Alopecia areata in all of its forms is a complex type of hair loss that is distinctly different from androgenetic alopecia, also known as male pattern baldness, which develops with age.
Alopecia areata is an autoimmune skin disease that can cause hair loss, usually in patches, on the scalp, face, as well as other parts of the body, most commonly starting in childhood.
In the United States roughly 6.6 million men, women and children of all races will experience the onset of alopecia areata at some point during their lifetime. While this disease is not physically disabling, patients and their families can suffer from anxiety, depression, anger, guilt and shame.
At Armani Medical our one and only mission it to improve the lives of our patients. If you think your hair is thinning, no matter the location or pattern, we urge you to seek medical attention to identify the cause and rule out other health conditions. For a comprehensive and confidential assessment call Dr. Abraham Armani MD today at his Dallas office at (972) 2- ARMANI.
What is Alopecia Areata?
The visible symptoms of this cyclical disease most commonly begin when the patient loses hair in small round patches on the scalp, but hair loss can occur anywhere on the body that grows hair. While Alopecia areata can be triggered by viruses, stress, metabolic or endocrine disorders, and even nutritional deficiencies, it often occurs in otherwise healthy patients. The three types alopecia areata are:
- Alopecia Areata Patchy – Most common form, patches of baldness typically on the scalp
- Alopecia Areata Totalis – Rare form, total hair loss on the scalp
- Alopecia Areata Universalis – Rarest form, total hair loss over the scalp and body
While this may feel quite staggering, the good news is that while the hair follicles have minimized and stopped producing hair, most affected follicles have not actually died. That means the hair may grow back, with or without treatment, and sometimes many years after the hair loss first occurred.
Causes
Alopecia areata is an autoimmune disease, which means the white blood cells, which we know attack viruses and other maladies, turn their attention to assailing hair follicles that have lost their “immune privilege.” The follicles go into a defensive resting state, minimize, and stop or slow down the production of hair, but they usually do not die.
Researchers have determined that Alopecia areata is an inherited polygenic disease, with links to at least eight genes. Studies examining alopecia areata in twins have also shown that possessing the genes alone does not predetermine the onset of alopecia areata. Rather genetic predisposition and triggers, like those mentioned above, must both be present at the same time for the collapse of immune privilege and the disease to develop. It is believed other environmental factors may also trigger the disease, but that aspect has yet to be fully explored.
Methods of treatment
At this time the Food and Drug Administration (FDA) has not approved any method or medication to specifically treat any of the three types of alopecia areata. There are, however, a number of pharmaceutical treatments that have shown promise, but have produced inconsistent results.
Additionally, methods of treatment also vary according to the specific type of alopecia areata and the severity of the disease. These medications are injected, taken orally, or applied topically, and include corticosteroids, minoxidil (Rogaine®), anthralin, and immunotherapy.
It is extremely rare for alopecia areata to be treated surgically, and is not recommended. In July 2015 the FDA announced that it selected alopecia areata for the Patient-Focused Drug Development Initiative (PFDDI), which means the administration will research the efficacy of the treatments mentioned above, with a focus on the patient perspective.
Experiencing hair loss? Dr. Armani is a nationally recognized hair restoration expert who has won the Patients Choice Award five years in a row. Find out what treatments are available by making an appointment today by calling (972) 2- ARMANI.