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It is a condition in which hair is lost from some or all areas of the body.
These patches can take many shapes, they are usually round or oval.
About 0.15% of people are affected at any one time, and 2% of people are affected at some point in time.
It results, oftentimes, in a few bald spots on the scalp.
The underlying skin is unscarred and looks superficially normal.
Different areas of the skin may exhibit hair loss and regrowth at the same time.
The area of hair loss may tingle or be mildly painful.
The hair tends to fall out over a short period of time, with the loss commonly occurring more on one side of the scalp than the other.
In most cases that begin with a small number of patches of hair loss, hair grows back after a few months to a year.
In patients with a greater number of patches, hair can either grow back or progress to alopecia areata totalis or, in rare cases, alopecia areata universalis.
Usual onset in childhood.
It is common in children.
- Females are affected at higher rates than males.
Alopecia areata most often affects the scalp and beard, but may occur on any part of the body with hair.
Causes-Autoimmune disorder: The underlying mechanism involves failure by the body to recognize its own cells, with subsequent immune-mediated destruction of the hair follicle.
Risk factors: Family history, female gender, rheumatoid arthritis, type 1 diabetes, celiac disease.
Patients also tend to have a slightly higher incidence of conditions related to the immune system, such as asthma, allergies, atopic dermatitis, and hypothyroidism.
Differential diagnosis: Trichotillomania, alopecia mucinosa, postpartum alopecia.
The diagnosis does not affect life expectancy, and patients are generally healthy.
Frequency about 2% of people in the US.
Most cases unassociated with an obvious trigger.
It is distinctive from the hair loss pattern among males.
Risk factors include a positive family history.
Alopecia areata is not contagious.
It occurs more frequently in people who have affected family members, suggesting heredity may be a factor.
Among identical twins, if one is affected, the other has about a 50% chance of also being affected.
There are, at least. four regions in the genome that are likely to contain associated genes.
AA shares genetic risk factors with other autoimmune diseases, including rheumatoid arthritis, type 1 diabetes, and celiac disease.
It may be the only manifestation of celiac disease.
There is immune-mediated destruction of the hair follicle.
Exclamation point hairs, narrowing along the length of the strand closer to the base, producing a characteristic appearance, are often present.
Exclamation point hairs are very short (3–4 mm), and can be seen surrounding the bald patches.
In cases of alopecia areata, hair tends to pull out more easily along the edge of the patch where the follicles are already affected by the body’s immune system than away from the patch where they are still healthy.
No cure for the condition is known.
In some cases, the hair regrows, and the condition does not reoccur, while in others, hair loss and regrowth occurs over years.
On individuals in whom all body hair is lost, fewer than 10% recover.
Nails may have pitting or trachyonychia.
In AA, the hair follicle is attacked by the immune system, with T-cells congregating at the roots, killing the follicle: resulting in baldness.
These T cell lymphocyte clusters occur around affected follicles, causing inflammation and subsequent hair loss.
AA, a systemic autoimmune disorder in which the body attacks anagen hair follicles and suppresses or stops hair growth.
Hair follicles normally state are kept secure from the immune system, by immune privilege., which is breached in alopecia areata.
Endogenous retinoids metabolic defect is a key part of the pathogenesis of the alopecia areata.
More than 129 single nucleotide polymorphisms have been identified that are associated with alopecia areata.
Genes that are identified include those involved in controlling the activation and proliferation of regulatory T cells, cytotoxic T lymphocyte-associated antigen 4, interleukin-2, interleukin-2 receptor A, and Eos as well as the human leukocyte antigen.
Two genes, PRDX5 and STX17, that are expressed in the hair follicle.
DIAGNOSIS: usually diagnosed based on clinical features.
Trichoscopy may aid in establishing the diagnosis,as it shows regularly distributed yellow dots of hyperkeratotic plugs, small exclamation-mark hairs, and black dots of destroyed hairs in the hair follicle opening.
Discrete areas of hair loss surrounded by exclamation mark hairs is sufficient for clinical diagnosis.
Reddening of the skin may also be present in the balding area.
Rarely, histologic confirmation is needed for the diagnosis: peribulbar lymphocytic infiltration, shift of anagen-to-telogen ratio towards telogen, and dilated follicular infundibulae, possibly pigment incontinence in the hair bulb and follicular stelae.
TREATMENT:
Treatment efficacy is very difficult and spontaneous remission is unpredictable, and hair may regrow spontaneously in many cases.
None of the existing therapeutic options are curative or preventive.
Limited success has been achieved by using corticosteroid injections, or cream.
Other medications that have been used are minoxidil, irritants (anthralin or topical coal tar), and topical immunotherapy cyclosporin, ruxolitinib.
Topical corticosteroids frequently fail to enter the skin deeply enough, and oral corticosteroids may decrease the hair loss, but only for the period during which they are taken.
No singular treatment is effective in all cases, and some patients may show no response to any treatment.
Alopecia areata associated with celiac disease treated with a gluten-free diet may allow for regrowth of scalp and other body hair in many people: Improvement is probably due to the normalization of the immune response as a result of gluten withdrawal from the diet.
Patients may also have aberrant nail formation because keratin forms both hair and nails.
Hair may grow back and then fall out again later.
Onset of alopecia areata before puberty predispose to chronic recurrence of the condition.
Patients may experience social phobia, anxiety, and depression.
Among identical twins, if one is affected, the other has about a 50% chance of also being affected.
Preliminary findings show that ruxolitinib restored hair growth in three individuals with long-standing and severe disease.
The oral Janus kinase (JAK) inhibitor baricitinib demonstrated efficacy and a higher rate of hair regrowth than placebo.
The FDA approved the first treatment for a type of hair loss in which the immune system attacks hair follicles, alopecia areata.
The drug, called baricitinib, was already approved for the treatment of another autoimmune disorder, rheumatoid arthritis.
It works by inhibiting the activity of enzymes known as Janus kinases, which in turn may block some of the molecular signals that cause autoimmune disease.
In clinical trials, the drug was better than placebo at promoting hair regrowth in people with severe alopecia areata.