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alopecia areata

What is alopecia areata

Alopecia areata is also called autoimmune alopecia or autoimmune hair loss, is a common autoimmune skin disease, where  your body’s immune system attacks your hair cells, causing hair loss on the scalp, face and sometimes on other areas of your body 1. The term “alopecia” means hair loss and “areata” refers to the patchy nature of the hair loss that is typically seen with alopecia areata. Alopecia areata represent an attack on the hair roots by the body’s own immune system. The hair loss can be total (including facial hair such as the eyelashes and eyebrows) or partial, resulting in a bald spot. Any disorder in which the body attacks its own cells is called an autoimmune disorder, and alopecia areata is an example of this kind of disorder. Alopecia areata affects people of all ages, both sexes and all ethnic groups can develop alopecia areata. Approximately 20% of affected patients are children 2. Alopecia areata affects as many as 6.8 million people in the U.S. with a lifetime risk of 2.1% 3. Alopecia areata affects 0.1–0.2% of the population worldwide 4. Alopecia areata often first appears suddenly during childhood and young adults with one or more round bald patches appear suddenly, most often on the scalp, but it can be different for everyone who has it. Alopecia areata’s manifestations vary, from a well-defined alopecic patch, multiple patches, total scalp alopecia (alopecia totalis), to complete body hair loss (alopecia universalis) 5. The hair loss associated with alopecia areata is not painful or disabling. However, alopecia areata impacts quality of life because it causes changes in a person’s appearance and has major psychological effects for men and women, especially in social acceptance and psychological well-being 6. In some people, alopecia areata can lead to depression, anxiety, and other emotional or psychological issues. The good news is that with alopecia areata, your hair follicles remain alive and hair can regrow at any time and those affected by alopecia areata sometimes experience regrowth of their hair. Hairs that do grow back often lack color or may be either temporarily or permanently white. This hypopigmentation is not seen in other forms of alopecia.

People with mild early alopecia areata may need no treatment, as their hair is likely to come back anyway without it. Some treatments can induce hair growth, though none is able to alter the overall course of the disease. Any treatments that carry serious risks should be avoided, as alopecia areata itself has no adverse effect on physical health. Alopecia areata treatment for adults with less than 50% of scalp involvement is intralesional triamcinolone acetonide injected intradermally using a 0.5-inch, 30-gauge needle 7. Maximal volume is 3 mL per session 8. Treatment may be repeated every four to six weeks until resolution or for a maximum of six months. Local adverse effects include transient atrophy and telangiectasia.

Other therapies for the treatment of alopecia areata include topical mid- to high-potency corticosteroids, minoxidil, anthralin, immunotherapy (squaric acid dibutylester [SADBE] and diphenylcyclopropenone [diphencyprone, DPCP]), and systemic corticosteroids 9. Currently available therapies often yield unsatisfactory results, and some clinicians rely on the high rate of spontaneous remission or recommend a hairpiece or wig if remission does not occur 10.

Key facts

  • Alopecia areata is the third most common cause of hair loss. Hair loss occurs over a period of weeks. The hair usually grows back after several months, although it may fall out again. In some cases, unpredictable cycles of hair loss followed by regrowth can last for years. In addition to hair loss, some affected individuals have fingernail and toenail abnormalities, such as pits on the surface of the nails.
  • The lifetime risk in the general population is 1.7%.
  • Alopecia areata represents a T-cell-mediated immune attack on the hair causing bald spots.
  • The target allergen is related to melanin. Thus, patients with both black and white hair can preferentially loose the dark hair.
  • About half of patients have onset of the alopecia before 15 years of age.
  • About 10% of patients have nail changes including pitting, trachyonychia, and longitudinal ridging.
  • A study of treatment with intralesional steroid Kenalog (triamcinolone acetonide) concentration showed 2.5 mg/mL to be just as effective as 5 or 10 mg/mL.
  • Many studies have found Vitamin D levels to be lower in alopecia areata patients compared to controls.

Figure 1. Alopecia areata

alopecia areata

Figure 2. Alopecia areata in children (hair loss involving the eyebrows and eyelashes)

alopecia areata in children

Physiology of hair growth

The scalp contains, on average, 100,000 hairs 11. You lose up to 100 hairs from your scalp every day. That’s normal, and in most people, those hairs grow back. A hair shaft grows within a hair follicle at a rate of about 1 – 1.5 cm per month. It is due to cell division within the hair bulb at the base of the hair follicle. The cells produce the three layers of the hair shaft (medulla, cortex, cuticle), which are mainly made of the protein keratin (which is also the main structure of skin and nails). Hair growth follows a cycle and the hair growth cycle is divided into three phases: anagen (active growing stage, about 90 % of hairs), catagen (degeneration stage, less than 10% of hairs) and telogen (resting stage, 5% to 10% of hairs). Hair is shed during the telogen phase. When telogen hairs are shed, new anagen hairs grow to replace them, beginning a new cycle 12, 13. These phases are not synchronized, and any hair may be at a particular phase at random. Hair length depends on the duration of anagen. Short hairs (eyelashes, eyebrows, hair on arms and legs) have a short anagen phase of around one month. Anagen lasts up to 6 years or longer in scalp hair. In addition to the ratio of anagen hair to telogen hair, the diameter of the hair follicles determines scalp coverage. Vellus hairs have a hair-shaft diameter of less than 0.03 mm, whereas terminal hairs have a diameter greater than 0.06 mm. The optimal hairs for scalp-hair growth and scalp coverage are anagen and terminal hairs.

Timespan of the hair growth cycle

  • The anagen phase constitutes about 90% (1000 days or more) of the growth cycle. Anagen hairs are anchored deeply into the subcutaneous fat and cannot be pulled out easily.
  • The catagen phase (10 days) and telogen phase (100 days) constitute only 10% of the hair growth cycle.
  • During the catagen and telogen phase of the hair growth cycle, as hairs are at the shedding and rest-from-growth period, no bald spots are shown as hairs are randomly distributed over the scalp.

Anagen (active growing stage, about 90 % of hairs) stage

Your hair grows around 1 – 1.5 cm per month, faster in summer than in winter.

  • The anagen stage is the growing period of a hair follicle.
  • This stage typically lasts about 3 to 5 years. Asian hair can last 5-7 years
  • Full length hair can be upto 100 cm long

Catagen (degeneration stage, less than 10% of hairs) stage

At the end of the anagen phase, your hair enters the catagen phase.

The catagen stage is the intermediate period of hair growth.

  • Hair follicles prepare themselves for the resting phase.
  • It lasts around 1-2 weeks.
  • During this phase, the deeper portions of the hair follicles start to collapse.

Telogen (resting stage, 5% to 10% of hairs) stage

During the telogen phase each hair is released and falls out

  • The telogen stage is the resting and shedding period of the hair cycle.
  • The follicle remains inactive for 3 to 4 months.
  • At the end of this period, older hairs that have finished their life will fall out and newer hairs will begin to grow.
  • As compared with anagen hair, telogen hair is located higher in the skin and can be pulled out relatively easily. Normally, the scalp loses approximately 100 telogen hairs per day.

Hair loss, hair thinning and problems with hairgrowth occur when the growth cycle is interrupted/disrupted. This can be triggered by conditions such as nutritional and medical situations, illness or stress. For instance 6 weeks after intensive dieting or stress you can experience hair loss. This occurs because the growing stage (Anagen) is cut short and hairs enter the falling (Telogen) stage at the same time.

Figure 3. Hair growth cycle

hair growth cycle

Types of alopecia areata

Alopecia areata most commonly begins as isolated patchy hair loss, usually in one or more coin-sized (usually round or oval) patches on the scalp or other places on the body that grow hair — such as the beard, eyebrows, eyelashes or extremities (arms, legs, hands and feet).

  • Patchy alopecia areata: Patchy alopecia areata is the form with one or more coin-sized (usually round or oval) patches on the scalp or other places on the body that grow hair. This type may convert into either alopecia totalis (hair loss across the entire scalp) or alopecia universalis (hair loss across the entire body), but most commonly it remains patchy.
  • Persistent patchy alopecia areata: Persistent patchy alopecia areata is characterized by patchy scalp hair loss that continues over a long period of time without ever developing into extensive alopecia areata such as totalis or universalis.
  • Alopecia totalis: total or near-total loss of hair on the scalp.
  • Alopecia universalis: total to near-total loss of hair on all haired surfaces of the body. Alopecia universalis results in hair loss across the entire scalp and face (including eyebrows and eyelashes), plus the rest of the body (including pubic hair).
  • Alopecia incognita: diffuse total hair loss with positive pull test, yellow dots, short, miniaturized regrowing hairs, but without nail involvement.
  • Diffuse alopecia areata: Diffuse alopecia areata results in sudden and unexpected thinning of the hair all over the scalp. It can be hard to diagnose because it looks a lot like other forms of hair loss such as telogen effluvium or male or female pattern hair loss.
  • Ophiasis: hair loss in a band-like shape along the circumference of the head, more specifically along the border of the temporal and occipital bones. Ophiasis alopecia areata can be more difficult to treat, because it does not respond as quickly to medication.
  • Sisaipho: extensive alopecia except around the periphery of the scalp.
  • Marie Antoinette syndrome also called canities subita: acute episode of diffuse alopecia with very sudden “overnight” greying with preferential loss of pigmented hair 14.

Who gets alopecia areata?

Alopecia areata can affect males and females at any age. Alopecia areata starts in childhood in about 50% of cases and before the age of 40 years in 80%. Lifetime risk is 1–2% and is independent of ethnicity.

  • A family history of alopecia areata and/or of other autoimmune conditions is present in 10–25% of patients.
  • At least 8 susceptibility genes have been detected.
  • Patients with alopecia areata have higher than expected rates of thyroid disease, vitiligo and atopic eczema.
  • There is increased prevalence in patients with chromosomal disorders such as Down syndrome.
  • It’s possibly drug-induced when arising in patients on biologic medicines.

Is alopecia areata hereditary?

There is a genetic predisposition to alopecia areata. About 20% of people with alopecia areata have a family history. The inheritance pattern of alopecia areata is unclear because multiple genetic and environmental factors appear to be involved. Overall, the risk of developing alopecia areata is greater for first-degree relatives (such as siblings or children) of affected individuals than it is in the general population. People with alopecia areata are also more likely to have family members with other autoimmune disorders.

What does alopecia areata look like?

Typically, alopecia areata starts as one or more bald, smooth patches on the scalp, which are not inflamed or scaly. Alopecia areata tends to affect the pigmented hair so there may be some white hairs left within the bald area in older people. Sometimes the hair loss is diffused rather than well-circumscribed patches. Short, tapered hairs, known as exclamation mark hairs that are characteristic of alopecia areata, may be seen at the edge of the bald patch. Regrowth usually starts at the centre of the bald patch with fine white hair that thickens with time and usually regains its color. Some people with alopecia areata develop small pits on their nails, similar to the dimples seen on a thimble.

Figure 4. Clinical manifestations of alopecia areata

alopecia areata symptoms

Footnotes: a) Limited patchy alopecia areata (<50% scalp involvement). b) Extensive patchy alopecia areata (>50% scalp involvement). c) Active patch of alopecia areata showing exclamation point hairs (arrow) and slight skin erythema. d) Alopecia universalis. e) Ophiasis pattern of alopecia areata. f) Sparing of white hairs in alopecia areata. g) Nail pitting and longitudinal striations (trachyonychia) associated with alopecia areata.

[Source 1 ]

Can alopecia areata be cured?

No, alopecia areata cannot be cured. Depending on the extent of hair loss there is a good chance that, for 4 out of 5 affected people, complete regrowth will occur within 1 year without treatment. There may, however, be further episodes of hair loss in the future. If there is very extensive hair loss from the start, the chances of it regrowing are not as good. Those with more than half the hair lost at the beginning or with complete hair loss at any stage have only about a 1 in 10 chance of full recovery. The chances of regrowth are not so good in young children and those with the condition affecting the hairline at the front, side or back.

What is the prognosis for alopecia areata?

In 80% of patients with a single bald patch, spontaneous regrowth occurs within a year. Even in the most severe cases of alopecia totalis and alopecia universalis, recovery may occur at some future date. This is an important difference between alopecia areata and the scarring forms of alopecia, which destroy the hair follicle and result in irreversible hair loss. Referral centers indicate that 34–50% of patients will recover spontaneously within 1 year, although most will experience multiple episodes of the alopecia, and 14–25% of patients will progress to alopecia totalis or alopecia universalis, from which full recovery is unusual (<10% of patients) 15. One Japanese study reported spontaneous remission in 80% of patients within 1 year for those with a small number of circumscribed patches of hair loss 16. The best indication for a prognosis is the extent of hair loss when first diagnosed 15. A less favorable prognosis is observed with childhood onset alopecia areata and ophiasis 17. A later age of onset correlates with less extensive alopecia 5. Severe alopecia areata (alopecia totalis and alopecia universalis) usually occurs before 30 years of age 5 and is often associated with nail dystrophy (trachyonychia) 18.

Research has shown:

  • 40% of patients with a single patch of hair loss have full hair regrowth within 6 months.
  • 27% of patients with multiple patches of hair loss have full regrowth within 12 months.
  • 33% of patients with alopecia areata have chronic hair loss.

Poor prognostic factors include:

  • Extensive disease
  • Bald patches persisting for more than 1 year
  • Ophiasis pattern of hair loss
  • Alopecia areata of the nails
  • Onset of alopecia areata before puberty
  • Family members with alopecia areata
  • Personal or family history of other autoimmune diseases
  • Down syndrome

New monoclonal antibody biologic agents targeting cytokine pathways offer promise for future treatment of alopecia areata.

Alopecia areata symptoms

Hair loss most commonly occurs on the scalp, but it can also target the eyebrows, eyelashes, beard, and other body sites. Symptoms may include the following:

  • Round, patchy areas of non-scarring hair loss, ranging from mild to severe
    • Mild: 1–5 scattered areas of hair loss on the scalp and beard
    • Moderate: More than 5 scattered areas of hair loss on the scalp and beard
    • Severe: loss of all of the hair on the scalp and body
  • Scalp burning (without redness), accompanying lesions
  • Pitting and ridging of the fingernails

Several clinical patterns are described. More severe disease is associated with young age, concurrent atopic eczema, and chromosomal abnormalities.

Most patients have no symptoms, and a bald patch or thinning hair is noted incidentally, often discovered by a hairdresser. Other patients describe a burning, prickly discomfort in the affected areas—this is known as trichodynia.

Alopecia areata typically presents with round, bald spots on the scalp. The beard, eyebrows, or eyelashes may be affected but it is unusual for isolated lesions elsewhere on the body. One or more may be present at any one time. The exclamation point hair is characteristic and appears as a short terminal hair, tapered at the proximal end. There is no scarring, scale, or other alteration of the scalp skin.

The follicular openings are not lost in contrast to a scarring alopecia.

Patients may rarely go on to lose extensive amounts of hair of the scalp and body, but again, this is unusual. Most patients regrow their hair. The term alopecia totalis refers to patients who have lost all of their scalp hair. The term alopecia universalis refers to patients who have lost all hair on the scalp and body. All nasal hair may be lost and this can lead to increased nasal inflammation and irritation.

A new subtype of alopecia areata called “acute diffuse and total alopecia of the female scalp” has been described where the woman suffers complete hair loss within one month of presentation. The histology is that of alopecia areata except for a significant eosinophilic tissue infiltrate. Fortunately, the vast majority of these women do well with cosmetically acceptable hair regrowth at six months with or without steroid administration.

Patchy alopecia areata

Patch alopecia areata can affect any hair-bearing area, most often the scalp, eyebrows, eyelashes and beard.

Patchy alopecia areata has three stages:

  1. Sudden loss of hair
  2. Enlargement of bald patch or patches
  3. Regrowth of hair

The bald areas may have a smooth surface, completely devoid of hair or with scattered “exclamation mark” hairs.

  • Exclamation mark hairs are 2- to 3-mm in length, broken or tapered, with a club-shaped root. Microscopy shows a thin proximal shaft and normal caliber distal shaft.
  • Regrowing hairs are often initially colored white or grey; they may be curly when previously straight.
  • It may take months and sometimes years to regrow all the hair.
  • One patch can be falling out while another is regrowing.

Alopecia totalis

  • Affects up to 5% of patients with autoimmune hair loss
  • All or nearly all scalp hair is lost

Alopecia universalis

  • Affects less than 1% of cases
  • All hair or nearly all hair on the entire body is lost

Ophiasis

  • Pattern of alopecia areata affecting occipital and lateral scalp
  • Bald area can encircle scalp

Diffuse alopecia areata

  • Sometimes called alopecia areata incognita
  • Presents with sudden diffuse thinning of scalp hair
  • Persisting hair tends to grey, thus descriptions of ‘turning white overnight’
  • Positive hair pull test
  • May be confused with telogen effluvium or hair loss due to medications

Alopecia areata of the nails

  • Nail disease affects 10–50% of those with alopecia areata
  • Regular pitting and ridging are the most common findings
  • May also cause koilonychia, trachyonychia, Beau lines, onychorrhexis, onychomadesis, onycholysis and red spots on the lunula

Figure 5. Alopecia areata of fingernails (nail pitting)

Alopecia areata of fingernails

Alopecia areata complications

Alopecia areata patients are at risk for psychosocial consequences of their disease, such as depression and anxiety. Psychological support may be beneficial.

Alopecia areata patients should be assessed for atopy, vitiligo, thyroid disease, and other autoimmune conditions.

Alopecia areata is associated with several concurrent diseases (comorbidities) including depression, anxiety, and several autoimmune diseases including thyroid disease (hyperthyroidism, hypothyroidism, goiter ant thyroiditis), lupus erythematosus, vitiligo, psoriasis, rheumatoid arthritis and inflammatory bowel disease 19. The frequency of these concurrent diseases varies between geographically separate populations, which may suggest genetic variability within these different populations. A retrospective study in Taiwan found that patients with alopecia areata had higher hazard ratios for autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and psoriasis within the 3-year follow-up period than healthy controls 20. In addition, increased prevalence of other forms of inflammatory skin disease such as atopic dermatitis, vitiligo, psoriasis and lichen planus were found than in controls, suggesting that patients with alopecia areata are at increased risk of developing variety of T-cell driven inflammatory skin diseases 21. Severe alopecia areata might be accompanied by nail changes 22. Atopic diseases, such as sinusitis, asthma, rhinitis, and especially atopic dermatitis, are also more common than expected in populations with alopecia areata 23 and are associated with early-onset and more severe forms of hair loss. In a Korean population, atopic dermatitis was significantly more common in patients with early-onset alopecia areata, whereas thyroid disease was the most common in late-onset disease 24; findings were similar in Sri Lanka 22. In a review of 17 studies, investigators found higher odds of atopic dermatitis in patients with alopecia totalis or alopecia universalis compared to those with patchy alopecia areata 24. In a large-scale epidemiological study in Taiwan investigators found a correlation between prior herpes zoster outbreaks with alopecia exposure within 3 years, suggesting that stress might trigger alopecia areata 25. Several studies, with and without controls, demonstrated a high prevalence of thyroid autoimmunity associated with alopecia areata 26, whereas others found lower frequencies than in earlier studies, indicating that there is no need for detailed investigations into these diseases without a clinical history to suggest they are present 27.

Alopecia areata causes

Alopecia areata is classified as an autoimmune disorder with a genetic predisposition, progressing from disruption of immune privilege of hair follicles 1. Emerging evidence suggests that a collapse in hair follicle immune privilege is the leading cause of alopecia areata 28. When this process develops, hair follicles present surface autoantigens, resulting in inflammatory cells attacking hair follicles and eventually resulting in an alopecic patch. Other factors such as genetics, stress, and environment are also responsible for development of alopecia areata 29.

A 55% concordance rate between identical twins has also been observed 30. Recent genome-wide association studies metanalysis have localized the human leukocyte antigen (HLA) signal of alopecia areata mostly to the HLA-DRB1 30. One locus harboring the genes that encode the natural killer cell receptor D (NKG2D) was implicated in alopecia areata and not in other autoimmune diseases, which suggests a key role in pathogenesis. Therefore, CD8+ NKG2D T cells have been a subject of study and found to be the major effectors in alopecia areata 1.

Alopecia areata is histologically characterized by T (lymphocyte) cells around the hair follicles. These CD8(+)NK group 2D-positive (NKG2D(+)) T cells release pro-inflammatory cytokines and chemokines that reject the hair. The exact mechanism is not yet understood.

Immune privilege protects hair follicle components from immune attacks by various mechanisms. Physical barriers, including the extracellular matrix, have reduced lymphatic permeability and guard hair bulbs against infiltrating immune cells 31. It also downregulates major histocompatibility complex (MHC) class I expression and MHC class I pathway molecules (β2-microglobulin and transporter associated with antigen processing [TAP-2]). Downregulation of MHC class I is caused by the local production of immunosuppressive factors, such as α-melanocyte-stimulating hormone (α-MSH), transforming growth factor-β (TGF-β), indoleamine‐2,3‐dioxygenase (IDO), protein red encoded by IK gene (red/IK), interleukin (IL)‐10, calcitonin gene‐related peptide, insulin‐like growth factor‐1, and somatostatin 32. Reduction of MHC class II expression on hair follicle Langerhans cells impairs antigen-presenting cell (APC) function 33. In addition, immune privilege expresses “no danger” signals using type-1 transmembrane glycoprotein CD200, which lowers antigen-presenting cell (APC) activity and pro-inflammatory cytokines secretion 34.

The immune privilege environment normally suppresses natural killer (NK) cell activation by downregulating MHC class I chain-related gene A (MICA) and UL16-binding protein (ULBP) in resident immune cells. These would otherwise bind to NKG2D‐activating receptors on CD8+ T cells and NK cells inducing inflammation and damaging local tissues. Supporting evidence shows that there are few perifollicular NK cells in healthy hair follicles 35. Next, killer cell Ig-like receptors, which are MHC class I inhibitory receptors, were significantly higher in controls than in alopecia areata patients 36. Killer cell Ig-like receptors help NK cells distinguish between normal cells and target cells, which prevents damage to healthy cells. Lastly, macrophage migration inhibitory factor, a pleiotropic cytokine presented in several immune privilege sites, prevents the release of cytolytic perforin granules from NK cells 37.

The onset or recurrence of hair loss is sometimes triggered by:

  • Viral infection
  • Trauma
  • Hormonal change
  • Emotional/physical stressors

Moreover, sporadic cases of alopecia areata developing during anti-TNF-α therapy have been reported 38. One third of the cases had a positive (personal or family) history of alopecia areata. Most of presented with rapid extensive alopecia areata, usually involving the ophiasis area. Prognosis was usually poor, with slight response to treatments. In the cases where anti-TNF-α therapy was maintained, the course did not seem to change.

Table 1. Alopecia areata associations

Age of OnsetAssociated Disease
< 10 yearsatopic dermatitis, lupus
11-20 yearspsoriasis, rheumatoid arthritis
21-60 yearsatopic and autoimmune diseases
> 60 yearsthyroid disease
All agesanxiety, depression, and obsessive compulsive disorders

Alopecia areata genetic factors

Several lines of evidence support the notion that alopecia areata has a genetic basis. In general, the prevalence of adult patients with a family history is estimated to be between 0% and 8.6%2 39, whereas in children data between 10% and 51.6% are reported 40. One study found that men were more likely to have a positive family history than women 41. The occurrence of alopecia areata in identical twins 42, siblings 43 and families with several generations of affected individuals 44 indicates that this alopecia areata has a heritable basis. Most of the early human genetic studies were candidate gene association studies, in which linkage to specific genes or groups of genes was the focus. These studies focused on the human leukocyte antigen class II (HLA-D) region on human chromosome 6 as the most likely region for genes that regulate susceptibility or resistance to alopecia areata 45. Family-based linkage studies and genome-wide association studies (GWAS) analyses, which were greatly enabled by the repository of the National Alopecia Areata Registry, identified linkage or association on many chromosomes, which suggests that alopecia areata is a very complex polygenic disease 46. These results confirmed earlier quantitative trait locus (QTL) analysis studies using an alopecia areata mouse model, often with similar, if not identical results 47.

Alopecia areata pathophysiology

The pathomechanism of alopecia areata involves the complex interaction between innate and adaptive immunities 48. The hair follicle immune privilege environment is highly regulated and usually prevents autoimmune hair loss. Emerging evidence suggests that the collapse of hair follicle immune privilege contributes to alopecia areata pathogenesis. MHC class I and class II expression on the hair matrix and follicular epithelium are found in alopecia areata-affected patients 33. The local production of immunosuppressive factors including α-MSH, TGF-β, IDO, and red/IK are downregulated in peri-lesional and lesional alopecia areata 49. Histological features from alopecia areata patient scalp biopsies showed infiltrating peri-follicular CD4+ T cells, intrafollicular CD8+T cells 1, mast cells 50, NK cells 36 and APCs.28 MICA immunoreactivity occurred throughout alopecia areata-affected hair follicles, which activated NKG2D+ NK cells and CD8+ T cells around alopecia areata lesions, but not in normal hair follicles 51.

Recent hypothesis of the disease mechanism focuses on the collapse of immune privilege of hair follicles and autoreactive lymphocytes. Under normal conditions, hair follicles form an area where autoantigens cannot be recognized due to the lack of major histocompatibility complex (MHC) in the proximal outer root sheath and matrix cells 52. In alopecia areata, the immune privilege is disrupted by specific triggers, such as microtrauma, viral infection, or endocrine dysfunction, resulting in immune dysregulation 49. Furthermore, ectopic expression of MHC class I, recognized by autoreactive CD8+ T cells, could directly and adversely affect anagen hair follicles, leading to follicular apoptosis 49.

Several studies have demonstrated the role of inflammatory cytokines, especially Th1-mediated cytokines, in the occurrence of alopecia areata via two possible mechanisms, either activation of the CD8+ T cell pathway or induction of cessation of hair growth cycle. Interferon (IFN)-γ, the hallmark cytokine of Th1-mediated pathway, is regarded as a key cytokine in alopecia areata 52. A large amount of IFN-γ is produced by autoactivated CD8+ cells and antigen presenting cells (APCs) after initial inflammatory insult on hair follicles 53, resulting in further upregulation of MHC class I and II molecules in the bulb of hair follicles and activation of CD8+ and CD4+ T cells 54. Serum from patients has been reported to contain a higher level of IFN-γ, interleukin (IL)-2, IL-12, and IL-18 compared to that from control subjects 55. Serum levels of IFN-γ tend to be elevated with disease severity 56. IL-1B, IL-2, and IL-6 are also present in human scalp lesions 57. Furthermore, the Th17 pathway may be involved in disease development by collaboration with the Th1 pathway via IL-17A and IL-17F 58.

Recent studies have reported significantly increased serum levels of Th2 cytokines, such as IL-4 and IL-10, which were suspected to be critical players in disease suppression. Serum level of IL-4 was found to be higher in patients with patch-type alopecia areata, a mild form of the disease, than in those with other subtypes 59. Apart from the Th2-mediated pathway, regulatory T cells are also responsible for the suppression of exaggerated Th1- and Th2-related inflammation via TGF-β and IL-10 56. Without a definite conclusion about its mechanism, the majority of the studies have shown no significant difference in regulatory cytokines between patients with alopecia areata and normal controls 60.

Alopecia areata triggers

In the majority of cases, no obvious explanation for the onset of an episode of alopecia areata can be found, but a variety of trigger factors have been proposed. The most commonly reported is emotional or physical stress, such as following bereavement or injury 19. Others include vaccinations, febrile illness, and drugs. A low frequency of alopecia areata was reported to arise shortly after vaccinations against a variety of human pathogens including Japanese encephalitis 61, hepatitis B virus 62, Clostridium tetani 63, herpes zoster virus 64 and papillomavirus 65. By contrast, one report showed that alopecia areata was triggered or exacerbated by swine flu virus infection 66. However, hepatitis B vaccine trials using large numbers of C3H/HeJ spontaneous, adult-onset mouse model of alopecia areata, in which diphtheria and tetanus toxoids were added as controls, suggested that alopecia areata associated with vaccination was in the normal, predicted incidence range 67.

How can alopecia areata be prevented?

Scientists do not yet know how to prevent the onset of alopecia areata.

How is alopecia areata diagnosed?

Alopecia areata is diagnosed clinically. Although usually straightforward, additional tests are sometimes needed to confirm the diagnosis.

  • Trichoscopy (use of a dermatoscope to examine hair and scalp)
  • Skin biopsy (histopathology)

Alopecia areata treatment

There is not yet any reliable cure for alopecia areata and other forms of autoimmune hair loss. Because spontaneous regrowth is common in alopecia areata, and research has often been of poor quality, the effectiveness of reported treatments is mostly unknown.

  • Observation
  • Intralesional injection triamcinolone 2.5 mg/mL monthly
  • Hydroxychloroquine
  • Methotrexate or azathioprine
  • Topical immunotherapy with diphenylcyclopropenone (DPCP) and anthralin
  • Fexofenadine
  • Measure Vitamin D and supplement if low.

Systemic therapy is reserved for patients with:

  • More than 20% of scalp hair loss
  • Rapid hair loss
  • Chronic hair loss
  • Severe distress.

Alopecia areata need not be treated as it is a benign condition and regrowth is typical. In fact, spontaneous remission occurs in up to 80% of patients with limited disease within a year. However, alopecia areata often causes great embarrassment and thus therapy is often desired to speed regrowth.

Figure 6. Alopecia areata treatment algorithm

alopecia areata treatment algorithm
[Source 68 ]

Intralesional steroids, first-line

Individual lesions may be injected with Kenalog (triamcinolone acetonide) every month. This usually induces hair regrowth for isolated areas although atrophy of the skin may occur. The injection should be done into the deep dermal/upper subcutaneous plane using a 0.5-inch, 30-gauge needle 7. One may cover several square centimeters of skin with one injection point by fanning out in various directions with the needle and injecting while withdrawing. This helps distribute the medication more evenly than multiple small injection points. The maximum dose often cited is 20 mg per month, e.g., 8 mL of 2.5 mg/mL 8. In a double blind placebo controlled clinical trial comparing injection with 2.5, 5, and 10 mg/mL in alopecia areata of < 50% of the scalp, the 2.5 mg/mL concentration was just as effective as the 5 and 10 69. Treatment may be repeated every four to six weeks until resolution or for a maximum of six months. Local adverse effects include transient atrophy and telangiectasia.

Vitamin D

Deficient serum 25(OH)D (calcidiol or 25-hydroxyvitamin D) levels are present in patients with alopecia areata and inversely correlate with disease severity. Thus, screening patients and supplementing, if indicated, seems prudent 70. It would also be reasonable to screen patients for iron and zinc deficiency and supplement as appropriate 71.

Fexofenadine

Some use fexofenadine 120-180 mg/day for adults either as monotherapy or as an adjunct for other therapies. In a retrospective study of extensive alopecia treated with contact immunotherapy, the mean regrowth score of the fexofenadine group was 1.33 and that of the control 0.47 72.

Topical treatments

Several topical treatments used for alopecia areata are reported to result in temporary improvement in some people. Their role and efficacy are unknown. The hair may fall out when they are stopped. These include 9:

  • Potent or ultrapotent topical steroids
  • Minoxidil solution or foam
  • Dithranol (anthralin) ointment
  • Immunotherapy (diphenylcyclopropenone, squaric acid dibutylester)

Any alopecia areata patient may benefit from a class 1 topical steroid for several months, although the area should be monitored for the development of atrophy. For example, topical clobetasol (given as a foam) grew modestly more hair than placebo in a double blind placebo controlled clinical trial.

Steroid creams and scalp applications

Potent or ultrapotent topical steroids are applied to the bald patches, usually twice a day, for a limited time.

Topical Minoxidil

Minoxidil 5% is recommended by many, but its use is off-label in the US. In one study, topical minoxidil applied twice daily and nightly occluded with petrolatum for 1 year outperformed placebo modestly, but the hair is often fine and not of much use.

Topical Bimatoprost

A study in which 30 patients applied mometasone cream once daily or bimatoprost 0.03% solution (Lumigan, Allergan, 3 ml) twice daily to two separate patches of alopecia areata found that bimatoprost grew hair sooner and better than mometasone 73.

Dithranol cream

Dithranol cream which is usually used to treat another skin condition called psoriasis, causes irritation of the skin, and occasionally this appears to stimulate the hair to regrow when applied to the bald areas. There is only weak evidence for this but it is safe to use so doctors may offer it. Dithranol stains the skin and hair a purple-brown colour, which is particularly prominent in blond and fair-headed people.

Alopecia of Eyebrows

  • Intralesional steroid injection.
  • Topical Bimatoprost.

Intralesional injection of steroid may be done by an ophthalmologist. Forty-one subjects with alopecia areata universalis without ocular disease applied 0.03% bimatoprost to the eyelid margin once a day over the course of 1 year 74. 43% of patients had moderate or total regrowth.

One may use intralesional triamcinolone 2.5 mg/mL every month, but the patient must accept the rare risk of ocular complications. For example, intralesional Kenalog (triamcinolone acetonide) 40 mg for vitiligo of the forehead (a much higher dose than would be used for alopecia areata) caused immediate stroke and blindness in a 15-year-old boy 75. One patient who had not had eyebrows for 20 years developed reasonable regrowth after several injections.

Intralesional triamcinolone 2.5 mg/mL may be injected every cm–about 0.1 mL per injection. When the patient returns often there is regrowth in tufts. One can then inject in between the tufts.

Alopecia Areata in a Child

  • First-line 5% minoxidil and topical steroid (e.g., clobetasol, mometasone cream)
  • Second-line, if extensive, immunocontact therapy
  • Hydroxychloroquine
  • Once over 10 years of age, or can tolerate, add intralesional triamcinolone as above
  • Oral Tofacitinib did well in 8 patient 12-19 years of age with alopecia universals 76.

Treatment Options for Extensive Disease

Hydroxychloroquine

Hydroxychloroquine improved the clinical appearance in 5/9 children after 6 months 77. Patients were 12-16 years of age. A typical dose was 200 mg twice daily.

Systemic Steroids

Systemic steroids are usually only considered for extensive disease because of potential side effects. Most physicians agree that long-term systemic steroid treatment is not justified because of potential and actual adverse effects. Taking steroids by mouth over a period of time can cause many side effects including raised blood pressure, diabetes, stomach ulcers, cataracts and osteoporosis as well as weight gain. In one study, pulse oral prednisone 300 mg every 4 weeks was used. Otherwise, one may give the steroid daily orally and taper to the lowest effective dose. Alternatively, Kenalog (triamcinolone acetonide) 60 mg intramuscular monthly x 3 may be tried but no more should be given and the patient risks the hair falling out once treatment is stopped.

Azathioprine

In a small study, 14 patients with alopecia universalis were treated with azathioprine 2.5 mg/kg body weight per day. Forty-three percent achieved complete regrowth at a mean of 4.7 months 78 reviewed treatment of 31 patients and found regrowth greater than 50% was observed in 67.7% of patients, with the best responses observed in those with <5 years of disease progression (79%), age over 40 years (73.3%), male patients (72.8%), cumulative dose of methotrexate 1000-1500 mg, and multifocal alopecia areata (93%).

Short Contact Anthralin

Inducing an irritant contact dermatitis can sometimes cause regrowth. Typically, one has the patient apply 1% anthralin for 1 hour and then wash off. The main side effect is irritation, but that is the goal. Rarely, there can be facial edema, vesicles, blisters, etc., if the reaction is too severe.

Tofacitinib and other JAK Inhibitors

Recently, the efficacy of leveraging Janus Kinase inhibitors (JAKis) in various autoimmune and hematologic diseases has seen increased interest. Janus Kinase inhibitors (JAKis) are selective, competitive inhibitors of adenosine triphosphate-binding sites on JAK/STAT 79. It predominantly blocks the downstream IFN-γ and γc cytokine receptors and reduces the recruitment of CD8+NKG2D+ T cells 80. It also interferes with Th1 cell and Th17 cell differentiation. Notably, activation and proliferation of hair follicle stem cells are promoted by JAKis, which accelerates hair follicle reentry into the anagen phase 81. Treatment of alopecia areata with JAK1/2 (IFN-γ pathway) and JAK3 (γc cytokines) blockers showed promising results. The therapeutic efficacy of oral tofacitinib (Xeljanz) and oral ruxolitinib (Jakafi) in treating severe and recalcitrant alopecia areata has an overall response rate of 30%–75%, with transient and minimal side effects 82.

Ninety patients with severe alopecia areata were treated with tofacitinib 5 mg twice daily for 2-3 months initially. Then, non-responders were eligible for pulse prednisone or higher doses of tofacitinib 83. Seventy-seven percent achieved a clinical response, with 58% achieving a greater than 50% improvement in SALT score over 4-18 months. There were no serious adverse events.

68% (9/13) pediatric patients with severe alopecia areata experienced clinically significant regrowth of hair in a study using tofacitinib (5 mg twice daily x 5 months) 84. Most of the patients studied had either alopecia universalis or totalis. No serious side effects were reported.

Topical 2% tofacitinib ointment applied twice daily (topical) had a modest effect, perhaps similar to clobetasol ointment under occlusion 85.

Oral ruxolitinib (a JAK1 and JAK2 blocker) led to almost complete hair regrowth in 3 alopecia areata patients in 5 months 86. In another study, 9/12 patients achieved at least 50% regrowth most by 6 months 87. Also Ruxolitinib-induced reversal of alopecia universalis in a patient with essential thrombocythemia 88.

Other Therapy

A wig or hair piece may be needed for more extensive disease. Patients with more diffuse hair loss, e.g., alopecia totalis or universalis, may desire more aggressive therapy. Intramuscular triamcinolone 40-60 mg or a tapering course of systemic steroids may be tried although controlled studies are lacking. Cyclosporin has been tried. Topical immunotherapy, with e.g., phenol, has been reported.

Adalimumab did not help alopecia areata in one report but did in another 89. Apremilast did not help 9 patients with severe alopecia areata 90.

Treatment with platelet-rich plasma was studied in 45 patients with alopecia areata 91. Intralesional platelet-rich plasma grew more hair than intralesional triamcinolone 2.5 mg/mL or placebo without significant side effects. The platelet-rich plasma was prepared by drawing the patient’s own blood, centrifuging it for 8 minutes at 70 “G”s, and separating the platelet-rich plasma fraction.

A combination of the lipid lowering agents simvastatin and ezetimibe (which have immunomodulating effects) has been reported to be effective 92. Besides their efficacy in reducing atherosclerotic cardiovascular risk, statins are also anti-inflammatory and immunomodulatory agents. In vitro (test tube) and in vivo (animal) studies showed that statins downregulate Th1 cytokines and upregulate Th2 cytokines via modulation of the JAK/STAT pathway. Furthermore, it can directly modulate APCs to increase Treg cell activation 93. Evidence also suggests that statins downregulate leukocyte activation, proliferation, differentiation, adhesion, and extravasation into target tissues 94. The combination of statins and ezetimibe (non-statin lipid-lowering medication) showed promising results with 30%–80% hair regrowth in 28% of recalcitrant alopecia areata patients 92. However, another study reported unsatisfactory results as none of the patients achieved hair regrowth 95. The relapse rate was significantly lower in statin-treated patients than in the control group 96. Thus, lipid-lowering agents, when combined with other therapies, show promise for preventing disease relapses; however, further studies to elucidate this are required.

There is no convincing data to support the use of methotrexate, sulfasalazine, azathioprine, ciclosporin or phototherapy.

Topical immunotherapy

Topical immunotherapy is currently considered as the first-line treatment, representing the most effective modality for treating extensive or recalcitrant alopecia areata 97. Despite being commonly used, the exact mechanism underlying topical immunotherapy for the treatment of alopecia areata has not yet been elucidated. Accumulating evidence has shown advantage of topical immunotherapy over no treatment; however, comparison of the efficacies across different clinical studies and different substances is difficult owing to variations of treatment protocols, evaluation methods, and study durations.

Diphenylcyclopropenone

Diphenylcyclopropenone (DPCP) is a topical sensitizer, efficacy of which was primarily reported by Happle et al in 1983 98. Currently, diphenylcyclopropenone (DPCP) is the most commonly used substance owing to the following reasons. First, it is nonmutagenic in Ames assay, with no report of systemic absorption 99. Second, no long-term adverse effect has been documented yet. Finally, it is less expensive and more stable in acetone solution compared to squaric acid dibutylester (SADBE) 100. In 2012, the British Association of Dermatologists’ guideline also recommended the use of diphenylcyclopropenone (DPCP) as the first-line topical sensitizer for the treatment of alopecia areata 101.

Several studies have evaluated the efficacy of diphenylcyclopropenone (DPCP) in patients with alopecia areata; hair regrowth rate was found to be 6–77%. A systematic review had previously reported an overall hair regrowth rate of 53.75% in diphenylcyclopropenone (DPCP)-treated patients 102. Severity of alopecia areata was found to be a significant factor associated with hair regrowth. The highest efficacy of diphenylcyclopropenone (DPCP) was reported by Tosti et al 103 with 77% complete hair regrowth in patients with mild alopecia areata. The largest retrospective study involving 757 patients with all subtypes of alopecia areata was published in 2020 104. The overall hair regrowth rate has been reported to be 60.1% and the satisfactory hair regrowth (>75% hair regrowth) rate was 16.3% 104. Comparison across subtypes of alopecia areata showed patch-type alopecia areata to have 2.56 times higher satisfactory hair regrowth while alopecia universalis had 2.6 times lower response in comparison to other subtypes 104. The satisfactory hair regrowth rate of diphenylcyclopropenone (DPCP) for patch-type alopecia areata was reported ranging between 55.4% and 63.4% 105, 106. When the efficacy of diphenylcyclopropenone (DPCP) on alopecia totalis or alopecia universalis subtype was considered, two meta-analyses showed different results. Lee et al 105 reported 28.3% of patients with satisfactory hair regrowth while Gupta et al 106 reported a higher rate of 87.9%.

Very few studies to date have demonstrated the efficacy of diphenylcyclopropenone (DPCP) in children with alopecia areata. The efficacy of satisfactory hair regrowth has been reported to range from 11–33%. A prospective study using diphenylcyclopropenone (DPCP) in 12 pediatric patients with extensive alopecia areata reported initial hair regrowth in 67% of patients and complete hair regrowth in 33% after a mean treatment duration of 7.3 months 107. Another retrospective study investigated the efficacy of diphenylcyclopropenone (DPCP) in 108 children with alopecia areata, and found only 13% and 11% of patients to have achieved complete hair regrowth after six and 12 months of treatment, respectively 108.

Although efficacy of diphenylcyclopropenone (DPCP) has been widely investigated for hair regrowth, few studies have focused on the relapse rate after cessation of treatment. A comparative study in this regard showed that patients who continued using diphenylcyclopropenone (DPCP) as a maintenance therapy had a lower relapse rate (24.4%) compared to those who did not (68.2%) 109. Hull and Cunliffe 110 reported 63% relapse rate after six months of successful therapy without maintenance treatment. Male gender, high severity of disease, and body hair involvement were established as negative factors determining recurrence. In contrast, a study on 25 patients with complete hair regrowth showed no relapse after discontinuing diphenylcyclopropenone (DPCP), over a mean period of 15 months 111. The importance of maintenance therapy in topical immunotherapy still remains inconclusive.

Although diphenylcyclopropenone (DPCP) is the best-documented treatment for extensive or recalcitrant alopecia areata, not all patients achieve a good response, and some might withdraw due to adverse effects. Patients with high serum IgE levels may have more severe adverse events following diphenylcyclopropenone (DPCP) application 112. Regarding safety, most patients were found to be tolerant to diphenylcyclopropenone (DPCP) and no systemic absorption has yet been reported 113. Most adverse effects have been recorded without long-term complications; common side effects include dermatitis and urticaria 114. Angioedema, anaphylaxis, fever, erythema multiforme-like reactions, postinflammatory hypopigmentation, and depigmentation have been reported as infrequent complications 115.

Topical combination therapy using diphenylcyclopropenone (DPCP)

Topical combination therapy using diphenylcyclopropenone (DPCP) and anthralin on 25 patients with severe alopecia areata resulted in complete regrowth of hair in 72% of patients 116. On the contrary, two studies and one case series showed nonsuperior efficacy of diphenylcyclopropenone (DPCP) and anthralin combination therapy compared to diphenylcyclopropenone (DPCP) monotherapy 117, 118. Regarding diphenylcyclopropenone (DPCP) combination with 5% minoxidil, Shapiro et al 119 found no significant difference in satisfactory hair regrowth between combined regimen and diphenylcyclopropenone (DPCP) monotherapy. When combined with imiquimod, however, superior efficacy of combination therapy to diphenylcyclopropenone (DPCP) monotherapy was evident 120.

Note that topical immunotherapy diphenylcyclopropenone (diphencyprone) provokes contact allergic dermatitis in treated areas. The resultant dermatitis is irritating and may be unsightly. It is often accompanied by a swollen lymph gland.

Since the standard treatment protocol of contact sensitizers may take a long time until acceptable treatment response is achieved, modified protocols have been introduced to address this issue. Sriphojanart et al 121 and Thuangtong et al 122 had reported the use of a multiconcentration diphenylcyclopropenone (DPCP) treatment on patients’ scalps at the first visit. A concentration that created an optimal eczematous reaction would then be selected as the starting solution for application. Multi-concentration protocol showed similar efficacy as the standard protocol, with a shorter duration till significant hair regrowth is achieved 121. Another study had also investigated the efficacy across various application intervals. Results showed the three-week treated group to have higher efficacy than the one-week interval group, with 54% and 46% response rates, respectively 123. A subsequent retrospective study reported no significant difference of efficacy between home-based diphenylcyclopropenone (DPCP) therapy and clinic-based therapy; however, the home-based group had better compliance compared to the clinic-based group 124.

Topical Squaric Acid Dibutylester

Squaric acid dibutylester (SADBE) or 3,4-dibutoxycyclobut-3-ene-1,2-dione, its topical application induces an allergic contact dermatitis and can grow hair both in adults and children 125. Various protocols exist, but one common approach is to first do an application on the arm to induce sensitivity and then one month later, start topical application of 5% squaric acid dibutylester (SADBE) on the affected areas of the scalp. Patients return monthly to monitor progress and for reapplication of the 5% if the hair is regrowing. If there is too much reaction (e.g., burning, blistering), the concentration is reduced to 2.5%. If no hair is growing, then the concentration can be increased to 10%.

The response rate of squaric acid dibutylester (SADBE) in the treatment of alopecia areata ranges between 19% and 79.6% 97. A meta-analysis by Lee et al 105, including 45 studies with 2227 patients, showed 51.8% of patients with patch-type alopecia areata and 25% of patients with alopecia totalis or alopecia universalis to have achieved satisfactory hair regrowth. A network meta-analysis by Gupta et al 106 suggested that 35% and 49.7% of patients with patch-type alopecia areata and alopecia totalis or alopecia universalis, respectively, demonstrated satisfactory hair regrowth.

One randomized placebo-controlled trial of squaric acid dibutylester (SADBE) was published in 1986, which demonstrated complete hair regrowth in 64% of patients with patch-type alopecia areata 103. The largest prospective study of squaric acid dibutylester (SADBE), conducted in 144 patients with variable severities of alopecia areata, reported 80% and 49% response rates in mild and severe forms of alopecia areata, respectively 126. Satisfactory results were reported by Happle et al 125, Dall’oglio et al 127 and Chua et al 128, with complete hair regrowth rates of 87%, 79.6%, and 68%, respectively. In contrast, Caserio 129 and Gianetti and Orecchia 130 reported unsatisfactory results with complete response rate of 28.5% and 19%, respectively.

Adverse effects of squaric acid dibutylester (SADBE) include redness, swelling, and itching at the application site. However, some patients might experience more severe reactions, such as blistering, burning of the skin, and spreading of rash to other areas. Uncommon adverse effects reported include spread of generalized eczema, persistent contact dermatitis, and severe angioedema 131. Postinflammatory hypopigmentation and depigmentation have also been reported after the application of squaric acid dibutylester (SADBE), and lesions were obviously visible in patients with skin phototype V or VI 132.

Dinitrochlorobenzene

Dinitrochlorobenzene (DNCB) or 1-chloro-2,4-dinitrobenzene was the earliest contact allergen introduced in 1912 97. Dinitrochlorobenzene (DNCB) used to be popular for the treatment of extensive or recalcitrant alopecia areata, with hair regrowth ranging around 25–89% and complete regrowth rates being 6.7–25% 97. However, in 1985, dinitrochlorobenzene (DNCB) was found to be mutagenic and carcinogenic in Ames test and had to be discontinued thereafter 133.

What else should be considered for alopecia areata?

Counseling

Some people with alopecia areata seek and benefit from professional counseling to come to terms with the disorder and regain self-confidence.

Camouflaging hair loss

Scalp

A hairpiece is often the best solution to disguise the presence of hair loss. These cover the whole scalp or only a portion of the scalp, using human or synthetic fibers tied or woven to a fabric base.

  • A full wig is a cap that fits over the whole head.
  • A partial wig must be clipped or glued to existing hair.
  • A hair integration system is a custom-made hair net that provides artificial hair where required, normal hair being pulled through the net.
  • Hair additions are fibers glued to existing hair and removed after 8 weeks

Styling products include gels, mousses and sprays to keep hair in place and add volume. They are reapplied after washing or styling the hair.

Eyelashes

Artificial eyelashes come as singlets, demilashes and complete sets. They can be trimmed if necessary. The lashes can irritate the eye and eyelids. They are stuck on with methacrylate glue, which can also irritate and sometimes causes contact allergic dermatitis.

Eyeliner tattooing is permanent and should be undertaken by a professional cosmetic tattooist. The color eventually fades and may move slightly from the original site. It is extremely difficult to remove the pigment, should the result turn out to be unsatisfactory.

Eyebrows

Artificial eyebrows are manufactured from synthetic or natural human hair on a net that is glued in place.

Eyebrow pencil can be obtained in a variety of colors made from inorganic pigments.

Tattooing can also be undertaken to disguise the loss of eyebrows, but tends to look rather unnatural because of the shine of hairless skin.

Living with alopecia areata

Alopecia areata may affect your sense of well-being. Because hair loss and regrowth from alopecia areata is unpredictable and sometimes cyclical (comes back again and again), having alopecia areata can be frustrating and emotionally challenging for many people. There are some common emotions that many people who have alopecia areata and the people around them say that they experience. These include feelings of grief, anxiety, loss, fear, embarrassment, loneliness and anger.

However, there are many things you can do to cope with the effects of alopecia areata, including:

Get support

  • Learn as much as you can about the disease, and talk with others who are dealing with it. Many people find that the support of a group or an individual who also has alopecia areata is helpful in processing the emotions connected to living with the disease. Connect with community by joining a support group such as the National Alopecia Foundation (https://www.naaf.org/find-support/support-groups)
  • Visit a mental health professional if you experience higher levels of stress, depression, or anxiety.

Protect bare skin and stay comfortable

  • Use sunscreens for any bare areas.
  • Wear wigs, hairpieces, hats, or scarves to protect your scalp from the sun and to keep your head warm.
  • Wear eyeglasses or sunglasses to protect your eyes from sun and dust if you have lost hair from your eyebrows or eyelashes.

Consider cosmetic solutions

  • Wear a wig, hairpiece, or bandana to cover up hair loss. Some people choose to shave their heads to mask patchy hair loss.
  • Use fake eyelashes or apply stick-on eyebrows if you lose hair from your eyelashes or eyebrows.

Take care of your health

Visit your primary care doctor regularly. People with alopecia areata have a higher risk of certain other diseases, and early diagnosis is important.

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