Alopecia Areata: Clinical Guidelines

List of Abbreviations

ALT – alanine aminotransferase

AST – aspartate aminotransferase

Abs – antibodies

ICD – International Classification of Diseases

PUVA therapy – irradiation with ultraviolet light of 320–400 nm wavelength using photosensitizing drugs

RCTs – randomized controlled trials

REG – rheoencephalogram

Tg – thyroglobulin

TSH – thyroid-stimulating hormone

TPO – thyroid peroxidase

FT3 – free triiodothyronine

FT4 – free thyroxine

HLA (Human Leukocyte Antigens) – major histocompatibility complex

Terms and Definitions

Alopecia areata is a chronic organ-specific autoimmune inflammatory disease with genetic predisposition, characterized by damage to hair follicles and sometimes nail plates (in 7–66% of patients), persistent or temporary non-scarring hair loss.

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Alopecia areata is a chronic organ-specific autoimmune inflammatory disease with genetic predisposition, characterized by damage to hair follicles and sometimes nail plates (in 7–66% of patients), persistent or temporary non-scarring hair loss [1].

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

The development of the disease is thought to be based on a local autoimmune mechanism of hair follicle damage, which leads to a breakdown of immune tolerance of the cells forming the follicle and cessation of specific reception from its dermal papilla [1].

Predisposition to alopecia areata is genetic. A family history of the disease is present in 10–20% of patients, and the true incidence is likely even higher, as mild cases may go unnoticed. The genetic predisposition has a polygenic nature. An association of alopecia areata with specific class II HLA alleles, particularly DQB1*03 and DRB1*1104, is observed. HLA alleles DQB1*0301 (HLA-DQ7) and DRB1*1104 (HLA-DR11) may be associated with alopecia totalis and alopecia universalis.

Triggering factors for the disease can include stress, vaccination, viral diseases, infectious diseases, antibiotic therapy, anesthesia, etc.

Conditions associated with alopecia areata.

Autoimmune thyroid diseases are observed in 8–28% of patients; however, the presence of thyroid antibodies in the blood does not clinically correlate with the severity of alopecia areata. Vitiligo is observed in 3–8% of patients with alopecia areata. Atopy is recorded in AA patients twice as frequently compared to the general population.

The most common comorbid conditions in patients with alopecia areata include chromosome 21 trisomy (Down syndrome), pernicious anemia, autoimmune polyglandular syndrome, celiac disease, iron deficiency, vitamin D deficiency, and trichotillomania.

Relatives of patients with alopecia areata have an increased risk of developing type 1 diabetes; conversely, the incidence rate in the patients themselves may be lower compared to the general population. Patients exhibit a high rate of psychiatric disorders, particularly anxiety and depressive disorders [1].

1.3 Epidemiology of the Disease or Condition

Alopecia areata is a common type of hair loss. The incidence and prevalence of alopecia areata depend on geographical and ethnic differences, as well as the immunogenetic background of the patients. Individuals of both sexes are susceptible to the disease. The frequency of alopecia areata accounts for 0.7–3.8% of patients seeking help from a dermatologist. The lifetime risk of developing the disease is 1.7%. Alopecia areata occurs equally in men and women. The first patch of hair loss appears in 20% of patients during childhood, in 60% of patients under the age of 20, and in 20% of patients over the age of 40 [1].

Up to 50% of patients recover within a year even without treatment (spontaneous remission). At the same time, 85% of patients experience more than one episode of the disease. When alopecia areata manifests before puberty, the probability of developing alopecia totalis is 50%. With alopecia totalis/universalis, the probability of complete recovery is less than 10%.

The prognosis is worsened by early age of disease onset, its duration, family history, affected area size, nail changes, and the presence of concomitant atopy and other autoimmune diseases [2–4].

1.4 Features of Coding the Disease or Condition

Alopecia areata (L63):

L63.0 – Alopecia totalis;

L63.1 – Alopecia universalis;

L63.2 – Ophiasis;

L63.8 – Other alopecia areata;

L63.9 – Alopecia areata, unspecified.

1.5 Classification of the disease or condition

Depending on the extent and type of hair loss, the following clinical forms of alopecia areata are distinguished:

local (limited);

subtotal;

total;

universal.

Other forms of alopecia areata include:

multifocal (reticular) pattern of hair loss patches;

ophiasis;

sisapho (inverse ophiasis);

diffuse form.

1.6 Clinical presentation of the disease or condition

In the local (limited) form of alopecia areata, one or more well-defined round patches of hair loss are identified on the scalp.

In the subtotal form of alopecia areata, more than 40% of hair is absent on the scalp.

In ophiasis, the patches of hair loss are ribbon-shaped, involving the entire marginal hair growth zone in the occipital and temporal regions.

In sisapho (inverse ophiasis), ribbon-shaped patches of hair loss extend to the frontoparietal and temporal regions.

The diffuse form of alopecia areata is characterized by partial or complete diffuse thinning of the hair on the scalp.

In the total form of alopecia areata, there is a complete loss of terminal hair on the scalp.

In the universal form of alopecia areata, hair is absent on the scalp, eyebrows, eyelashes, and body skin.

Severe forms of alopecia areata include: hair loss of ≥50% of the scalp area, total, and universal forms.

2. Diagnostics, medical indications and contraindications for diagnostic methods

Criteria for establishing the diagnosis/condition: the diagnosis of alopecia areata is established based on the clinical manifestations of the disease.

2.1 Complaints and Anamnesis

In most cases, the disease proceeds without subjective sensations. In rare cases, with a disease duration of less than 1 month, the following subjective symptoms may occur: hyperemia, burning sensation, itching in the area of hair loss [2–4].

2.2 Physical Examination

In the active (progressive) stage, subjective symptoms are generally absent; some patients may complain of itching, burning, or pain in the affected areas. Typical lesions present as non-scarring hair loss patches of round or oval shape with unchanged skin color. Moderately red or peach-colored patches are less common. Proximally narrowed and distally wide exclamation mark hairs are a characteristic feature, often noticeable on the affected area or at its periphery. In the active phase of the disease, the hair pull test may be positive at the borders of the lesions — the zone of so-called "loose hairs". The width of this zone does not exceed 0.5–1 cm.

AA patients (in 7–66%) may exhibit specific dystrophic nail changes: pinpoint nail pitting, trachyonychia, Beau's lines, onychorrhexis, nail thinning or thickening, onychomadesis, koilonychia, punctate or transverse leukonychia, red spotted lunulae, and wavy alterations of the free edge.

Trichoscopy: presence of "yellow dots" (follicles filled with hyperkeratotic masses), "black dots" (cadaverized hairs representing comedo-like follicular plugs), exclamation mark hairs (dystrophically altered hairs narrowed in the proximal part); broken hairs, conical, tulip-shaped, pigtail-like coiled hairs, monilethrix-like hairs, and zigzag hairs may also be present.

AA can affect almost any hair-bearing area, but the scalp is affected in approximately 90% of patients. Initially, the disease does not affect grey hair.

In the stationary stage, the zone of "loose hairs" is not detected around the alopecia patch, and the skin within the patch is unchanged.

Trichoscopy: yellow dots and vellus hairs may be present.

In the regressive stage, the growth of vellus hair—fine depigmented hair—as well as partial growth of terminal pigmented hair is observed within the alopecia patch. When hair growth resumes, initial hairs are typically hypopigmented, but over time the color usually returns [2–5].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

2.3 Laboratory Diagnostics

Comments: Histologically, AA in the active stage is characterized by a pronounced lymphohistiocytic infiltrate located perivascularly and perifollicularly with penetration into the hair bulb, with a predominance of T-lymphocytes; perivascular edema is possible. However, the histopathological signs of AA depend on the stage of the disease; in the case of chronic patches, classical signs may be absent. In the chronic stage, fibrous and atrophic processes predominate with perifollicular and perivascular sclerosis, minimal lymphohistiocytic infiltrate, and reduction and partial atrophy of hair follicles.

Blood test for thyroid-stimulating hormone (TSH), determination of anti-thyroperoxidase antibodies in the blood, blood test for free triiodothyronine ($FT_3$), blood serum test for free thyroxine ($FT_4$), determination of anti-thyroglobulin antibodies in blood serum [6].

GGR BLOC 2Grade of Recommendation B (Level of Evidence – 2)

Blood test for 25-OH vitamin D to rule out 25-OH vitamin D deficiency and address the need for 25-OH vitamin D supplementation [7, 8].

GGR BLOC 2Grade of Recommendation B (Level of Evidence – 2)

2.4 Instrumental Diagnostics

Comments: Differential diagnosis is carried out with trichotillomania, diffuse toxic alopecia, traumatic alopecia, scalp trichophytosis, and scarring alopecias.

In trichotillomania, patches of alopecia have an irregular shape, may resemble "flame tongues," and are typically located in the temporal and parietal areas, as well as the eyebrows and eyelashes. Terminal hair growth is often observed in the central part of the patch. Hairs within the patch may be broken at varying heights. The pull test at the edge of the patch reveals no zone of loose hair. Trichotillomania can occur against the background of alopecia areata (AA), which is sometimes characterized by itching, and scratching can become a habit.

Diffuse toxic alopecia is typically associated with acute toxic conditions: heavy metal poisoning, chemotherapy, antitumor drug administration, and prolonged fever.

In traumatic alopecia, hairs are evenly broken at the same height in the center of the patch, there are no signs of inflammation, and the anamnesis reveals an episode of abuse or mechanical damage by styling devices.

In scalp trichophytosis, examination reveals an inflammatory rim at the periphery of the patch and the presence of "stumps"—hairs broken at a level of 2–3 mm from the skin surface. The disease may be accompanied by inflammation and scaling, which are generally not absent in AA. Microscopic examination of hair for dermatophytes reveals fungal mycelium and spores inside and outside the hair shaft.

In scarring alopecia, the skin within the affected area is shiny, and the follicular apparatus is absent. Clinical manifestations sometimes complicate diagnosis, in which case a histological examination is recommended.

In children with a congenital solitary patch of hair loss in the temporal region, differential diagnosis with temporal triangular alopecia should be performed.

2.5 Other Procedures

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

Currently, there is no cure for the disease. Therapy is administered to restore hair growth, but proving its long-term efficacy is not feasible. The probability of spontaneous remission in patchy alopecia areata is as follows: 1/3 within 6 months, 1/2 within 1 year, 2/3 within 5 years; after this period, complete remissions are rare. The relapse rate within 5 years is 80%, and within 20 years it is 100%. The rate of complete remission in totalis and universalis alopecia with a disease duration of 5 years is 1% in children and less than 10% in adults.

3.1 Conservative Treatment

For children - Level of Evidence C (Reliability of Evidence 3)

For adults - Level of Evidence C (Reliability of Evidence 4)

#prednisolone**, starting at 40 mg per day orally (with a gradual dose reduction) for 6 weeks [1]

#prednisolone** 200 mg per week orally for 3 months [1]

or

#prednisolone** 300 mg orally once a month for 3 months [1, 56, 57]

or

#methylprednisolone** 250 mg intravenously twice a day for 3 days [1]

GCR CLEL 5Grade of Recommendations C (Level of Evidence 5)

#prednisolone** 5 mg/kg/month orally for 3 months [55, 57]

or

#prednisolone** 300 mg/month orally for 3 months [1, 57]

or

#prednisolone** 0.5–0.8 mg/kg/day orally (with a gradual dose reduction) for 8 weeks, not exceeding a treatment duration of 12 weeks [57]

GCR CLEL 5Grade of Recommendations C (Level of Evidence 5)

Comments: systemic therapy with #prednisolone** may be prescribed to children starting from 15 years of age. The risk of side effects and the probable efficacy of systemic therapy with #prednisolone** should be weighed.

#methotrexate** at a target dose of 15–25 mg per week for 1–31 months [1, 14–16]. When used in children under 18 years of age, the target dose is 0.38 mg/kg/week [52].

For children - Level of Evidence C (Reliability of Evidence 4)

For adults - Level of Evidence C (Reliability of Evidence 5)

or

Sparing therapy: #methotrexate** 15–20 mg once a week in combination with #prednisolone** 10–20 mg per day orally [1, 15].

LeR CLoE 5Level of Recommendation C (Level of Evidence — 5)

Comments: the average duration of treatment with #methotrexate** can take from 6 to 12 months. Tablet forms in 2 divided doses 12 hours apart, injections once a week. #methotrexate** therapy may be prescribed to children starting from 15 years of age. The risk of side effects and the probable efficacy of #methotrexate** therapy should be weighed. The efficacy of #methotrexate** therapy in children is lower than in adults. If no effect is observed within 6 months, therapy is discontinued. No earlier than 24 hours later – #folic acid** orally 5–10 mg/day [53, 54].

#cyclosporine** 3–5 mg per kg of body weight per day orally for 6–12 months. Upon achieving a positive clinical result, the dose is gradually reduced until complete discontinuation [14, 17, 18, 50].

or

Sparing therapy: #cyclosporine** 2.5–5 mg/kg per day orally in combination with #methylprednisolone** 20–24 mg/day with a reduction in the dose of #methylprednisolone** over 3 weeks to 4 mg/day, maintaining a #methylprednisolone** dose of 2–4 mg/day depending on the clinical outcome for no more than 24 weeks [18, 50].

LoE BRoE 2Level of Evidence B (Reliability of Evidence 2)

Comments: sparing therapy in combination with #methylprednisolone** is more effective than #cyclosporine** monotherapy [17, 50]. Systemic therapy with #cyclosporine** may be prescribed to children starting from 15 years of age. The risk of side effects and the probable efficacy of systemic therapy with #cyclosporine** should be weighed.

#tofacitinib** 5 mg twice daily orally for 3–17 months [19, 20, 21, 51].

GCR CLOCE 4Grade of Recommendation C (Level of Evidence 4)

Comments: systemic therapy with #tofacitinib** may be prescribed to children starting from 15 years of age. The risk of side effects and the probable efficacy of systemic therapy with #tofacitinib** should be weighed.

baricitinib** 4 mg once daily orally for 36–52 weeks; if no efficacy is observed within 36 weeks, it is recommended to discontinue therapy [83, 87].

LoE ARoE 2Level of Evidence A (Reliability of Evidence 2)

minoxidil, 5% solution topically to the patches of alopecia [68].

GCR BLOCE 1Grade of Recommendation B (Level of Evidence 1)

or

minoxidil, 2% topical solution applied to alopecia patches [1, 14, 62, 57, 65].

LeR CLoE 5Level of Recommendation C (Level of Evidence — 5)

or

minoxidil 2% three times daily for 6–14 weeks after discontinuation of systemic glucocorticoid therapy [69].

Level of Evidence CGrade of Recommendation 2Level of Evidence C (Grade of Recommendation 2)

Comments: topical minoxidil is contraindicated in individuals over 65 years of age

#minoxidil, 5% topical solution applied to alopecia patches twice daily [68, 84].

GCR BLOCE 1Grade of Recommendation B (Level of Evidence 1)

#minoxidil 2% three times daily for 6–14 weeks after discontinuation of systemic glucocorticoid therapy [69].

Level of Evidence CGrade of Recommendation 2Level of Evidence C (Grade of Recommendation 2)

Comments: #minoxidil topical therapy is approved for children from 9 years of age.

#triamcinolone every 4 weeks as intradermal injections spaced 0.5–1 cm apart, 0.1 ml each [1, 50].

LeR CLoE 5Level of Recommendation C (Level of Evidence — 5)

Comments: The maximum dose of #triamcinolone per session should not exceed 20 mg [22–25]. It is administered at an average concentration of 2.5–5 mg/ml or not exceeding 10 mg/ml [14]. If no positive effect is observed 6 months after starting treatment, intralesional administration of the drug should be discontinued.

Intralesional administration of #triamcinolone may be prescribed to children aged 12 years and older. The risk of side effects should be weighed against the expected efficacy of intralesional #triamcinolone.

Side effects include transient atrophy and telangiectasia. The risk of developing cataracts or increased intraocular pressure rises when glucocorticoids are administered near the eyes, such as in the eyebrow area. To reduce the risk of adverse events, it is necessary to decrease the drug volume and the number of injections at the site, as well as avoid intraepidermal injections.

To reduce injection pain, topical local anesthetics are applied before the procedure [26, 27].

or

#betamethasone: intradermal administration into the lesion at a dose of 0.2 ml/cm². The drug is administered every 4–6 weeks; the total amount of the drug administered across all sites within a week must not exceed 1 ml [28, 50].

LeR CLoE 5Level of Recommendation C (Level of Evidence — 5)

Comments: intralesional administration of #betamethasone may be prescribed to children aged 12 years and older. The risk of side effects should be weighed against the expected efficacy of intralesional #triamcinolone. Side effects include transient atrophy and telangiectasia. The risk of developing cataracts or increased intraocular pressure rises when glucocorticoids are administered near the eyes, such as in the eyebrow area. To reduce the risk of adverse events, it is necessary to decrease the drug volume and the number of injections at the site, as well as avoid intraepidermal injections.

#betamethasone 0,05% spray 2 times daily with a treatment duration of up to 12 weeks [64].

GRC CLEL 2Grade of Recommendation C (Level of Evidence 2)

#betamethasone** 0,05% cream once daily for 3 months [63, 86]

LeR CLoE 5Level of Recommendation C (Level of Evidence — 5)

#clobetasol 0.05% ointment under an occlusive dressing at night 6 days a week, treatment duration – up to 6 months [1, 35, 36, 50].

GCR CLOCE 4Grade of Recommendation C (Level of Evidence 4)

#clobetasol 0.05% cream as a thin layer on lesions 2 times daily for 12 weeks [73, 38]

Grade of Recommendation 2 (Level of Evidence C)

#betamethasone 0,05% spray 2 times daily with a treatment duration of up to 12 weeks [64]

Level of Evidence CGrade of Recommendation 2Level of Evidence C (Grade of Recommendation 2)

#clobetasol 0.05% cream as a thin layer on lesions 2 times daily, 2 courses of 6 weeks with 6-week washout periods, total duration – 24 weeks [37].

LoE AGoE 2Level of Evidence A (Grade of Recommendation 2)

#clobetasol 0.05% cream as a thin layer on lesions 2 times daily for 12 weeks [38].

Level of Evidence CGrade of Recommendation 2Level of Evidence C (Grade of Recommendation 2)

#calcipotriol ointment 2 times daily for 12 weeks [34]

GCR CLOCE 4Grade of Recommendation C (Level of Evidence 4)

#betamethasone+calcipotriol topical ointment 2 times daily for 3 months [61]

GPR BLEL 2Grade of Recommendation B (Level of Evidence 2)

#bimatoprost 0.03% solution 2 times daily for 12 weeks [30]

GPR BLEL 2Grade of Recommendation B (Level of Evidence 2)

#pimecrolimus** 1% cream daily 2 times daily for 12 weeks [38].

Comments: recommended for children from 3 years of age [38].

Grade of Recommendation 2 (Level of Evidence B)

#tacrolimus** 0.1% ointment daily once daily at night under occlusion for 24 weeks [60]

Grade of Recommendation 4 (Level of Evidence C)

Comments: recommended for children from 6 years of age [60].

topical administration of prostaglandin analogues [40];

#bimatoprost 0.03% solution applied daily in the evening to the base of the upper eyelashes for 1–4 months; therapy may be continued upon achieving a clinical effect [40, 58];

For adults - Grade of Recommendation C (Level of Evidence 4)

For children - Grade of Recommendation B (Level of Evidence 2)

Comments: recommended for children from 5 years of age.

or

#latanoprost 0.005% solution applied daily in the evening to the base of the upper eyelashes for 1–4 months; therapy may be continued upon achieving a clinical effect [40, 59, 70];

GCR CLOCE 4Grade of Recommendation C (Level of Evidence 4)

Comments: recommended for children from 11 years of age.

3.2 Surgical Treatment

Not applicable.

3.3 Other Treatment

Narrow-band phototherapy using a 308 nm excimer laser. Initial laser radiation dose at 50 mJ/cm2 of the minimal erythema dose; subsequently, the radiation dose is increased by 50 mJ/cm2 every two sessions. The affected area is treated 2 times a week, for a course of no more than 24 sessions [41–43].

LoR CLE 3Level of Recommendation C (Level of Evidence 3)

Comments: recommended for children from 4 years of age.

Intradermal administration of platelet-rich autologous plasma into the scalp every 2–4 weeks for a total of 3 procedures [45, 46, 71, 72].

Comments: recommended for children from 15 years of age.

GRC BLEL 2Grade of Recommendation B (Level of Evidence 2)

non-ablative fractional photothermolysis (1550 nm wavelength): laser radiation dose 30–45 mJ/cm², 6–8 treatment zones, 8–10 passes, 2–3 sessions at 3–6 week intervals [47, 48]

or

non-ablative fractional photothermolysis (1550 nm wavelength): laser radiation dose 10–15 mJ, MTZ 300/cm²/pass, 2 passes per session, a course of 24 sessions at weekly intervals [48]

or

for localized, total, and universal forms:

non-ablative fractional photothermolysis: laser radiation dose 10-15 mJ, MTZ 300/cm²/pass, once every 2 weeks for 10 sessions at 2-week intervals combined with 5% minoxidil 2 times daily applied immediately after the photothermolysis session [48, 49].

GCR CLOCE 4Grade of Recommendation C (Level of Evidence 4)

non-ablative fractional photothermolysis: laser radiation dose 10–15 mJ, MTZ 300/cm²/pass, once every 2 weeks – 10 sessions at 2-week intervals combined with 5% minoxidil 2 times a day daily, applied immediately after the photothermolysis session [49].

GCR CLOCE 4Grade of Recommendation C (Level of Evidence 4)

Medical nutrition therapy is not used.

Anesthesia: not used

4. Medical Rehabilitation and Sanatorium-Resort Treatment

Rehabilitation and spa treatment are not used.

5. Prevention and Dispensary Observation

Not applicable.

6. Organization of Medical Care

Treatment is carried out on an outpatient basis in a dermatovenereological medical institution. Indications for hospitalization: none.

7. Additional Information

Currently, there is no cure for the disease. Therapy is administered to restore hair growth, but proving its long-term efficacy is not feasible. The probability of spontaneous remission in alopecia areata with patches is as follows: 1/3 within 6 months, 1/2 – within 1 year, 2/3 – within 5 years; after this period, complete remissions are rare. The relapse rate within 5 years is 80%, and within 20 years – 100%. The rate of complete remission in totalis and universalis alopecia with a disease duration of 5 years or more is 1% in children and less than 10% in adults.

Management in case of treatment failure: medical tattooing (trichopigmentation, permanent makeup, microblading, etc.), wigs, hairpieces, hair integration systems, camouflage products for topical application to the scalp and hair (thickeners, powders, hair fibers).

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

1. Kubanov Alexey Alekseevich – Academician of the RAS, Doctor of Medical Sciences, Professor, Director of the State Research Center of Dermatovenereology and Cosmetology of the Russian Ministry of Health, President of the Association of Dermatovenereologists and Cosmetologists, Moscow.

2. Kondrakhina Irina Nikiforovna – Doctor of Medical Sciences, Head of the Consultative and Diagnostic Center of the State Research Center of Dermatovenereology and Cosmetology of the Russian Ministry of Health, member of the Association of Dermatovenereologists and Cosmetologists, Moscow.

3. Gallyamova Yulia Albertovna – Doctor of Medical Sciences, Professor, Head of the Course of Dermatovenereology and Cosmetology at the Department of Allergology and Immunology with a Course of Dermatovenereology and Cosmetology, Penza Institute for Advanced Medical Training – branch of the Russian Medical Academy of Continuous Professional Education of the Russian Ministry of Health, member of the Association of Dermatovenereologists and Cosmetologists, Penza.

4. Asoskova Anastasia Valerievna – Candidate of Medical Sciences, Associate Professor at the Department of Dermatovenereology and Cosmetology, Russian Medical Academy of Continuous Professional Education of the Russian Ministry of Health, dermatovenereologist at the Consultative and Diagnostic Center of the State Research Center of Dermatovenereology and Cosmetology of the Russian Ministry of Health, member of the Association of Dermatovenereologists and Cosmetologists, Moscow.

Conflict of interest:

The authors declare no conflict of interest.

Appendix A2. Methodology for Developing Clinical Guidelines

Target audience for these clinical guidelines:

Medical specialists: dermatovenereologists, pediatricians.

Residents and trainees of continuing professional education programs in the specified specialties.

Table A1. Scale for assessing levels of evidence (LoE) for diagnostic methods (diagnostic interventions)

Table P2. Scale for assessing levels of evidence (LE) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, and rehabilitative interventions)

Table A3. Scale for assessing the levels of evidence (LE) for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions)

Procedure for updating clinical guidelines

The draft guidelines are reviewed by independent experts. Comments received from experts are systematized and discussed by the members of the working group. Resulting changes to the guidelines or reasons for declining changes are recorded.

The draft guidelines are posted for discussion on the website of the State Research Center of Dermatovenereology and Cosmetology of the Russian Ministry of Health so that individuals not involved in guideline development can participate in discussing and improving the guidelines.

For the final edition and quality control, the guidelines are re-analyzed by the members of the working group.

Appendix A3. Reference Materials

These clinical guidelines were developed taking into account the following regulatory legal documents:

Order of the Ministry of Health of the Russian Federation No. 924n dated November 15, 2012, "On Approval of the Procedure for Providing Medical Care to the Population in the Profile 'Dermatovenereology'."

Appendix B. Physician Action Algorithms

Flowchart 1. Patient management algorithm

Appendix C. Patient Information

Patients with prolonged absence of eyebrows may be offered dermatography or medical tattooing (trichopigmentation).

Various topical camouflage products (hair powders, pencils, sprays), hair prostheses, wigs, hair integration systems, hairpieces, and other hair additions are recommended for patients with AA during therapy or in case of treatment failure.

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

Not applicable.