HAIR DISORDERS
Hair-follicle is a cup-like invagination of epidermis into dermis, present all over skin except over palm and soles. Human hair consists of a bulbous root at the bottom of hair follicle and a keratinized shaft.
Hair growth is cyclical, with a growing phase (anagens) and resting phase (telogens). Hair follicles, if destroyed, can't regenerate again. Androgens are major determinant of secondary hair growth during puberty.Hair abnormalities may be intrinsic or secondary to inflammatory dermatosis, biochemical/metabolic or endocrinal defects or traction trauma.
Hypertrichosis (excess hair growth) or Hirsutism, i.e. androgenic hair pattern in females, may be due to: (a) familial tendency, (b) endocrinal disorders, e.g. Cushing syndrome, virilizing tumors, (c) drugs: steroids, minoxidil, etc. or (d) genetic errors, e.g. mucopolysaccharidoses. Local hypertrichosis (tuft of hair) is seen in spina bifida occulta or hairy nevi.
Alopecia (hair loss) or hypotrichosis (deficient hair growth) may be partial or total, due to many factors (Table 25.12). True familial alopecia is rare in children. Mechanical alopecia in children includes Traction alopecia (due to tight braids, head-bands or curlers), Pressure alopecia (due to constant pressure in bed-ridden patients or normal infants) and trichotillomania.
Alopecia areata denotes rapid or complete loss of hair in round/oval patches over scalp, though rare variants include alopecia totalis (complete hair loss over scalp) or
| TABLE 25.12: Causes of Alopecia* in children | ||
| • | Familial | Usually in males |
| • | Mechanical | Traction/pressure alopecia |
| Trichotillomania | ||
| • | Toxic | Chemo/radiotherapy |
| • | Nutritional | PEM, zinc deficiency, Vit. A excess |
| • | Hereditary | MKHS, cartilage-hair dysplasia |
| • | Inflammatory | T. captis, atopic eczema |
| • | Autoimmune | Alopecia areata, SLE |
| • | Structural defects | Trichorrhexis, pili torti |
*Or abnormally sparse, brittle and hypopigmented hair MKHS: Menkes-Kinky-Hair syndrome.
alopecia universalis (complete hair loss over scalp and body). Nearly 60% cases are children and adolescents lt; 20 years of age.
Exact etiology is unknown, though it has been found to be associated with emotional stress, similar family history, Down syndrome and autoimmune disorders.
Treatment is often ineffective, though topical steroids or topical minoxidil may be used in localized lesions. Extensive lesions may benefit from oral steroids or PUVA therapy.
Prognosis is unpredictable but spontaneous resolution may occur after 6-12 months in mild cases.
Trichotillomania is characterized by compulsive pulling, twisting or breaking of hairs, usually in mentally retarded or psychiatrically abnormal (obsessive-compulsive neurosis) children, leading to irregular and incomplete hair loss mostly in parietal region. Trichobezoar, i.e. accumulation of hairs in stomach is common in these cases.
Intrinsic structural defects of hair mainly include Trichorrhexis nodosa, i.e. dry, brittle, lustreless hair with multiple fractures of hair shaft presenting as grayish white nodes on shaft due to a congenital defect or wrong combing technique; and Pili torti, i.e. spangled, brittle and coarse hair of different length over entire scalp.
Menkes-kinky-hair syndrome, a rare x-linked recessive disorder of copper metabolism is characterized by short, fine, brittle, light-colored hair along with progressive psychomotor retardation and hypopigmented skin.
25.11.2