Alopecia
Catherine S. Zorc
INTRODUCTION
Tinea capitis, trichotillomania, alopecia areata, and telogen effluvium account for >95% of cases of alopecia in children. The growth cycle of hair consists of an active growth phase (anagen), a transition phase (catagen), and a resting phase (telogen). After the telogen phase, the hair is shed and replaced by a new anagen bulb. On a normal scalp, approximately 85% to 90% of the hair is in the anagen phase. There are 100,000 hairs on the normal scalp. Hair loss is only clinically apparent when a person has lost 25% to 50% of his hair.
DIFFERENTIAL DIAGNOSIS LISTInfectious Causes
Tinea capitis
Secondary syphilis
Toxic Causes
Cytotoxic agents
Anticonvulsants
Radiation
Hypervitaminosis A
Anticoagulants
Neoplastic Causes
Histiocytosis
Traumatic Causes
Trichotillomania
Traction alopecia
Friction alopecia
Congenital Causes
Aplasia cutis congenita
Nevus sebaceous
Epidermal nevus
Hemangioma
Loose anagen syndrome
Ectodermal dysplasia
Hair shaft defects
Metabolic or Genetic Causes
Androgenic alopecia
Acrodermatitis enteropathica
Anorexia nervosa
Malnutrition
Hypo- or hyperthyroidism
Hypopituitarism
Diabetes mellitus
Inflammatory Causes
Alopecia areata
Systemic lupus erythematosus
Scleroderma
Miscellaneous Causes
Atopic dermatitis
Seborrheic dermatitis
Psoriasis
Telogen effluvium
Anagen effluvium
DIFFERENTIAL DIAGNOSIS DISCUSSION
Tinea Capitis
Etiology
Caused by dermatophyte infection of the scalp hairs, tinea capitis is responsible for <50% of cases of hair loss in children. Currently, the most prevalent fungus causing tinea capitis is Trichophyton tonsurans in the United States.
Clinical Features
Tinea capitis is seen most commonly in school-aged children. The infection causes patchy hair loss that may or may not be accompanied by scale. Some areas may seem completely bald and indistinguishable from alopecia areata, but on closer examination the scalp contains very short hairs, called “ black-dot” tinea capitis. There may be posterior cervical or occipital lymphadenopathy.
Evaluation
Unlike Microsporum canis, which caused epidemic outbreaks of tinea capitis during the 1940s, T. tonsurans does not show immunofluorescence under Wood lamp examination. Diagnosis can be confirmed using a potassium hydroxide (KOH) preparation and by fungal culture of the hair and scale. A KOH preparation reveals organisms inside the hair shaft.
Treatment
Oral griseofulvin dosed at 20 to 25 mg/kg/day microsize (or 10 to 15 mg/kg/day ultramicrosize) once daily for 6 to 8 weeks is the standard therapy for tinea capitis in children. It is best absorbed when taken with fatty foods. The medication is safe in children; it is not necessary for the patient to undergo laboratory testing before initiating drug therapy. Newer antifungal medications such as fluconazole, itraconazole, and terbinafine may also be effective and require a shorter course of therapy. An antifungal or selenium shampoo may hasten resolution in combination with systemic antifungal medication. An effort should be made to identify and treat infected household contacts to avoid reinfection.
HINT: The infection may be accompanied by a hypersensitivity reaction called a “kerion,” which is a boggy, inflammatory mass. The surface may contain pustules, and cervical lymphadenopathy is usually present. Although it may appear to be superinfected, the lesion can usually be treated successfully with griseofulvin and oral prednisone.
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