What is Alopecia Areata?

Alopecia areata (AA) is a non-scarring alopecia that can appear in a patchy, confluent, or diffuse form. Hair loss may occur in part or all portions of the body, with the scalp being the most affected. The illness can spread to the entire scalp (Alopecia totalis) or the entire epidermis in 1–2% of instances (Alopecia universalis). Men and women are equally affected by AA, which has a reported incidence of 0.1–0.2% and a lifetime risk of 1.7 percent (Safavi et al., 1995).

 

For years, the genesis of AA has eluded experts, and as a result, a plethora of correlations have been hypothesised by trichologists.

 

The incidence of AA in conjunction with other autoimmune conditions such as vitiligo, lichen planus, morphea, atopic dermatitis, Hashimoto’s thyroiditis, pernicious anaemia, and diabetes mellitus supports this viewpoint (Brenner, 1979). It has recently been revealed that inpatients with AA had a high prevalence of mood, adjustment, depressive, and anxiety disorders.

 

This aspect of psychiatric illness has been commonly attributed to AA as both a cause and a consequence. As a result, in the treatment of such individuals, a multifaceted strategy is recommended. Though corti-costeroids have been the cornerstone of treatment, a wide range of evidence-based treatments for the treatment of AA have emerged. The current study aims to analyse the various features of alopecia areata’s natural history as well as the benefits and drawbacks of various treatment options.

 

What is Alopecia Areata?

Alopecia areata is a condition in which hair falls off in small, undetectable spots. These patches may, however, join and become visible. When the immune system targets the hair follicles, hair loss occurs.

 

Sudden hair loss can happen anywhere on the body, including the scalp, brows, eyelashes, and face. It might sometimes take years to develop and reoccur.

 

Alopecia universalis is a disorder that causes total hair loss and prevents hair growth. It’s possible that hair will fall out again when it grows back. Hair loss and regeneration differs in intensity from person to person.

 

 

  1. Hair Loss Dynamics

 

Hair follicle development happens in cycles. A long growing phase (anagen), a short transitional phase (catagen), and a short resting phase comprise each cycle (telogen). The hair falls out (exogen) at the conclusion of the resting period, and a new hair begins to develop from the follicle, restarting the cycle. The lengths of the three stages differ significantly, with the duration of the anagen affecting the type of hair generated, particularly its length.

 

Each day, around 100 strands of hair reach the end of their resting phase and fall out (Trueb, 2010). Hair loss in non-scarring alopecias, such as alopecia areata, is fundamentally a hair follicle cycle condition. An unidentified trigger is thought to induce an autoimmune lymphocyte attack on the hair bulb in AA. Anagen hairs are affected by this inflammation, which causes anagen hairs to stop growing.

 

Anagen effluvium (abnormal loss of anagen hairs) is clinically identified as dystrophic anagen hair with tapered proximal ends and no root sheaths when the growing phase is disrupted (anagen arrest). Telogen Effluvium is a related but different condition that affects many women.

 

This is an umbrella term for a variety of disorders in which the affected hairs suffer a rapid transition from anagen to telogen (anegan release), clinically manifested as localised telogen shedding and morphologically identified as hair with a depigmented bulb.

 

Etiopathogenesis

The aetiology of AA has shifted significantly over time, with several schools of thought assigning various etiologies to the disorder (Fig. 2). In the late 1970s, a viral aetiology was hypothesised, but further studies have shown that there is no link. Yang et al. discovered that 8.4% of patients had a positive family history of AA, indicating a polygenic additive mode of inheritance.

 

It is now widely assumed that AA is an organ-specific autoimmune disease with a hereditary predisposition and a trigger in the environment. There has been evidence of a link between AA and the human leukocyte antigen (HLA). HLA-A1, HLA-B62, HLA-DQ1, and HLADQ3 were found in patients with AA, according to Kavak et al (Ay Se et al.,2000). In the recent past, HLA-A1, HLA-B62, HLA-DQ1, and HLADQ3 were found in AA individuals (Ay Se et al.,2000). Barahmani et al. recently demonstrated in the United States that AA is associated with a non-HLA molecule containing the major histocompatibility complex class I chain-related gene A (MICA).

 

It could be a candidate gene and a component of an extended HLA haplotype that contributes to the vulnerability and severity of this condition (Barahmani et al.,2006). Antigens are presented to CD8+T cells via HLA class I molecules, which are found on nearly all nucleated cells including platelets.

 

HLA class II molecules are divided into three subclasses (DR, DQ, and DP) and are found on immune cells such as B cells, activated T cells, macrophages, keratinocytes, and dendritic cells, where they present peptides to CD4+ T cells.

 

Causes of Alopecia Areata

 

When white blood cells attack the cells in hair follicles, causing them to shrink and hair growth to plummet. It’s unclear what sets off the immune system’s assault on hair follicles.

 

While the cause of these changes is unknown, it appears that genetics have a role since alopecia areata is more common among people with a family member who has the disease. One in every five persons with alopecia areata has a family member who suffers from the disease.

 

According to further research, many people with a family history of alopecia areata have a personal or family history of other autoimmune diseases, such as atopy, which is characterized by an inclination to scratch.

 

Stress isn’t the cause of alopecia areata, according to popular belief. Extreme stress may be a trigger for the condition, but most recent research points to a genetic causation.

 

 

 

Treatment of Alopecia Areata

 

Alopecia areata is not curable, however it can be treated and hair can regrow. Alopecia is frequently treated using medications that are also used to treat other disorders. Alopecia areata can be treated in a variety of ways, including:

 

Anti-inflammatory medications called corticosteroids are commonly used to treat autoimmune illnesses. Corticosteroids can be injected into the scalp or other regions, taken orally (as a pill), or administered topically (as an ointment, cream, or foam) to the skin. It is possible that a patient’s response to therapy will be gradual.

 

Rogaine ® (minoxidil) is a topical medication that is already used to treat pattern baldness. Rogaine treatment normally takes about 12 weeks before hair starts to grow.

 

Other treatments used to treat alopecia include psoriasis medications and topical sensitizers, which have varied degrees of success (drugs that are applied to the skin and cause an allergic reaction that can cause hair growth).

 

Aside from pharmacological treatments, patients with alopecia might try a variety of aesthetic and defensive techniques. These are some of them:

 

  1. Makeup can be used to conceal or decrease hair loss.

 

  1. Protect your eyes from the sun and the surroundings by wearing sunglasses (if there is loss of eyelashes).

 

  1. Protect the head from the weather by using wigs, hats, or scarves.

 

4.Consume a healthy, well-balanced diet. Hair growth is a process that is reliant on vitamins and minerals. Hair loss is common among people who follow fad diets (although not specifically related to alopecia areata.)

 

5.Reduce your stress levels. Many persons with new onset alopecia areata have had recent stresses in their lives, including work, family, deaths, surgeries, accidents, and so on, despite the fact that this has never been confirmed by big trials and examinations.

 

Diagnosis of Alopecia Areata

After weeks or months of shock, fear, and perplexity, a dermatologist’s diagnosis of alopecia are frequently the result of considerable time.

The disease’s slow hair loss is signified by a bald patch that feels when putting hair up, odd quantities of hair on a pillow, clumps of hair clogging the shower drain, or a comment made by a hairdresser.

Although no two alopecia areata cases are alike, the discovery of hair loss and the disease’s diagnosis may cause individuals to feel similar sentiments.

The majority of persons who suffer from alopecia areata have patchy alopecia areata, which causes hair loss in patches that return without therapy.

The NAAF, on the other hand, understands the worry that comes with any sort of hair loss and offers treatments to fit the needs of all alopecia areata patients.

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