ICD 10 alopecia areata. Alopecia, Diseases and treatment with folk remedies and medicines

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2017

Alopecia totalis (L63.0), Alopecia universalis (L63.1), Alopecia areata (L63), Alopecia areata, unspecified (L63.9), Alopecia areata (LAND FORM), Other alopecia areata (L63.8)

Dermatovenereology

general information

Short description

Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated June 29, 2017
Protocol No. 24

Alopecia is a pathological hair loss caused by various influences on the hair follicle and clinically manifested by the formation of lesions with a complete absence of hair on the head, beard, eyebrows, eyelashes and torso.

INTRODUCTORY PART

ICD-10 code(s):

Date of development of the protocol: 2017

Abbreviations used in the protocol:

Protocol users: general practitioners, pediatricians, therapists, dermatovenerologists.

Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
B	High-quality (++) systematic review of cohort or case-control studies, or High-quality (++) cohort or case-control studies with very low risk of bias, or RCTs with low (+) risk of bias, the results of which can be generalized to an appropriate population .
C	Cohort or case-control study or controlled trial without randomization with low risk of bias (+). The results of which can be generalized to the relevant population or RCTs with very low or low risk of bias (++ or +), the results of which cannot be directly generalized to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best clinical practice.

Classification

Classification:
By type:
· ordinary;
· prehypertensive;
· atopic;
· autoimmune;
· mixed.

By form:
· local;
· ribbon-like;
· subtotal;
· total;
· universal (malignant) form;
· alopecia areata with damage to the nail plates.

By severity:
· light up to 25% of the area, single lesions up to 3-5 cm in diameter;
· average 25-50% of the area, lesions 5-10 cm in diameter;
· heavy up to 75% of the area.

With the flow:
· acute;
· subacute;
· chronic.

By degree of activity:
progressive;
· stationary;
· regressing.

Diagnostics

METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

Diagnostic criteria

Complaints:
· for hair loss.

History of the disease:
age of onset of the disease;
· connection with provoking factors;
· presence of this pathology in close relatives, concomitant diseases.

Physical examination:
Pathognomonic symptoms:
· presence of foci of alopecia with clear boundaries;
· the presence of broken hair in the hearth or along its edge;
presence of light vellus hair in the growth area

Laboratory research[ UD - B] :
· general blood analysis: increased platelet count (endogenous intoxication);
· identification by microscopy of dystrophic proximal ends of hair epilated from the lesion in the form of a “broken rope”;
microscopic examination for fungi;
· trichoscopy of skin in lesions;
· blood chemistry: determination of glucose, total protein, cholesterol, bilirubin, creatinine, urea, ALT, ACaT immunogram levels I and II; blood for the content of sex hormones (estrogen, progesterone), T-4, T-4, TSH.

Instrumental studies: are not specific and mandatory; if pathogenetic cause-and-effect relationships are identified, it is recommended:
· echoencephalography(to exclude pathological processes in the structure of the brain);
· radiography of the sella turcica(primarily with total and universal forms to exclude space-occupying formations);
· Rheovasography of cerebral vessels or Dopplerography of the vessels of the head and neck.

Indications for consultation with specialists:
· consultation with a therapist - in the presence of concomitant therapeutic pathology that worsens the course of the skin process;
· consultation with a neurologist - to establish pathogenetic cause-and-effect relationships of hair loss;
· consultation with an endocrinologist - to establish the pathogenetic cause-and-effect relationships of hair loss;
· consultation with a psychotherapist - for medical and social rehabilitation.

Diagnostic algorithm:(scheme)

Differential diagnosis

Differential diagnosis and rationale for additional studies:

*Diagnosis*	*Rationale for*	*Surveys*	*Criteria*
	*differential*		*exclusion of diagnosis*
	*diagnostics*
Trichotillomania	Foci of bizarre shape, with uneven contours, often with preservation of hair within the foci of baldness, with the absence of vellus and an area of loose hair.	Diagnosis is based on the histology of the biopsy specimen (hemorrhages and ruptures of the membranes, absence of hair in the telogen phase.	1. Disease refers to disorders of the patient’s habits and desires; 2. Noticeable hair loss after repeated unsuccessful attempts to suppress the desire to pull it out; 2. Among the patients, females aged 11-16 years predominate; 3. Areas of baldness are usually located symmetrically
Mycosis of the scalp	An inflammatory ridge is detected along the periphery of the lesion and the presence of stumps of hair broken off at a level of 2-3 mm from the surface of the skin.	To confirm the diagnosis, a microscopic examination is performed for mycosis; fungal drusen are detected inside and outside the hair shaft.	1. Most often found in children and adolescents 2. On the scalp there are round-shaped lesions with moderate hyperemia, skin peeling and hair breaking at a level of 1-2 or 5-6 mm from the skin level. 3. Glow under a Wood's fluorescent lamp
Toxic alopecia	There is a clear dependence with the use of cytostatics, anticoagulants, chemotherapy, psychotropic drugs and severe infectious process	The diagnosis is established on the basis of anamnesis of the disease, clinical picture in the form of focal or complete alopecia on the scalp and/or torso	1.The disease often begins with severe symptoms of intoxication 2. At the same time, there may be involvement of internal organs in the process

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Treatment

Drugs (active ingredients) used in treatment

Treatment (outpatient clinic)

TREATMENT TACTICS AT AN OUTPATIENT LEVEL: all patients with this diagnosis are treated at an outpatient level.

Non-drug treatment:
Diet: table No. 15, in the diet it is necessary to increase the amount of water consumed based on an increase in blood viscosity, signs of peripheral blood thickening).

Physiotherapy:
- narrowband phototherapy using an excimer laser with a wavelength of 308 nm (C). The initial dose of laser radiation is 50 mJ/cm 2 less than the minimum erythemal dose; subsequently, the radiation dose is increased by 50 mJ/cm2 every two sessions. The affected area is treated 2 times a week, no more than 24 sessions.

For severe forms of HA- PUVA therapy (C). Psoralen and its derivatives are used at a dose of 0.5 mg per kg of body weight 2 hours before the procedure. Radiation dose - with a gradual increase from 1 J per 1 cm 2 to 15 J per 1 cm 2.

Drug treatment: the use of these drugs can be presented in the form of various treatment options, depending on the form (the note indicates the indications for choosing this treatment method). For example, the choice of systemic corticosteroids is necessary for severe forms of alopecia - total or rapidly progressive subtotal in adults and children. Topical corticosteroids (creams, ointments, lotions) are used starting from the focal form of alopecia in combination with vitamins, microelements and immunomodulators, the duration of therapy is from 4 to 8 weeks. If topical corticosteroids are ineffective, peripheral vasodilators, dithranol, physical therapy (PUVA) and systemic corticosteroids (standard therapy or pulse therapy) are used.

When identifying the role of the immune system in the development of alopecia areata, immunosuppressive drugs are used - cyclosporine, methotrexate. Prescription of drugs is primarily for persons with long-term total alopecia, with a tendency to recurrent course and refractory to traditional therapy.

If the patient is prone to depression and emotional lability, consultation with a psychologist or psychiatrist is recommended.
It should be noted that the best option for patients with a single focus of baldness is observation tactics, because In 80% of patients with single spots present for less than a year, the alopecia spontaneously regresses.

List of essential medicines(having a 100% probability of application):

Drug group	Medicines	Indications	Dosage, method of application	Level of evidence	Note
Topical glucocorticosteroids	Prednisolone		cream, ointment 0.5% 2 times a day	WITH	In order to normalize local immunity, relieve inflammation
	Betamethasonavalerate	All forms of alopecia areata, except universalis	cream 0.1% 2 times a day	WITH
	Betamethasone dipropionate	All forms of alopecia areata, except universalis	0.05% ointment 2 times a day	WITH
	Hydrocortisone butyrate	All forms of alopecia areata, except universalis	cream 0.1% 2 times a day	IN
	Methylprednisolone aceponate	All forms of alopecia areata, except universalis	cream 0.1% 1 time per day	WITH
	Mometasonafuroate	All forms of alopecia areata, except universalis	cream 0.1% 1 time per day	WITH
	Betamethasone	All forms of alopecia areata, except universalis	Ampoule 1.0 ml iv 0.1 ml per 2 cm2 every 4-6 weeks	WITH
	Diprospan (synthetic derivative of prednisolone)	All forms of alopecia areata, except universalis	crystalline suspension, Ampoule 1.0 ml iv 0.1 ml per 2 cm2 every 2 weeks	WITH
	Triamcinolone acetonide,	All forms of alopecia areata, except universalis	suspension for injection every 4-6 weeks in the form of multiple intradermal injections with an interval of 0.5-1 cm of 0.1 ml is injected with a 30 gauge needle 0.5 inches long. The maximum dose per session should be be 20 mg	IN
	clobetasol propionate,	For severe forms of alopecia	ointment 0.05% 2 times a day externally under an occlusive dressing with a duration of therapy of up to 2 months.	IN
Peripheral vasodilator	Minoxidil	All forms of alopecia areata, except universalis	Lotion (2-5% r-raminoxidil) 2 times a day	A	The drug is a follicle stimulator
Dermatotropic agents	Dithranol	All forms of alopecia areata, except universalis	Ointment 1 time per day	WITH	Side effects: inflammatory reactions and pigmentation of surrounding healthy skin.
Microelements	Zinc sulfate	All forms of alopecia areata	Powder 0.2 g 1 time per day for 2 months	WITH
	Zinc oxide	All forms of alopecia areata	powder 0.1 g 0.02 - 0.05 g (children) 2 times a day for 2 months
Systemic glucocorticosteroids*	Prednisolone		tablet 5 mg (course dose 40-60 mg)	WITH	according to indications, depending on the severity (total form of alopecia)
Systemic glucocorticosteroids*	Betamethasone	Subtotal form of alopecia and fulminant course	ampoules 1.0 ml 1 time every 7-10 days (from 4 to 6 procedures)	WITH
Antimetabolites	methotrexate	Severe alopecia	- tablets, injection solution 15-30 mg 1 time per week. orally or subcutaneously for 9 months; upon receiving a positive effect - extension of therapy up to 18 months. - injection solution 15-30 mg once a week orally or subcutaneously in combination with prednisolone 10-20 mg per 24 hours orally until hair growth resumes. - if there is no positive effect, discontinue methotrexate.	WITH
Immunosuppressants. .	cyclosporine	Severe forms of alopecia	capsules, oral solution 2.5-6 mg per kg body weight per day orally for 2-12 months. Upon reaching positive clinical result, the dose is gradually reduced to complete cancellation	WITH

Note: * - medicines for which the evidence base today is not sufficiently convincing.

List of additional medicines:

Drug group	Medicines	Indications	Dose and method of administration	Level evidence	Note
Drugs that improve peripheral circulation*	Deproteinized hemoderivative from calf blood	Common forms and recurrent course	ampoules 5.0 ml, 1 month		To stimulate hair growth by activating blood microcirculation under the skin
Drugs that replenish potassium and magnesium deficiency*	Orotic acid	Forms of alopecia due to potassium and magnesium deficiency, during therapy with systemic corticosteroids	tablets 0.5 3 times a day		for the entire course of hormone therapy, to reduce side effects

Surgery: No.

Further management:
· balanced diet with a high content of vitamins and microelements;
· elimination of risk factors;
· treatment of concomitant pathology;
· courses of vitamin therapy, herbal medicine, adaptogens, lipotropic agents;
· Spa treatment.

Indicators of treatment effectiveness:
· Criteria for assessing the effectiveness of treatment:
0 points - no effect;
1 point - rare growth of vellus;
2 - growth of vellus and terminal hair;
3 - growth of terminal hair.
· restoration of the hair structure and healing of all lesions in all areas (scalp, mustache and beard areas in men and vellus hair on the body).

Hospitalization

INDICATIONS FOR HOSPITALIZATION, INDICATING THE TYPE OF HOSPITALIZATION

Indications for planned hospitalization: No.
Indications for emergency hospitalization: No.

Information

Sources and literature

Minutes of meetings of the Joint Commission on the Quality of Medical Services of the Ministry of Health of the Republic of Kazakhstan, 2017
1. 1) Skripkina Yu.K. Skin and venereal diseases [Text]: textbook - Moscow: GOETAR-Media, 2007.- 544 pp.: ill. 2) Federal clinical recommendations for the management of patients with alopecia areata. Moscow 2012 3) “Treatment of skin and venereal diseases.” // Guide for doctors. THEM. Romanenko V.V. Kaluga, SL Afonin. Moscow 2006 4) Rational pharmacotherapy of skin diseases and sexually transmitted infections. Guide for practicing physicians. // Ed. A.A. Kubanova, V.I. Kisina. Moscow, 2005 5) Evidence based (s3) guidelines for the treatment of androgenetic alopecia in women and in men // 2006 British Association of Dermatologists, British Journal of Dermatology, 149, 692–699. http://www.turkderm.org.tr/pdfs/S3_guideline_androgenetic_alopecia.pdf 6) Guidelines Guidelines for the management of alopecia areata // Accepted for publication April 17, 2007. 7) The therapeutic effect and the changed serum zinc level after zinc supplementation in alopecia areata patients who had a low serum zinc level. Park H, Kim CW, Kim SS, Park CW. // Ann Dermatol. 2009 May;21(2):142-6. Epub 2009 May 31. 8) Combination of topical garlic gel and betamethasone valerate cream in the treatment of localized alopecia areata: a double-blind randomized controlled study. // Indian J Dermatol Venereol Leprol. 2007 Jan-Feb;73(1):29-32. 9) Evidence based (s3) guidelines for the treatment of androgenetic alopecia in women and in men 2005 British Association of Dermatologists, British Journal of Dermatology.-149.-692–699 http://www.turkderm.org.tr/pdfs /S3_guideline_androgenetic_alopecia.pdf. 10) Wolff H, Fischer TW, Blume-Peytavi U, - DtschArzteblInt - May 27, 2016; 113(21); 377-86 11) Messenger AG, McKillop J, Farrant P, McDonagh AJ, Sladden M. British Association of Dermatologists" guidelines for the management of alopecia areata 2012. Br J Dermatol. 2012 May;166(5):916-26. 12) Gilhar A1, Etzioni A, Paus R,"Published April 19, 2012. The New England journal of medicine, Volume 366, Issue 16; Pages 1515-25. 13) Gilhar A, Etzioni A, Paus R, - N. Engl J. Med. - April 19, 2012; 366 (16); 1515-25 14) Stefanato C. M. Histopathology of alopecia: a clinicopathological approach to diagnosis. Histopathology 2010; 56, 24-38. 15) Inui S., Nakajima T ., Nakagawa K., Itami S. Clinical significance of dermoscopy in alopecia areata: analysis of 300 cases Int J Dermatol 2008 Jul;47 (7): 688-93. 16) Jain N, Doshi B, Khopkar U, - Int J Trichology - October 1, 2013; 5 (4); 170-8 17) Finner AM, Otberg N, Shapiro J, - DermatolTher - July 1, 2008; 21 (4); 279-94 18) Olsen E. A., Messenger A.G., Shapiro J., Bergfeld W.F., Hordinsky M.K., Roberts J.L., Stough D., Washenik K., Whiting D.A. Evaluation and treatment of male and female pattern hair loss // J. Am. Acad. Dermatol. – 2005. – Vol. 52(2). – P. 301–311. 19) Lee WS, Lee HJ, Choi GS, Cheong WK, Chow SK, Gabriel MT, Hau KL, Kang H, Mallari MR, Tsai RY, Zhang J, Zheng M, - J EurAcadDermatolVenereol - August 1, 2013; 27(8); 1026-34 20) Scarinci F, Mezzana P, Pasquini P, Colletti M, Cacciamani A, - CutanOculToxicol - June 1, 2012; 31(2); 157-9. 21) Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata. Dermatol Surg 2007;33:1483-1487. 22) Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata in children. PediatrDermatol 2009; 26:547-50. 23) Zakaria W, Passeron T, Ostovari N, Lacour JP, Ortonne JP. 308-nm excimer laser therapy in alopecia areata. J Am AcadDermatol 2004:51:837-838. 24) Raulin C, Gundogan C, Greve B, Gebert S. Excimer laser therapy of alopecia areata - side-byside evaluation of a representative area. J DtschDermatolGes 2005:3:524-526. 25) Gundogan C, Greve B, Raulin C. Treatment of alopecia areata with the 308-nm xenon chloride excimer laser: case report of two successful treatments with the excimer laser. Lasers SurgMed 2004: 34: 86-90. 26) Claudy AL, Gagnaire D. PUVA treatment of alopecia areata. Arch Dermatol 1983; 119:975-8. 27) Lassus A, Eskelinen A, Johansson E. Treatment of alopecia areata with three different PUVA modalities. Photodermatology 1984; 1:141-144. 28) Van der Schaar WW, Sillevis Smith JH. An evaluation of PUVA-therapy for alopecia areata. Dermatologica 1984; 168:250-252. 29) Mitchell AJ, Douglass MC. Topical photochemotherapy for alopecia areata. J Am Acad Dermatol 1985; 12:644-649. 30) Taylor CR, Hawk JL. PUVA treatment of alopecia areatapartialis, totalis and universalis: audit of 10 years’ experience at St John’s Institute of Dermatology. Br J Dermatol 1995;133:914-918. 31) Healy E, Rogers S. PUVA treatment for alopecia areata - does it work? A retrospective review of 102 cases Br J Dermatol 1993; 129:42-44. 32) Gupta AK, Ellis CN, Cooper KD et al. Oral cyclosporine for the treatment of alopecia areata. A clinical and immunohistochemical analysis. J AMAcadDermatol 1990; 22:242-50. 33) Fiedler-Weiss VC. Topical minoxidil solution (1% and 5%) in the treatments of alopecia areata. 34) Coronel-Perez IM, Rodriguez-Rey EM, Camacho-Martinez FM. Latanoprost in the treatment of eyelash alopecia in alopecia areatauniversalis. J Eur Acad Dermatol Venerol 2010; 24:481-5; 35) Faghihi G, Andalib F, Asilian A. The efficacy of latanoprost in the treatment of alopecia areata of eyelashes and eyebrows. Eur J dermatol 2009: 19:586-7. 36) Acikgoz G, Caliskan E, Tunca M. The effect of oral caclosporine in the treatment of severe alopecia areata. 37) Messenger AG, McKillop J, Farrant P, McDonagh AJ, Sladden M. British Association of Dermatologists’ guidelines for the management of alopecia areata 2012. British Journal of Dermatology 2012; 166:916-926. 38) Joly P. The use of methotrexate alone or in combination with low doses of oral corticosteroids in the treatment of alopecia totalis or universalis. J Am Acad Dermatol 2006; 55: 632-636. 39) Royer M, Bodemer C, Vabres P, et al. Efficacy and tolerance of methotrexate in severe childhood alopecia areata. Br J Dermatol 2011;165(2):407-10. 40) Gupta AK, Ellis CN, Cooper KD et al. Oral cyclosporine for the treatment of alopecia areata. A clinical and immunohistochemical analysis. J AM AcadDermatol 1990; 22:242-50. 41) Acikgoz G, Caliskan E, Tunca M. The effect of oral caclosporine in the treatment of severe alopecia areata.

Information

ORGANIZATIONAL ASPECTS OF THE PROTOCOL

List of developers:
1) Batpenova Gulnar Ryskeldyevna - Doctor of Medical Sciences, Professor, Head of the Department of Dermatovenerology of JSC Astana Medical University.
2) Dzhetpisbaeva Zulfiya Seitmagambetovna - Candidate of Medical Sciences, Associate Professor of the Department of Dermatovenereology of Astana Medical University JSC.
3) Tatyana Viktorovna Tarkina - Doctor of Medical Sciences, Associate Professor of the Department of Dermatovenereology of JSC Astana Medical University.
4) Natalya Olegovna Tsoi - PhD, assistant at the Department of Dermatovenereology of Astana Medical University JSC.
5) Mazhitov Talgat Mansurovich - Doctor of Medical Sciences, Professor of the Department of Clinical Pharmacology and Internship of Astana Medical University JSC, clinical pharmacologist.

Disclosure of no conflict of interest: absent

Reviewers:
1) Nurmukhambetov Zhumash Naskenovich - Doctor of Medical Sciences, Professor of the Department of Immunology and Dermatovenerology of Semey State Medical University.

Conditions for reviewing the protocol: review of the protocol 5 years after its publication and from the date of its entry into force or if new methods with a level of evidence are available.

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

Etiology and epidemiology

The basis for the development of the disease is assumed to be a local autoimmune mechanism of damage to the hair follicle, which leads to a violation of the immune tolerance of the cells that form the follicle and the cessation of specific reception from its hair papilla.

The incidence and prevalence of GA depend on geographical and ethnic differences, as well as on the immunogenetic background of patients. The disease affects people of both sexes.

Predisposition to GA is genetic. 10-20% of patients have a family history of the disease, and the true incidence of the disease is likely even higher, since mild cases may go undetected. Genetic predisposition is polygenic in nature. There is a connection between GA and certain HLA class II alleles, especially with DQB1*03 and DRB1*1104. HLA alleles DQB1*0301(HLA-DQ7) and DRB1*1104 (HLA-DR11) may be associated with alopecia totalis and alopecia universalis.

Trigger factors for the disease can be stress, vaccination, viral diseases, infectious diseases, taking antibacterial drugs, anesthesia, etc.

Conditions associated with GA.

Autoimmune diseases of the thyroid gland are observed in 8-28% of patients, while the presence of thyroid antibodies in the blood has no clinical correlation with the severity of GA. Vitiligo is observed in 3-8% of patients with HA. Atopy, compared to the general population, is registered in patients with HA 2 times more often.

Relatives of patients with HA have an increased risk of developing type 1 diabetes; on the contrary, the incidence rate in the patients themselves compared with the general population may be lower. Patients with GA have a high rate of mental illness, especially anxiety and depressive disorders.

The incidence of GA is 0.7-3.8% of patients seeking help from a dermatologist. Risk of occurrence
disease during life is 1.7%. GA occurs equally in both men and women. The first focus of baldness appears in 20% of patients in childhood, in 60% of patients under the age of 20, in 20% of patients over the age of 40.

Classification

L63.0 Alopecia totalis
L63.1 Alopecia universalis
L63.2 Area baldness (band-shaped)
L63.8 Other alopecia areata

Symptoms of alopecia areata

Depending on the volume and type of baldness, the following clinical forms of HA are distinguished:

local (limited);
subtotal;
total;
universal.

Other forms of GA are:

multifocal (mesh) arrangement of alopecia areas;
ophiasis;
inverse ophiasis (sisapho);
diffuse form.

With a local (limited) form of HA, one or more clearly defined round foci of alopecia are determined on the scalp.

In the subtotal form of HA, more than 40% of hair is absent from the scalp.

With ophiasis, alopecia foci have a ribbon-like shape and cover the entire marginal zone of hair growth in the occipital and temporal regions.

With inverse ophiasis (sisapho), ribbon-shaped foci of alopecia spread to the fronto-parietal and temporal regions.

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

In the total form of HA, complete loss of terminal hair on the scalp is observed.

With the universal form of HA, there is no hair on the scalp, in the area of eyebrows, eyelashes, or on the skin of the body.

Stages of the pathological process

Active (progradient, progressive) stage.

Subjective symptoms are usually absent; some patients may complain of itching, burning or pain in the affected areas. Typical lesions are areas of non-scarring baldness of a round or oval shape with unchanged skin color. Less commonly observed are lesions of moderate red or peach color. Proximally narrowed and distally broad exclamation point-shaped hairs are a characteristic feature often seen at or around the affected area. In the active phase of the disease, at the borders of the lesions, the hair tension test may be positive - the “loose hair” zone. The zone border does not exceed 0.5-1 cm.

HA can spread to almost any area of the scalp, but in approximately 90% of patients the scalp is affected. At the initial stage, the disease does not affect gray hair.

Stationary stage.

Around the alopecia lesion, the area of “loose hair” is not identified, the skin in the lesion is unchanged.

Regression stage.

In the area of alopecia, growth of vellus is observed - vellus depigmented hair, as well as partial growth of terminal pigmented hair. When hair regrowth occurs, the original hair is usually hypopigmented, but color usually returns over time.

In patients with GA, specific dystrophic changes in the nails may be observed: pinpoint ulceration of the nails, trachyonychia, Beau's lines, onychorrhexis, thinning or hardening of the nails, onychomadesis, koilonychia, pinpoint or transverse leukonychia, red spotted lunulae.

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

The prognosis is aggravated by the early age of onset of the disease, its duration, family history, the presence of concomitant atopy and other autoimmune diseases.

Diagnosis of alopecia areata

The diagnosis is made based on the clinical picture of the disease:

the presence of alopecia areas on the skin with clear boundaries;
the presence of stumps of hair in the lesion in the form of an exclamation mark and a “loose hair zone” at the border of the lesion (active stage);
detection during microscopic examination of hair epilated from the lesion of dystrophic proximal ends in the form of a “broken rope”;
the presence of light vellus hair in the growth area (in the regression stage); sometimes along one edge of the lesion there are fragments of hair in the form of an exclamation mark, and on the opposite - the growth of vellus;
detection of signs of onychodystrophy during examination of nails: thimble-shaped indentations, longitudinal striations, changes in the free edge in the form of wavy patterns;
detection during trichoscopy (dermatoscopy of the scalp) of “yellow dots”, cadaverized hair, hair in the form of exclamation marks.

In case of a doubtful diagnosis, as well as before prescribing treatment, laboratory tests are recommended:

microscopic examination of skin and hair for the presence of pathogenic fungi;
microscopic examination of hair epilated from the marginal zone of the lesion (detection of dystrophic hair ends - a sign pathognomonic for HA);
histological examination of a fragment of scalp skin. Histologically, HA is characterized by a predominantly T-cell inflammatory infiltrate in and around the anagen hair follicle bulbs. However, the histopathological signs of GA depend on the stage of the disease; in the case of a chronic course of the disease, classical signs may be absent;
clinical blood test;
serological studies to exclude lupus erythematosus and syphilis;
determination of cortisol levels in the blood (when planning treatment with systemic glucocorticoids - before treatment and 4 weeks after its completion);
biochemical blood test: ALT, AST, total protein, bilirubin, cholesterol, blood sugar, alkaline phosphatase (if toxic alopecia is suspected, and also before prescribing photochemotherapy with the use of photosensitizers orally);
general radiography of the skull (to exclude space-occupying formations in the sella region);
blood test for thyroid hormones (free T3, free T4, TSH, anti-TPO, anti-TG) to exclude thyroid pathology and prolactin to exclude prolactinemia.

According to indications, consultations with other specialists are prescribed: neurologist, endocrinologist, psychotherapist.

Differential diagnosis

Differential diagnosis is carried out with trichotillomania, diffuse toxic alopecia, trichophytosis of the scalp, cicatricial alopecia.

In trichotillomania, alopecia lesions have an irregular shape and are usually located in the temples, crown, eyebrows, and eyelashes. In the central part of the lesion, terminal hair growth is often observed. In the outbreak, hair can be broken off at different lengths. Microscopic examination reveals hair roots in the anagen or telogen stage; dystrophic hair is absent.

Diffuse toxic alopecia is usually associated with acute toxic conditions: poisoning with heavy metal salts, chemotherapy, taking cytostatics, prolonged rise in temperature to 39˚C and above.

In case of trichophytosis of the scalp, during examination, an inflammatory ridge is detected along the periphery of the lesion and the presence of “stumps” - hair broken off at a level of 2-3 mm from the surface of the skin. The disease may be accompanied by inflammation and peeling, which, as a rule, is not observed with GA. Microscopic examination of hair fragments for fungi reveals fungal drusen inside or outside the hair shaft.

With cicatricial alopecia, the skin in the lesion is shiny, the follicular apparatus is not expressed. Clinical manifestations of cicatricial alopecia sometimes cause diagnostic difficulties; in this case, histological examination is recommended.

In children with a congenital single area of baldness in the temporal zone, a differential diagnosis should be made with temporal triangular alopecia.

In rare cases of HA when the frontal hairline and temporal zone are affected, frontal fibrous alopecia, a scar-like hair loss that mainly affects postmenopausal women, should be excluded. The disease may be accompanied by perifollicular erythema and desquamation, which are not observed with GA.

More curable than alopecia areata

Treatment regimens

Drug therapy

Systemic therapy for severe forms of GA.

Glucocorticosteroid drugs.

prednisolone
methylprednisolone

Antimetabolites

methotrexate

Immunosuppressants.

cyclosporine

Systemic therapy for local (limited) GA:

zinc sulfate

External therapy for severe forms of GA.

minoxidil, solution 5%
clobetasol propionate, ointment 0.05%

External therapy for local (limited) GA: - Intralesional administration of glucocorticosteroid drugs.

triamcinolone acetonide
betamethasone dipropionate (2 mg)
Minoxidil
minoxidil, solution 2%
minoxidil, solution 5%

Topical glucocorticosteroid drugs:

fluocinolone acetonide, cream 0.25%
betamethasone valerate, foam 0.1%, cream
betamethasone dipropionate, lotion 0.05%, cream
clobetasol propionate, cream 0.05%
hydrocortisone butyrate, cream 0.1%, emulsion
mometasone furoate, cream 0.1%, lotion
methylprednisolone aceponate, cream 0.1%, emulsion

Prostaglandin F2a analogues are used in the formation of alopecia in the eyelash growth area (C).

latanoprost, solution 0.03%
bimatoprost, solution 0.03%

Non-drug therapy

For local HA – narrow-band phototherapy using an excimer laser with a wavelength of 308 nm

For severe forms of HA – PUVA therapy (C). Psoralen and its derivatives are used at a dose of 0.5 mg per kg of body weight

Indications for hospitalization

None.

Requirements for treatment results

Renewal of hair growth in areas of alopecia.

Tactics in the absence of treatment effects

Patients with long-term absence of eyebrows may be offered dermatography or medical tattooing. Hair prostheses, wigs, hairpieces and other extensions are recommended for patients with hypertension during the period of therapy or in the absence of treatment effect.

Prevention

There are no methods of prevention.

If you have any questions about this disease, please contact dermatovenerologist Adaev Kh.M:

WhatsApp 8 989 933 87 34

Email: [email protected]

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Medicine knows various types of hair and scalp diseases. One of the varieties of such diseases is alopecia areata. However, not everyone knows what this medical term means. We will tell you about this and much more in this article.

What is alopecia areata?

Alopecia areata is a disease associated with damage to the cells of the hair root system and is characterized by the sudden appearance of one or several oval or round shaped bald spots. There is no itching or pain in areas of receding hairline, the skin is smooth and natural in color.

Alopecia areata is uncommon and can either appear or disappear completely unexpectedly for the patient. Often the symptoms of the disease go away on their own, without any treatment. However, there are also relapses of this disease.

If the patient has a small single patch of baldness for the first time, then it is likely that it will heal on its own; you just need to calmly wait and monitor it for about three months.

If focal alopecia begins to develop into a multifocal form, the patient should consult a doctor.

It happens that this disease begins with a small spot of baldness, then it grows into quite large bald patches, or the same spots can appear not only on the scalp, but also in any other places on the body. This form of the disease alopecia areata is called subtotal.

When focal alopecia develops into a total or universal stage, patients experience hair damage throughout the body, which is also accompanied by damage to the nail plates. In such difficult cases, only a doctor can establish the correct diagnosis and prescribe effective treatment methods, but for this the patient must undergo a full examination and establish the causes of this disease.

Mature hair loss usually leads to a decrease in hair density and, quite rarely, to total alopecia. There are many reasons for mature hair loss; for example, due to physiological changes in the body during pregnancy, alopecia may occur after childbirth. Long-term use of retinoids, oral contraceptives and drugs that slow down blood clotting, especially in combination with constant stressful situations and endocrine disorders, quite often cause alopecia. Lack of iron, zinc in the body and other nutritional disorders also adversely affect hair density.
As a rule, alopecia begins gradually with the appearance of small bald patches in the parietal or frontal part of the head, the skin acquires a glossy shine, atrophy of the hair follicles is observed, and in the center of the lesions you can find single long hairs that have not changed in appearance.
If the cause of alopecia is loss of growing hair, then over time this can lead to complete hair loss. Pathogenetically, alopecia of this type is caused by mycoses, radiation therapy, poisoning with bismuth, arsenic, gold, thallium and boric acid. Hair loss and alopecia may be preceded by antitumor therapy using cytostatics.
Androgenetic alopecia is observed mainly in men; it begins to appear after puberty and develops by the age of 30-35. The development of alopecia in this case is associated with an increased amount of androgenic hormones, which is caused by hereditary factors. Clinically, androgenetic alopecia is manifested by the replacement of long hair with vellus hair, which over time becomes even shorter and loses pigment. Initially, symmetrical bald patches appear in both temporal areas with gradual involvement of the parietal zone in the process. Over time, the bald patches merge due to peripheral growth.
Scarring alopecia, in which hair loss is accompanied by the appearance of shiny and smooth areas of the scalp, is distinguished by the fact that such areas do not contain hair follicles. The cause of this type of alopecia may be a congenital anomaly and defects of the hair follicles. But much more often, infectious diseases such as syphilis, leprosy and herpetic infections lead to cicatricial alopecia. Changes in the ovaries and pituitary gland such as hyperplasia and polycystic disease, basal cell carcinoma, long-term use of steroid drugs also provoke cicatricial alopecia. Exposure to aggressive chemicals, burns, and frostbite of the scalp are the most common exogenous causes of cicatricial alopecia.
Alopecia areata, when areas of baldness are not accompanied by scarring and are located in the form of rounded lesions of different sizes, appears suddenly. The causes of alopecia areata are not known, but meanwhile, areas with alopecia tend to grow peripherally, which can lead to total hair loss. Most often, alopecia areata is observed on the scalp, but the process of baldness can affect the area of the beard, mustache, eyebrows and eyelashes. Initially, alopecia lesions are small, up to 1 cm in diameter, the condition of the skin is not changed, but sometimes slight hyperemia may be observed.
The openings of the hair follicles in the affected area are clearly visible. As the alopecia lesions grow peripherally, they become scalloped and merge with each other. In the circumference of the areas there is a zone of loose hair, which can be easily removed with minor impact; the hair in this zone at its root is devoid of pigment and ends in a club-shaped thickening in the form of a white dot. They are called "exclamation point hair." The absence of such hair indicates that alopecia areata has entered the stationary stage and the progression of hair loss has ended. After a few weeks or months, hair growth in alopecia areas is restored. At first they are thin and colorless, but over time their color and structure become normal. The fact that hair growth has resumed does not exclude the possibility of relapse.
Seborrheic alopecia occurs in approximately 25% of cases of seborrhea. Baldness begins during puberty and reaches its maximum severity by 23-25 years. At first, the hair becomes oily and shiny, and looks like it has been greased with oil. The hair is stuck together in strands, and on the scalp there are dense, fatty yellowish scales. The process is accompanied by itching and often accompanied by seborrheic eczema. Baldness begins gradually, at first the lifespan of the hair is shortened, it becomes thin, thins out and gradually long hair is replaced by vellus hair. As seborrheic alopecia develops, the process of hair loss begins to increase, and the bald spot becomes noticeable, it begins from the edges of the frontal zone towards the back of the head or from the parietal zone towards the frontal and occipital. The area of baldness is always bordered by a narrow band of healthy and tightly fitting hair.

Alopecia- absence or thinning of hair on the skin in places where it usually grows (usually on the scalp).

Code according to the international classification of diseases ICD-10:

L63 - Alopecia areata
L64 - Androgenetic alopecia
L65- Other non-scarring hair loss
L66- Scarring alopecia
Q84. 0 - Congenital alopecia

Frequency

By the age of 50, 50% of men have clear signs of male pattern baldness. 37% of postmenopausal women report some signs of alopecia.

Predominant age

the frequency of androgenetic alopecia increases in proportion to age; dermatomycosis of the scalp and traumatic alopecia occur more often in children.

Alopecia: Causes

Etiology

Mature hair loss: . After childbirth as a consequence of physiological changes in the pregnant woman’s body. Medicines (oral contraceptives, anticoagulants, retinoids, beta-blockers, antitumor drugs, interferon [IFN]). Stress (physical or mental). Endocrine pathology (hypo- or hyperthyroidism, hypopituitarism). Nutritional factors (malnutrition, iron, zinc deficiency). Loss of growing hair: . Mycosis fungoides. X-ray therapy. Medicines (antitumor drugs, allopurinol, bromocriptine). Poisoning (bismuth, arsenic, gold, boric acid, thallium). Scar alopecia: . Developmental anomalies and congenital defects. Infections (leprosy, syphilis, herpes infection, cutaneous leishmaniasis). Basal cell carcinoma. Epidermal nevi. Exposure to physical factors (acids and alkalis, extreme temperatures [burns, frostbite], radiation). Cicatricial pemphigus. Lichen planus. Sarcoidosis. Androgenic alopecia: . Hyperplasia of the adrenal cortex. Polycystic ovary syndrome. Ovarian hyperplasia. Carcinoid. Pituitary hyperplasia. Medicines (testosterone, danazol, ACTH, anabolic steroids, progesterones). Gnezdnaya alopecia. Etiological factors are unknown, autoimmune nature is possible; inherited forms are described. Traumatic alopecia: . Trichotillomania (uncontrollable urge to pull out one's own hair). Damage caused by braiding hair or tying bows tightly. Dermatomycosis of the scalp: . Fungi of the genus Microsporum. Fungi of the genus Trichophyton.

Genetic aspects

There are at least 90 known inherited diseases and syndromes accompanied by alopecia. Congenital alopecia with keratosis of the palms and soles (104100, Â) . Congenital total alopecia(*104130, Â): combined with giant pigmented nevi, periodontitis, seizures, mental retardation. Gnezdnaya alopecia(104000, В) . Family alopecia(transformation anagen - telogen, foci of baldness, 104110, Â). Total alopecia(203655, 8p12, HR gene, r) . Various degrees of hypotrichosis, up to complete absence of hair, are characteristic of hereditary ectodermal dysplasia (see Ectodermal dysplasia).

Risk factors

Family history of baldness. Physical or mental stress. Pregnancy. Gnezdnaya alopecia— Down syndrome, vitiligo, diabetes.

Types

Mature hair loss (telî gen effluvium) is diffuse hair loss, leading to a decrease in hair density, but not to complete baldness. Loss of growing hair (anà gen effluvium) - diffuse hair loss, including growing hair, with possible complete baldness. Scar alopecia- the presence of shiny, smooth areas on the scalp that do not contain hair follicles. Androgenic alopecia- hair loss, usually developing in both sexes; possibly due to the effect of male sex hormones on the cells of the hair follicles. Gnezdnaya alopecia(alopecia) is acquired hair loss in the form of rounded lesions of varying sizes in certain areas of the scalp, eyebrows, and beard area, not accompanied by scarring. Traumatic alopecia- hair loss in certain areas of the skin due to chronic trauma, which in the early stages is not accompanied by scarring. Dermatomycosis of the scalp (tinea capitis) - the presence of limited foci with the absence of hair on the scalp, possibly combined with an inflammatory reaction; caused by a fungal infection.

Alopecia: Signs, Symptoms

Clinical picture

Hair loss. With dermatomycosis of the scalp - itching, flaking, inflammation. With dermatomycosis of the scalp and traumatic alopecia - hair breaking. With alopecia areata: sudden appearance on the scalp and face of several rounded areas of complete hair loss without any other changes; hair along the periphery of the lesions is easily pulled out; the lesions can grow, merge and lead to total baldness.

Alopecia: Diagnosis

Laboratory research

Study of thyroid function. Complete blood test (to identify possible dysfunctions of the immune system). Levels of unconjugated testosterone and dihydroepiandrosterone sulfate in women with androgenetic alopecia. Plasma ferritin concentration. Von Wasserman reaction to exclude syphilis. The number of T - and B - lymphocytes (sometimes reduced in patients with alopecia areata).

Special studies

Hair pulling test: gently tugging (without force) on the hair shaft to remove it; positive (hair is easily removed) for alopecia areata. Microscopic examination of the hair shaft. Examination of areas of peeling using potassium hydroxide; positive for ringworm of the scalp. The use of antifungal drugs may lead to false positive results. Examination of areas of peeling for the presence of fungi. A biopsy of the scalp with conventional microscopy and direct immunofluorescence study allows the diagnosis of dermatomycosis of the scalp, diffuse alopecia areata and cicatricial alopecia developed against the background of SLE, lichen planus and sarcoidosis.

Alopecia: Treatment Methods

Treatment

Lead tactics

Mature hair loss. Hair loss maximum 3 months after the causative effect (drugs, stress, nutritional factors); Once the cause is eliminated, hair growth is quickly restored. Loss of growing hair. Hair loss begins a few days or weeks after the causative effect, hair growth is restored after the cause is eliminated. Scar alopecia. The only effective treatment method is surgical (skin graft transplantation or excision of scarring areas). Androgenic alopecia. After 12 months of topical use of minoxidil, 39% of patients noted hair growth of varying severity. An alternative treatment method is surgery. Gnezdnaya alopecia. Usually the disease goes away on its own within 3 years without treatment, but relapses often occur. Traumatic alopecia. Cure can occur only after hair pulling stops. Intervention from a psychologist or psychiatrist may be required. Successful treatment involves medication, behavior modification, and hypnosis. Dermatomycosis of the scalp: treatment is carried out for 6-8 weeks. Thorough hand washing and washing of hats and towels is necessary.

Drug therapy

Finasteride tablets. Good results have been obtained for various forms of alopecia. For androgenetic alopecia - minoxidil (2% r - r) for topical use. For alopecia areata. Sedatives, vitamins, irritating alcohol rubs. HA preparations for topical use. In severe cases - photosensitizing drugs (Beroxan) topically in combination with ultraviolet irradiation (UVR), HA orally. For dermatomycosis of the scalp - griseofulvin (adults 250-375 mg/day, children 5, 5-7, 3 mg/kg/day) or ketoconazole 200 mg once a day for 6-8 weeks.

Surgery

Skin transplantation.

Course and prognosis

Mature and growing hair loss: Permanent baldness is rare. Scar alopecia: Hair follicles are constantly damaged. Androgenic alopecia: prognosis and course depend on treatment. Gnezdnaya alopecia: Spontaneous recovery is possible, but relapses are common; in the total form, the hair usually does not recover. Traumatic alopecia: the prognosis and course depend on the success of correcting the patient’s behavior. Ringworm of the scalp: usually completely resolved.

Synonyms

Atrichia. Atrichosis. Baldness. Baldness

ICD-10. L63 Gnezdnaya alopecia. L64 Androgenic alopecia. L65 Other non-scarring hair loss. L66 Scarring alopecia. Q84. 0 Congenital alopecia