Alopecia Areata

A Brief Description
Alopecia Areata, AA, is an autoimmune disorder that causes localized areas, or patches, of hair loss. (Alopecia is the medical term for hair loss, and areata is the medical term for patch).

In AA, the CD4 T cells (a type of lymphocyte), which normally have a protective role, attack hair follicles in a very localized area, or patch, on the scalp. The reason for this immune malfunction is not clear. Typically during the early onset of AA the affected scalp hair follicles shed rapidly, leaving a roundish bald spot(s).

Although AA is caused by lymphocytes attacking hair follicles, curiously, there are no visible signs of inflammation in the area of hair loss. In contrast, when lymphocytes attack hair follicles, in primary cicatricial alopecia (PCA), there is severe inflammation that causes scarring.

Exclamation point hairs can be seen in the affected area, indicating anagen effluvium hair loss, as well as other changes indicating telogen effluvium hair loss, (effluvium is the medical term for hair “shedding”)

Anagen efflivium occurs when hair follicles that are actively growing, (hair follicles in the anagen phase of the growth cycle), are exposed to a severe toxic, inflammatory or other insult. The rapidly dividing cells (germinal matrix cells undergoing mitotic activity surrounding the hair follicle papilla), that cause the hair shaft to lengthen are affected. A disruption of normal mitotic activity causes the lengthening hair shaft to become progressively narrow and very frail. Eventually the base of the hair is too narrow to support the hair strand; at that point the hairs can break off, and shed.

It would therefore appear that the offending T cells are targeting, to some degree, the actively dividing cells within the follicle germinal matrix.

AA Biopsy Findings
In the acute setting (i.e. early stage of the disease) Histopathology (i.e. skin biopsy findings) show lymphocytes surrounding the normal hair follicle bulb (i.e. the papilla area).

There is also an increase in telogen follicles, and in the more chronic stage there is progressively miniaturization, similar to Androgenetic Alopecia. There is no scarring or loss of follicular ostia (i.e. pores) as seen in Lymphocytic Primary Cicatricial Alopecia (PCA).

AA Cause
Like most autoimmune disorders the cause is not known. There appears to be some genetic factor or predisposition since 20% of affected people have a family member with Alopecia Areata, and identical twins have a 50% chance of their monozygotic sibling having AA. There is also an increased incidence of other autoimmune diseases in individuals with AA, as well as nail abnormalities and atopy. Atopy consists of asthma, allergic rhinnitis, and atopic dermatitis.

Alopecia Totalis
Alopecia Totalis (AT) is thought to be an advanced form of AA causing severe or complete hair loss, of the scalp and face.

Alopecia Universalis
Similar to AT, Alopecia Universalis (AU) is felt to be an extremely advanced form of autoimmune apolecia that is characterized by loss of hair, on the scalp, face, as well as loss of body hair.

Treatment Options
Treatment depends on multiple factors and should be tailored to each patients unique condition. Benefits from treatment can vary widely, especially when relapse is considered. Spontaneous regrowth does occur without treatment and there are reports of patients having spontaneous regrowth many years after the initial hair loss. Generally speaking around 50% of patients with moderate disease, will respond. The response is less in patients with more advanced disease, and usually much better in patients with mild disease.

Ninety percent of patients with a small patch of hair loss will have spontaneous regrowth within 2 years. Understandably, this group also responds well to most treatments. In contrast, early age of onset (i.e. less than 5 years old), nail abnormalities, atopy, advanced hair loss, such as AT or AU, indicate a poor prognosis and poor response to therapy.

Presently, there is no standard or FDA approved treatment for AA, AT, or AU. Treatments may include topical steroids, intralesional steroids (injected into affected area), topical minoxidil, topical anthralin, immunosuppressant drugs like, methotrexate and cyclosporin.

Some newer therapies may include diphenylcyclopropenone (DPCP), squaric acid dibutylester (SADBE), photodynamic therapy (PDT), cyclosporine in combination with methylprednisolone, JAK inhibitors, such as Tofacitinib, Ruxolitinib and others.

Please consult with your physician before considering any of the drugs or treatments discussed on this website