Alopecia areata (AA) is a kind of alopecia that affects the retina pigment epithelium, nails, and hairline follicles sporadically. It is a kind of hair loss that doesn’t leave scars and often manifests as rounded patches.
It is a kind of hair loss that doesn’t leave scars and often manifests as rounded patches. A rough estimate of the overall incidence is 20.2 per 100,000 person/year. In the overall population, there is a 2% chance that they may develop AA in their lifetime. Depending on the region and the ethnic group, the prevalence of AA ranges from 0.1% to 0.2%.
Between 0 to 8.6% of adult patients are believed to have a family history. Although the typical age of beginning seems to be between 25 & 36 years old, the incidence of AA appears to rise practically linearly with age. Early onset AA (between the ages of 5 and 10) typically manifests as a more severe variant.
Data indicate no discernible sex preference. It has links to a total risk increase of other autoimmune disorders (16 percent), such as thyroid disorders, vitiligo, & lupus erythematosus. In 39 percent of cases, there is also a connection to atopic dermatitis.
The comparative immune privilege of the hair shaft, which is an important characteristic, is primarily established by the inhibition of surface molecules necessary for expressing autoantigens to MHC class I CD8+ T lymphocytes and by the creation of a signaling setting that is inhibitive locally. One important cause of AA has been attributed to the hairline follicle’s immunological privilege breaking down.
The condition of hairline follicle cycling known as AA occurs when inflamed cells attack the hairline follicle matrix epithelial while it is experiencing slightly earlier cortical differentiating (anagen hairline follicles), causing them to enter the catagen stage too soon. However, because the stem line cells in the hair follicle are not destroyed, the hairline follicle can continue to cycle and renew. Follicles re-enter the anagen stage as a result regularly. However, they do not progress past the anagen III/IV stage.
It is likely that the immunological privilege of a perfectly healthy hair shaft collapses when AA develops. Therefore, it might only happen in a person who is genetically programmed if proinflammatory signaling, such as IFN gamma and substance P, which are known to upregulate MHC class Ia in individual hair shaft epithelial, are exposed to underlying autoreactive CD8+ T cells. It is uncertain what specific circumstance leads to alopecia areata. Certain triggers, most frequently physical or mental stress, immunizations, viral diseases, and medications, have been observed.
There may be a hereditary component to AA. It has been found that identical twins have a concordance rate of 55%. Recent GWAS metanalysis has mostly located the HLA-DRB1 as the source of the AA HLA signal.
An important role in pathogenesis may be played by one locus that contains the genes for the NKG2D (natural killer cell receptor D), which was linked to AA but no other autoimmune disorders. As a result, CD8+ NKG2D T cells have been investigated and discovered to be the primary AA effectors.
Since the inflammatory reaction spares hair roots, particularly stem cells, the possibility of hair regeneration exists. Current treatments, however, appear to have difficulty inducing regrowth. Although most patients will undergo numerous episodes of alopecia, approximately 34-50% of individuals may recover within a year.
However, 14-25% of individuals will advance to alopecia universalis or totalis, from which complete recovery is uncommon (10% of cases). With childhood-onset alopecia areata & ophiasis, the level of loss of hair & age of the patient at first diagnosis appear to be prognosis factors, and then a later phase of onset is correlated with less severe alopecia.
Clinical History:
Alopecia areata’s natural course is unpredictable. Between patients, there are significant differences in the severity and length of the condition. The majority of people with alopecia areata are asymptomatic, although 14% of individuals report burning or itching in the afflicted area. When the condition first manifests, it usually is localised.
80% of alopecia areata individuals have just one patch, 12.5% have two patches, and 7.7% have several patches. There is no connection between the quantity of patches at the beginning and the severity over time. Although it can affect any portion of the body with hair, alopecia areata most frequently affects the scalp (66.8-95%).
Localized alopecia areata
Localized patchy alopecia areata episodes with less than 50% involvement are typically self-limited; with or without therapy, most patients experience spontaneous regrowth within a few months.
Extensive alopecia areata
Less frequently seen are extensive (>50% involvement) types of alopecia areata. According to reports, 7% of patients get alopecia totalis or universalis at some point, while 11% of patients experience alopecia areata, which causes more than 40% of hair to fall out.
Alopecia totalis sufferers seem to be less common with each passing decade of life.
Physical examination
Alopecic patches that are smooth, somewhat erythematous (peach-colored), or normal-colored are typical. Exclamation point hairs, or hairs that are tapered near the proximal end, are pathognomonic but are not always present. When the pull test near the edge of a plaque yields a positive result, the disease is typically active, and additional hair loss is to be anticipated.
Other hair-bearing areas losing hair also supports the diagnosis. One or more rounded-to-oval denuded patches are the most typical appearances. The hair loss is not accompanied by any changes to the epidermis.
The pattern of alopecia areata can be used to classify it. Most typically, localised and patchy hair loss occurs.
When there is more widespread hair loss and the patches congregate, a reticular pattern develops.
When hair loss is restricted to the sides and lower back of the head, an ophiasis pattern develops. In contrast, the sisaipho pattern manifests when hair loss spares the sides and back of the head (ophiasis spelt backwards).
Alopecia totalis results in complete scalp hair loss.
In alopecia universalis, all hair-bearing areas completely lose all of their hair. Usually, focal alopecia areata can become generalised and resemble telogen effluvium (TE) or the form of androgenetic alopecia that affects women.
Differential Diagnoses
Trichotillomania
Brocq Pseudopelade
Telogen Effluvium
Pediatric Syphilis
Androgenetic Alopecia
Tinea Capitis
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
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Alopecia areata (AA) is a kind of alopecia that affects the retina pigment epithelium, nails, and hairline follicles sporadically. It is a kind of hair loss that doesn’t leave scars and often manifests as rounded patches.
It is a kind of hair loss that doesn’t leave scars and often manifests as rounded patches. A rough estimate of the overall incidence is 20.2 per 100,000 person/year. In the overall population, there is a 2% chance that they may develop AA in their lifetime. Depending on the region and the ethnic group, the prevalence of AA ranges from 0.1% to 0.2%.
Between 0 to 8.6% of adult patients are believed to have a family history. Although the typical age of beginning seems to be between 25 & 36 years old, the incidence of AA appears to rise practically linearly with age. Early onset AA (between the ages of 5 and 10) typically manifests as a more severe variant.
Data indicate no discernible sex preference. It has links to a total risk increase of other autoimmune disorders (16 percent), such as thyroid disorders, vitiligo, & lupus erythematosus. In 39 percent of cases, there is also a connection to atopic dermatitis.
The comparative immune privilege of the hair shaft, which is an important characteristic, is primarily established by the inhibition of surface molecules necessary for expressing autoantigens to MHC class I CD8+ T lymphocytes and by the creation of a signaling setting that is inhibitive locally. One important cause of AA has been attributed to the hairline follicle’s immunological privilege breaking down.
The condition of hairline follicle cycling known as AA occurs when inflamed cells attack the hairline follicle matrix epithelial while it is experiencing slightly earlier cortical differentiating (anagen hairline follicles), causing them to enter the catagen stage too soon. However, because the stem line cells in the hair follicle are not destroyed, the hairline follicle can continue to cycle and renew. Follicles re-enter the anagen stage as a result regularly. However, they do not progress past the anagen III/IV stage.
It is likely that the immunological privilege of a perfectly healthy hair shaft collapses when AA develops. Therefore, it might only happen in a person who is genetically programmed if proinflammatory signaling, such as IFN gamma and substance P, which are known to upregulate MHC class Ia in individual hair shaft epithelial, are exposed to underlying autoreactive CD8+ T cells. It is uncertain what specific circumstance leads to alopecia areata. Certain triggers, most frequently physical or mental stress, immunizations, viral diseases, and medications, have been observed.
There may be a hereditary component to AA. It has been found that identical twins have a concordance rate of 55%. Recent GWAS metanalysis has mostly located the HLA-DRB1 as the source of the AA HLA signal.
An important role in pathogenesis may be played by one locus that contains the genes for the NKG2D (natural killer cell receptor D), which was linked to AA but no other autoimmune disorders. As a result, CD8+ NKG2D T cells have been investigated and discovered to be the primary AA effectors.
Since the inflammatory reaction spares hair roots, particularly stem cells, the possibility of hair regeneration exists. Current treatments, however, appear to have difficulty inducing regrowth. Although most patients will undergo numerous episodes of alopecia, approximately 34-50% of individuals may recover within a year.
However, 14-25% of individuals will advance to alopecia universalis or totalis, from which complete recovery is uncommon (10% of cases). With childhood-onset alopecia areata & ophiasis, the level of loss of hair & age of the patient at first diagnosis appear to be prognosis factors, and then a later phase of onset is correlated with less severe alopecia.
Clinical History:
Alopecia areata’s natural course is unpredictable. Between patients, there are significant differences in the severity and length of the condition. The majority of people with alopecia areata are asymptomatic, although 14% of individuals report burning or itching in the afflicted area. When the condition first manifests, it usually is localised.
80% of alopecia areata individuals have just one patch, 12.5% have two patches, and 7.7% have several patches. There is no connection between the quantity of patches at the beginning and the severity over time. Although it can affect any portion of the body with hair, alopecia areata most frequently affects the scalp (66.8-95%).
Localized alopecia areata
Localized patchy alopecia areata episodes with less than 50% involvement are typically self-limited; with or without therapy, most patients experience spontaneous regrowth within a few months.
Extensive alopecia areata
Less frequently seen are extensive (>50% involvement) types of alopecia areata. According to reports, 7% of patients get alopecia totalis or universalis at some point, while 11% of patients experience alopecia areata, which causes more than 40% of hair to fall out.
Alopecia totalis sufferers seem to be less common with each passing decade of life.
Physical examination
Alopecic patches that are smooth, somewhat erythematous (peach-colored), or normal-colored are typical. Exclamation point hairs, or hairs that are tapered near the proximal end, are pathognomonic but are not always present. When the pull test near the edge of a plaque yields a positive result, the disease is typically active, and additional hair loss is to be anticipated.
Other hair-bearing areas losing hair also supports the diagnosis. One or more rounded-to-oval denuded patches are the most typical appearances. The hair loss is not accompanied by any changes to the epidermis.
The pattern of alopecia areata can be used to classify it. Most typically, localised and patchy hair loss occurs.
When there is more widespread hair loss and the patches congregate, a reticular pattern develops.
When hair loss is restricted to the sides and lower back of the head, an ophiasis pattern develops. In contrast, the sisaipho pattern manifests when hair loss spares the sides and back of the head (ophiasis spelt backwards).
Alopecia totalis results in complete scalp hair loss.
In alopecia universalis, all hair-bearing areas completely lose all of their hair. Usually, focal alopecia areata can become generalised and resemble telogen effluvium (TE) or the form of androgenetic alopecia that affects women.
Differential Diagnoses
Trichotillomania
Brocq Pseudopelade
Telogen Effluvium
Pediatric Syphilis
Androgenetic Alopecia
Tinea Capitis
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
https://www.ncbi.nlm.nih.gov/books/NBK537000/
medtigo
Alopecia areata
Updated :
January 9, 2023
Alopecia areata (AA) is a kind of alopecia that affects the retina pigment epithelium, nails, and hairline follicles sporadically. It is a kind of hair loss that doesn’t leave scars and often manifests as rounded patches.
It is a kind of hair loss that doesn’t leave scars and often manifests as rounded patches. A rough estimate of the overall incidence is 20.2 per 100,000 person/year. In the overall population, there is a 2% chance that they may develop AA in their lifetime. Depending on the region and the ethnic group, the prevalence of AA ranges from 0.1% to 0.2%.
Between 0 to 8.6% of adult patients are believed to have a family history. Although the typical age of beginning seems to be between 25 & 36 years old, the incidence of AA appears to rise practically linearly with age. Early onset AA (between the ages of 5 and 10) typically manifests as a more severe variant.
Data indicate no discernible sex preference. It has links to a total risk increase of other autoimmune disorders (16 percent), such as thyroid disorders, vitiligo, & lupus erythematosus. In 39 percent of cases, there is also a connection to atopic dermatitis.
The comparative immune privilege of the hair shaft, which is an important characteristic, is primarily established by the inhibition of surface molecules necessary for expressing autoantigens to MHC class I CD8+ T lymphocytes and by the creation of a signaling setting that is inhibitive locally. One important cause of AA has been attributed to the hairline follicle’s immunological privilege breaking down.
The condition of hairline follicle cycling known as AA occurs when inflamed cells attack the hairline follicle matrix epithelial while it is experiencing slightly earlier cortical differentiating (anagen hairline follicles), causing them to enter the catagen stage too soon. However, because the stem line cells in the hair follicle are not destroyed, the hairline follicle can continue to cycle and renew. Follicles re-enter the anagen stage as a result regularly. However, they do not progress past the anagen III/IV stage.
It is likely that the immunological privilege of a perfectly healthy hair shaft collapses when AA develops. Therefore, it might only happen in a person who is genetically programmed if proinflammatory signaling, such as IFN gamma and substance P, which are known to upregulate MHC class Ia in individual hair shaft epithelial, are exposed to underlying autoreactive CD8+ T cells. It is uncertain what specific circumstance leads to alopecia areata. Certain triggers, most frequently physical or mental stress, immunizations, viral diseases, and medications, have been observed.
There may be a hereditary component to AA. It has been found that identical twins have a concordance rate of 55%. Recent GWAS metanalysis has mostly located the HLA-DRB1 as the source of the AA HLA signal.
An important role in pathogenesis may be played by one locus that contains the genes for the NKG2D (natural killer cell receptor D), which was linked to AA but no other autoimmune disorders. As a result, CD8+ NKG2D T cells have been investigated and discovered to be the primary AA effectors.
Since the inflammatory reaction spares hair roots, particularly stem cells, the possibility of hair regeneration exists. Current treatments, however, appear to have difficulty inducing regrowth. Although most patients will undergo numerous episodes of alopecia, approximately 34-50% of individuals may recover within a year.
However, 14-25% of individuals will advance to alopecia universalis or totalis, from which complete recovery is uncommon (10% of cases). With childhood-onset alopecia areata & ophiasis, the level of loss of hair & age of the patient at first diagnosis appear to be prognosis factors, and then a later phase of onset is correlated with less severe alopecia.
Clinical History:
Alopecia areata’s natural course is unpredictable. Between patients, there are significant differences in the severity and length of the condition. The majority of people with alopecia areata are asymptomatic, although 14% of individuals report burning or itching in the afflicted area. When the condition first manifests, it usually is localised.
80% of alopecia areata individuals have just one patch, 12.5% have two patches, and 7.7% have several patches. There is no connection between the quantity of patches at the beginning and the severity over time. Although it can affect any portion of the body with hair, alopecia areata most frequently affects the scalp (66.8-95%).
Localized alopecia areata
Localized patchy alopecia areata episodes with less than 50% involvement are typically self-limited; with or without therapy, most patients experience spontaneous regrowth within a few months.
Extensive alopecia areata
Less frequently seen are extensive (>50% involvement) types of alopecia areata. According to reports, 7% of patients get alopecia totalis or universalis at some point, while 11% of patients experience alopecia areata, which causes more than 40% of hair to fall out.
Alopecia totalis sufferers seem to be less common with each passing decade of life.
Physical examination
Alopecic patches that are smooth, somewhat erythematous (peach-colored), or normal-colored are typical. Exclamation point hairs, or hairs that are tapered near the proximal end, are pathognomonic but are not always present. When the pull test near the edge of a plaque yields a positive result, the disease is typically active, and additional hair loss is to be anticipated.
Other hair-bearing areas losing hair also supports the diagnosis. One or more rounded-to-oval denuded patches are the most typical appearances. The hair loss is not accompanied by any changes to the epidermis.
The pattern of alopecia areata can be used to classify it. Most typically, localised and patchy hair loss occurs.
When there is more widespread hair loss and the patches congregate, a reticular pattern develops.
When hair loss is restricted to the sides and lower back of the head, an ophiasis pattern develops. In contrast, the sisaipho pattern manifests when hair loss spares the sides and back of the head (ophiasis spelt backwards).
Alopecia totalis results in complete scalp hair loss.
In alopecia universalis, all hair-bearing areas completely lose all of their hair. Usually, focal alopecia areata can become generalised and resemble telogen effluvium (TE) or the form of androgenetic alopecia that affects women.
Differential Diagnoses
Trichotillomania
Brocq Pseudopelade
Telogen Effluvium
Pediatric Syphilis
Androgenetic Alopecia
Tinea Capitis
It is challenging to determine whether a therapy is effective because of the rate of spontaneous relapse/remission. For many people, letting AA untreated is an acceptable alternative. Intralesional & topical corticosteroids are the preferred first-line therapies for the majority of patients with patchy AA, despite the paucity of evidence supporting the effectiveness of medications. In 60 to 67% of instances, triamcinolone acetonide 5 to 10 mg/mL given every 2 to 6 weeks induces localized re-growth.
According to a study, hair regrowth rates were consistent across all intralesional triamcinolone acetonide concentrations (2.5, 5, and 10 mg/ml) used to treat AA on the scalp. However, at a higher dose (10mg/ml), the chance of cutaneous atrophy increased. It has been suggested to utilize intralesional betamethasone, but more research is required to determine its effectiveness.
Localized skin shrinkage, discomfort, and depigmentation are side effects. Strong topical glucocorticoids are frequently used to treat AA, however, there is little proof that they are beneficial. In patients who are unlikely to tolerate intralesional injections, topical steroids can be a viable treatment choice. The use of occlusive coverings leads to a greater response, improving more than 25% of cases.
Folliculitis brought on by glucocorticoids is a relatively frequent side effect of this method. Local immunotherapy may be used to treat patients with severe illness, which is frequently characterized as more than 50 percent scalp baldness. By employing this method, fewer injections are needed than if intralesional corticosteroids were being used. A strong contact allergen, such as SADBE (squaric acid dibutyl ester) or DPCP (diphenylcyclopropenone).
SADBE is used on the scalp once a week to encourage hair cell growth. A recent meta-analysis of contact immunotherapy for AA examined the clinical results. The percentage of hair regeneration was 74.6% in the subgroup with spotty alopecia & 54.4% in the subgroup with alopecia universalis/totalis. Individuals getting maintenance therapy experienced recurrence rates of 38.2%, compared to 49% for patients not obtaining maintenance therapy.
Minoxidil, PUVA, and anthralin are examples of second-line treatments.
Patients with chronic alopecia areata are typically the only ones who need systemic therapy. Systemic therapy with glucocorticoids may promote hair growth. They are not commonly utilized, nevertheless, primarily due to their negative side effects. Methotrexate, etanercept, azathioprine, and cyclosporine are further systemic treatments that have all demonstrated inconsistent clinical outcomes.
Recombinant IL-2, tofacitinib (JAK inhibitors), Platelet-rich plasma, simvastatin plus ezetimibe & excimer laser, and hydroxychloroquine are examples of current experimental therapies.
https://www.ncbi.nlm.nih.gov/books/NBK537000/
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