Hair loss may be present in the family, highlighting genetic causes. Causes
Causes of noncicatricial alopecia can be separated based on focal or diffuse hair loss:Diffuse:

Androgenetic alopecia: androgenic DHT leads to catagenic miniaturization of hair follicles. Diffuse alopecia areata: diffuse autoimmune destruction of hair follicles
Alopecia totalis: unknown but thought to be autoimmune
Telogen effluvium: emotional or physiologic stress
Anagen effluvium: cancer treatments such as radiation and alkylating agents
Dermatopathia pigmentosa reticularis: genetic autosomal dominant conditionFocal:

Alopecia areata: autoimmune destruction of hair follicles
Tinea capitis: fungal infection
Traction alopecia: pulling force applied to hair
Trichotillomania (Trichotillosis)

Diagnosis
There are a number of conditions that may cause non scarring hair loss and the first step is to determine the pattern: focal or diffuse. The next step is to identify if the hair loss is scarring or non scarring. A history and physical examination is necessary as this will provide clues to the ultimate diagnosis. It is essential to ask about the onset, observed pattern, hairstyles, family history, diet, and social history.Diffuse:

Androgenetic alopecia: history of gradual thinning of hair and characteristic pattern. Males start to lose hair in the front and temples while females lose hair at the top of the head
Diffuse alopecia areata: exclamation point hairs
Alopecia totalis: concomitant loss of facial and skull hair
Telogen effluvium: history of emotional or physiologic stress
Anagen effluvium: history cancer treatments such as radiation and alkylating agents
Dermatopathia pigmentosa reticularis: genetic autosomal dominant conditionFocal:

Alopecia areata: smooth and round lesions
Tinea capitis: black dots with broken hair strands, may see red, scaly lesions and swollen lymph nodes on the back of head.
Recently, evidence of hepatitis C infection has been reported in the majority of mixed disease cases with rates being 70-90% in areas with high incidences of hepatitis C. The most effective therapy for hepatitis C-associated cryoglobulinemic disease consists of a combination of anti-viral drugs, pegylated INFα and ribavirin; depletion of B cells using rituximab in combination with antiviral therapy or used alone in patients refractory to antiviral therapy has also proven successful in treating the hepatitis C-associated disease. Data on the treatment of infectious causes other than hepatitis C for the mixed disease are limited. A current recommendation treats the underlying disease with appropriate antiviral, anti-bacterial, or anti-fungal agents, if available; in cases refractory to an appropriate drug, the addition of immunosuppressive drugs to the therapeutic regimen may improve results. Mixed cryoglobulinemic disease associated with autoimmune disorders is treated with immunosuppressive drugs: combination of a corticosteroid with either cyclophosphamide, azathioprine, or mycophenolate or combination of a corticosteroid with rituximab have been used successfully to treated mixed disease associated with autoimmune disorders. See also
Cryofibrinogenemia
Cryoglobulinemic purpura
Cryoglobulinemic vasculitis
Dysfibrinogenemia
Hematopoietic ulcer
Hyperviscosity syndrome
Paraproteinemia
Plasma cell dyscrasias

References


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