenal source in women)

3. Alopecia areata
Well-circumscribed, circular areas of hair loss, 2–5 cm in diameter. In extensive cases, coalescence of lesions and/or involvement of other hair-bearing surfaces of the body. Pitting or sandpapered appearance of the nails. The germinative zones of the hair follicles are surrounded by T lymphocytes. Occasional associated diseases: hyperthyroidism, hypothyroidism, vitiligo, Down syndrome

4. Tinea capitis
Varies from scaling with minimal hair loss to discrete patches with “black dots” (broken infected hairs) to boggy plaque with pustules (kerion). Invasion of hairs by dermatophytes, most commonly Trichophyton tonsurans.



5. Traumatic alopecia
Broken hairs, often of varying lengths. Irregular outline. Traction with curlers, rubber bands, braiding. Exposure to heat or chemicals (e.g., hair straighteners) Mechanical pulling (trichotillomania). Discontinuation of offending hair style or chemical treatments; diagnosis of trichotillomania may require observation of shaved hairs (for growth) or biopsy, possibly followed by psychotherapy.