1. What is Alopecia Areata?
Alopecia areata is a disease that affects hair follicles, resulting in the usually non-permanent loss of hair in distinct round or oval areas about the size of a quarter, without any evident inflammation of the affected skin or scalp. Most cases involve a few patches of hair loss to the scalp; some involve a larger number, and rarely, the disease causes full hair loss on the head (alopecia totalis), face, and body (alopecia universalis).
2. What Does Alopecia Areata Look Like?
Alopecia areata appears as patches of normal, bare skin in places where hair once grew; each patch usually approximating the size of a quarter. The skin usually does not appear inflamed, swollen, or red, and no itching or pain is involved. “Exclamation-point” hairs may be seen at the margin of the patch. These are broken, short hairs that taper at the base. Pulling slightly on these hairs causes them to fall out. In some cases, patches of alopecia may spontaneously grow back, while new patches may form in other unaffected areas. As the disease varies from person to person, there is no way of indicating whether or not hair will grow back, or whether other patches will continue to form.
3. Who Does Alopecia Areata Affect?
Alopecia areata is a very common disease that affects about one percent of the population at least once in their lifetime. It most commonly affects children and young adults under the age of 25, and is seen equally among males and females, except in certain countries (Italy and Spain) where it is seen twice as much among females than males. Regrowth to the bare patches does often occur, and 80 percent of persons with alopecia beginning after puberty will eventually regrow hair at some later point in life. However, to alleviate the social burden and anxiety associated with this condition, individuals often seek to manage their condition immediately through a variety of available treatments, many of which have proven to be effective.
4. What Causes Alopecia Areata?
The actual cause of alopecia areata is yet unknown. However, it is understood that alopecia is an autoimmune disease in which the immune system mistakenly attacks some part of the body as if it were foreign. In alopecia, this attack is specifically targeted toward the hair follicles. Genetic factors seem to play an important role since there is a higher frequency of a family history of alopecia areata in people who are affected.
5. What Triggers Alopecia Areata?
Alopecia areata has been reported to follow sudden, prolonged, or excessive stress, physical or psychological trauma, post-surgery, bereavement, nervous breakdown, or even financial crisis. While research has shown that these and other stress factors may trigger the condition, it is nearly impossible to predict or prevent future alopecia events or remissions. In active episodes of alopecia areata, an unknown phenomenon causes all the hairs in a certain area to enter the telogen or catagen stage at the same time, and the hairs fall out.
6. How Can My Alopecia Areata Be Treated?
Although no cure for alopecia areata is currently available, treatments do exist that are effective in stimulating varied amounts of regrowth for some individuals. Topical steroid creams or oral steroid medications may be prescribed to help decrease the autoimmune response and stimulate hair regrowth. In addition, steroid injection to alopecia patches may be temporarily very effective. Newer approaches also include topical retinoid therapy and topical minoxidil (trade name: Rogaine). This treatment has shown cosmetically acceptable results in 30% of cases. Minoxidil does not stop the disease process so stopping applications after hair has started to grow back may cause the hair to fall out again. A combined treatment called PUVA (Psoralen plus UVA light) involving medication and UVA light therapy to the alopecia patch may also be effective for some individuals. For more information on these treatments for alopecia areata, or to schedule a visit, please call and speak with a representative at the Berman Skin Institute.