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Π‘ΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅
- 1 Practice Essentials
- 2 Background
- 3 Pathophysiology
- 4 Π‘ΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅
- 5 ΠΠΏΠΈΠ΄Π΅ΠΌΠΈΠΎΠ»ΠΎΠ³ΠΈΡ
- 6 Π€Π°ΠΊΡΠΎΡΡ ΡΠΈΡΠΊΠ° ΡΠ°Π·Π²ΠΈΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
- 7 ΠΠ»Π°ΡΡΠΈΡΠΈΠΊΠ°ΡΠΈΡ
- 8 ΠΡΠΈΡΠ΅ΡΠΈΠΈ, ΠΏΡΠΈΠΌΠ΅Π½ΡΠ΅ΠΌΡΠ΅ Π΄Π»Ρ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
- 9 ΠΠ΅Ρ Π°Π½ΠΈΠ·ΠΌΡ ΡΠ°Π·Π²ΠΈΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
- 10 ΠΠΎΠ΄Ρ ΠΎΠ΄Ρ ΠΊ Π»Π΅ΡΠ΅Π½ΠΈΡ
- 11 ΠΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠ° Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
- 12 ΠΠΈΠ΅ΡΠ°
- 13 ΠΡΠΎΠ³Π½ΠΎΠ·
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 diseasesβincluding food allergy, asthma, and allergic rhinitis, in orderβhas 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]βassociated) 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.
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)β4, 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 cellβassociated 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 cellβderived 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 cellβderived 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]
| ΠΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΉ Π΄Π΅ΡΠΌΠ°ΡΠΈΡ | |
ΠΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΉ Π΄Π΅ΡΠΌΠ°ΡΠΈΡ Ρ ΡΠ΅Π±ΡΠ½ΠΊΠ° |
|
| ΠΠΠ-10 | L 20 20. |
|---|---|
| ΠΠΠ-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 |
ΠΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΉ Π΄Π΅ΡΠΌΠ°ΡΠΈΡ (ΠΡΠ, Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠ°Ρ ΡΠΊΠ·Π΅ΠΌΠ°, ΡΠΈΠ½Π΄ΡΠΎΠΌ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠΊΠ·Π΅ΠΌΡ/Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ° [1] ) β Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΉ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΉ Π΄Π΅ΡΠΌΠ°ΡΠΈΡ; Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅, ΠΊΠΎΡΠΎΡΠΎΠ΅ ΡΠ°Π·Π²ΠΈΠ²Π°Π΅ΡΡΡ Ρ Π»ΠΈΡ Ρ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΏΡΠ΅Π΄ΡΠ°ΡΠΏΠΎΠ»ΠΎΠΆΠ΅Π½Π½ΠΎΡΡΡΡ ΠΊ Π°ΡΠΎΠΏΠΈΠΈ, ΠΈΠΌΠ΅Π΅Ρ ΡΠ΅ΡΠΈΠ΄ΠΈΠ²ΠΈΡΡΡΡΠ΅Π΅ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅, Π²ΠΎΠ·ΡΠ°ΡΡΠ½ΡΠ΅ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ. Π₯Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΠ΅ΡΡΡ ΡΠΊΡΡΡΠ΄Π°ΡΠΈΠ²Π½ΡΠΌΠΈ ΠΈ (ΠΈΠ»ΠΈ) Π»ΠΈΡ Π΅Π½ΠΎΠΈΠ΄Π½ΡΠΌΠΈ Π²ΡΡΡΠΏΠ°Π½ΠΈΡΠΌΠΈ, ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΡΡΠΎΠ²Π½Ρ ΡΡΠ²ΠΎΡΠΎΡΠΎΡΠ½ΠΎΠ³ΠΎ IgE ΠΈ Π³ΠΈΠΏΠ΅ΡΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡΡ ΠΊ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΌ (Π°Π»Π»Π΅ΡΠ³Π΅Π½Π½ΡΠΌ) ΠΈ Π½Π΅ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΡΠ°Π·Π΄ΡΠ°ΠΆΠΈΡΠ΅Π»ΡΠΌ. ΠΠΌΠ΅Π΅Ρ ΡΡΡΠΊΡΡ ΡΠ΅Π·ΠΎΠ½Π½ΡΡ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΡ: Π·ΠΈΠΌΠΎΠΉ β ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΡ ΠΈΠ»ΠΈ ΡΠ΅ΡΠΈΠ΄ΠΈΠ²Ρ, Π»Π΅ΡΠΎΠΌ β ΡΠ°ΡΡΠΈΡΠ½ΡΠ΅ ΠΈΠ»ΠΈ ΠΏΠΎΠ»Π½ΡΠ΅ ΡΠ΅ΠΌΠΈΡΡΠΈΠΈ.
Π‘ΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅
ΠΠΏΠΈΠ΄Π΅ΠΌΠΈΠΎΠ»ΠΎΠ³ΠΈΡ
Π Π°ΡΠΏΡΠΎΡΡΡΠ°Π½ΡΠ½Π½ΠΎΡΡΡ ΠΡΠ ΡΡΠ΅Π΄ΠΈ ΡΠ°Π·Π²ΠΈΡΡΡ ΡΡΡΠ°Π½ 10-20 %. ΠΠ°Π½ΠΈΡΠ΅ΡΡΠ°ΡΠΈΡ ΡΠΈΠΌΠΏΡΠΎΠΌΠΎΠ² ΠΡΠ Ρ Π΄Π΅ΡΠ΅ΠΉ ΠΎΡΠΌΠ΅ΡΠ°Π΅ΡΡΡ Π² Π²ΠΎΠ·ΡΠ°ΡΡΠ΅ 6 ΠΌΠ΅ΡΡΡΠ΅Π² Π² 60 % ΡΠ»ΡΡΠ°Π΅Π², Π΄ΠΎ 1 Π³ΠΎΠ΄Π° Π² 75 %, Π΄ΠΎ 7 Π»Π΅Ρ Π² 80-90 %. Π ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ ΠΏΠΎΡΠ»Π΅Π΄Π½ΠΈΡ Π΄Π΅ΡΡΡΠΈΠ»Π΅ΡΠΈΠΉ Π½Π°Π±Π»ΡΠ΄Π°Π΅ΡΡΡ ΡΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΉ ΡΠΎΡΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π΅ΠΌΠΎΡΡΠΈ ΠΡΠ, ΡΡΠ»ΠΎΠΆΠ½ΡΠ΅ΡΡΡ Π΅Π³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅, ΠΎΡΡΠ³ΠΎΡΠ°Π΅ΡΡΡ ΠΈΡΡ ΠΎΠ΄. Π XX Π²Π΅ΠΊΠ΅ Π±ΡΠ»Π° ΠΏΠΎΠ΄ΡΠ²Π΅ΡΠΆΠ΄Π΅Π½Π° ΡΠ²ΡΠ·Ρ ΠΡΠ, ΠΏΠΎΠ»Π»ΠΈΠ½ΠΎΠ·Π° ΠΈ Π±ΡΠΎΠ½Ρ ΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π°ΡΡΠΌΡ, ΠΊΠΎΡΠΎΡΡΡ ΠΎΠ±ΠΎΠ·Π½Π°ΡΠΈΠ»ΠΈ ΡΠ΅ΡΠΌΠΈΠ½ΠΎΠΌ «Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠ°Ρ ΡΡΠΈΠ°Π΄Π°». [2] . Π‘ΠΎΡΠ΅ΡΠ°Π½ΠΈΠ΅ ΠΡΠ Ρ Π±ΡΠΎΠ½Ρ ΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π°ΡΡΠΌΠΎΠΉ Π½Π°Π±Π»ΡΠ΄Π°Π΅ΡΡΡ Π² 34 % ΡΠ»ΡΡΠ°Π΅Π², Ρ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌ ΡΠΈΠ½ΠΈΡΠΎΠΌ β Π² 25 %, Ρ ΠΏΠΎΠ»Π»ΠΈΠ½ΠΎΠ·ΠΎΠΌ β Π² 8 %. ΠΡΠ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Π΄Π΅Π±ΡΡΠΎΠΌ «Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠ°ΡΡΠ°», ΠΊΠΎΠ³Π΄Π° Π² Π΄Π°Π»ΡΠ½Π΅ΠΉΡΠ΅ΠΌ Ρ ΡΠ°ΠΊΠΈΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² ΡΠΎΡΠΌΠΈΡΡΡΡΡΡ Π΄ΡΡΠ³ΠΈΠ΅ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ: ΠΏΠΈΡΠ΅Π²Π°Ρ Π°Π»Π»Π΅ΡΠ³ΠΈΡ, Π±ΡΠΎΠ½Ρ ΠΈΠ°Π»ΡΠ½Π°Ρ Π°ΡΡΠΌΠ°, Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠΈΠ½ΠΈΡ. ΠΡΠ, ΡΠ²ΡΠ·Π°Π½Π½ΡΠΉ Ρ ΠΏΠΈΡΠ΅Π²ΠΎΠΉ Π°Π»Π»Π΅ΡΠ³ΠΈΠ΅ΠΉ, ΡΡΠΊΠΎΡΡΠ΅Ρ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ «Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠ°ΡΡΠ°».
Π€Π°ΠΊΡΠΎΡΡ ΡΠΈΡΠΊΠ° ΡΠ°Π·Π²ΠΈΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
ΠΠ΅Π΄ΡΡΠ°Ρ ΡΠΎΠ»Ρ Π² ΡΠ°Π·Π²ΠΈΡΠΈΠΈ ΠΡΠ ΠΏΡΠΈΠ½Π°Π΄Π»Π΅ΠΆΠΈΡ ΡΠ½Π΄ΠΎΠ³Π΅Π½Π½ΡΠΌ ΡΠ°ΠΊΡΠΎΡΠ°ΠΌ (Π½Π°ΡΠ»Π΅Π΄ΡΡΠ²Π΅Π½Π½ΠΎΡΡΡ, Π°ΡΠΎΠΏΠΈΡ, Π³ΠΈΠΏΠ΅ΡΡΠ΅Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ ΠΊΠΎΠΆΠΈ, Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ ΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΡ ΠΈ Π±ΠΈΠΎΡ ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΡ ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² Π² ΠΊΠΎΠΆΠ΅), ΠΊΠΎΡΠΎΡΡΠ΅ Π² ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΠΈ Ρ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠΌΠΈ Π°Π»Π»Π΅ΡΠ³Π΅Π½Π½ΡΠΌΠΈ ΠΈ Π½Π΅Π°Π»Π΅ΡΠ³Π΅Π½Π½ΡΠΌΠΈ ΡΠΊΠ·ΠΎΠ³Π΅Π½Π½ΡΠΌΠΈ ΡΠ°ΠΊΡΠΎΡΠ°ΠΌΠΈ (ΠΏΡΠΈΡ ΠΎΡΠΌΠΎΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ Π½Π°Π³ΡΡΠ·ΠΊΠΈ, ΡΠ°Π±Π°ΡΠ½ΡΠΉ Π΄ΡΠΌ) ΠΏΡΠΈΠ²ΠΎΠ΄ΡΡ ΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΡΠΈΠ½Ρ ΠΡΠ. Π ΠΎΡΠ½ΠΎΠ²Π΅ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΡΠ Π»Π΅ΠΆΠΈΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ½Π½Π°Ρ (ΠΌΡΠ»ΡΡΠΈΡΠ°ΠΊΡΠΎΡΠΈΠ°Π»ΡΠ½ΡΠΉ ΠΏΠΎΠ»ΠΈΠ³Π΅Π½Π½ΡΠΉ ΡΠΈΠΏ Π½Π°ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ) ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΡ ΠΈΠΌΠΌΡΠ½Π½ΠΎΠ³ΠΎ ΠΎΡΠ²Π΅ΡΠ° Π½Π° ΠΏΠΎΡΡΡΠΏΠ»Π΅Π½ΠΈΠ΅ Π°Π»Π»Π΅ΡΠ³Π΅Π½ΠΎΠ². Π₯Π°ΡΠ°ΠΊΡΠ΅ΡΠ½ΡΠ΅ ΡΠ΅ΡΡΡ ΠΈΠΌΠΌΡΠ½Π½ΠΎΠ³ΠΎ ΠΎΡΠ²Π΅ΡΠ° Π°ΡΠΎΠΏΠΈΠΊΠΎΠ²: ΠΏΡΠ΅ΠΎΠ±Π»Π°Π΄Π°Π½ΠΈΠ΅ Π’-Ρ Π΅Π»ΠΏΠ΅ΡΠΎΠ² II, Π³ΠΈΠΏΠ΅ΡΠΏΡΠΎΠ΄ΡΠΊΡΠΈΡ ΠΎΠ±ΡΠ΅Π³ΠΎ IgE ΠΈ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΡ IgE-Π°Π½ΡΠΈΡΠ΅Π». Π‘ΠΊΠ»ΠΎΠ½Π½ΠΎΡΡΡ ΠΊ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΠΊΠΎΠΆΠΈ β ΠΎΡΠ½ΠΎΠ²Π½ΠΎΠΉ ΡΠ°ΠΊΡΠΎΡ, ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΡΡΠΈΠΉ ΡΠ΅Π°Π»ΠΈΠ·Π°ΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π² Π²ΠΈΠ΄Π΅ ΠΡΠ. Π ΠΈΡΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΡΠ Ρ Π΄Π΅ΡΠ΅ΠΉ Π²ΡΡΠ΅ Π² ΡΠ΅ΠΌΡΡΡ , Π³Π΄Π΅ ΡΠΎΠ΄ΠΈΡΠ΅Π»ΠΈ ΠΈΠΌΠ΅ΡΡ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΈΠ»ΠΈ ΡΠ΅Π°ΠΊΡΠΈΠΈ: Π΅ΡΠ»ΠΈ ΠΎΠ±Π° ΡΠΎΠ΄ΠΈΡΠ΅Π»Ρ Π·Π΄ΠΎΡΠΎΠ²Ρ, ΡΠΈΡΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ Ρ ΡΠ΅Π±ΡΠ½ΠΊΠ° ΠΡΠ ΡΠΎΡΡΠ°Π²Π»ΡΠ΅Ρ 10-20 %, Π΅ΡΠ»ΠΈ Π±ΠΎΠ»Π΅Π½ ΠΎΠ΄ΠΈΠ½ ΠΈΠ· ΡΠΎΠ΄ΠΈΡΠ΅Π»Π΅ΠΉ β 40-50 %, Π΅ΡΠ»ΠΈ Π±ΠΎΠ»ΡΠ½Ρ ΠΎΠ±Π° ΡΠΎΠ΄ΠΈΡΠ΅Π»Ρ β 60β80 %.
ΠΠ»Π°ΡΡΠΈΡΠΈΠΊΠ°ΡΠΈΡ
Π‘ΡΠ°Π΄ΠΈΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΡ, ΠΏΠ΅ΡΠΈΠΎΠ΄Ρ ΠΈ ΡΠ°Π·Ρ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ
- ΠΠ°ΡΠ°Π»ΡΠ½Π°Ρ ΡΡΠ°Π΄ΠΈΡ
- Π‘ΡΠ°Π΄ΠΈΡ Π²ΡΡΠ°ΠΆΠ΅Π½Π½ΡΡ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ
- ΠΡΡΡΠ°Ρ ΡΠ°Π·Π°
- Π₯ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠ°Ρ ΡΠ°Π·Π°
- ΠΠΎΠ΄ΠΎΡΡΡΠ°Ρ ΡΠ°Π·Π°
ΠΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΡΠΎΡΠΌΡ Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ Π²ΠΎΠ·ΡΠ°ΡΡΠ° [1]
- ΠΠ»Π°Π΄Π΅Π½ΡΠ΅ΡΠΊΠ°Ρ (ΠΎΡ 1 ΠΌΠ΅ΡΡΡΠ° Π΄ΠΎ 2-Ρ Π»Π΅Ρ);
- ΠΠ΅ΡΡΠΊΠ°Ρ (Ρ 2 Π΄ΠΎ 13 Π»Π΅Ρ);
- ΠΠΎΠ΄ΡΠΎΡΡΠΊΠΎΠ²Π°Ρ (ΡΡΠ°ΡΡΠ΅ 13 Π»Π΅Ρ);
ΠΠΎ ΡΡΠΆΠ΅ΡΡΠΈ
- Π‘ΡΠ΅Π΄Π½Π΅ΡΡΠΆΠ΅Π»ΠΎΠ΅
- Π’ΡΠΆΠ΅Π»ΠΎΠ΅
ΠΠ»ΠΈΠ½ΠΈΠΊΠΎ-ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π²Π°ΡΠΈΠ°Π½ΡΡ
- Π‘ ΠΏΡΠ΅ΠΎΠ±Π»Π°Π΄Π°Π½ΠΈΠ΅ΠΌ Π°Π»Π»Π΅ΡΠ³ΠΈΠΈ:
- ΠΠΈΡΠ΅Π²ΠΎΠΉ
- ΠΠ»Π΅ΡΠ΅Π²ΠΎΠΉ
- ΠΡΠΈΠ±ΠΊΠΎΠ²ΡΠΉ
- ΠΡΠ»ΡΡΠ΅Π²ΠΎΠΉ ΠΈ ΠΏΡ.
ΠΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΡ
- ΠΠΈΠΎΠ΄Π΅ΡΠΌΠΈΡ
- ΠΠΈΡΡΡΠ½Π°Ρ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡ
- ΠΡΠΈΠ±ΠΊΠΎΠ²ΠΎΠ΅ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠ΅
ΠΡΠΈΡΠ΅ΡΠΈΠΈ, ΠΏΡΠΈΠΌΠ΅Π½ΡΠ΅ΠΌΡΠ΅ Π΄Π»Ρ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
(Hanifin, Rajka. Acta Derm. 92^44,1980)
ΠΠΎΠ»ΡΡΠΈΠ΅ (ΠΎΠ±ΡΠ·Π°ΡΠ΅Π»ΡΠ½ΡΠ΅) ΠΊΡΠΈΡΠ΅ΡΠΈΠΈ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ
- ΠΡΡΡΠΈΠ³ΠΎ (Π·ΡΠ΄) ΠΏΡΠΈ Π½Π°Π»ΠΈΡΠΈΠΈ Π΄Π°ΠΆΠ΅ ΠΌΠΈΠ½ΠΈΠΌΠ°Π»ΡΠ½ΡΡ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ Π½Π° ΠΊΠΎΠΆΠ΅
- Π’ΠΈΠΏΠΈΡΠ½Π°Ρ ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡ ΠΈ Π»ΠΎΠΊΠ°Π»ΠΈΠ·Π°ΡΠΈΡ (Π»ΠΈΡΠΎ, ΡΠ΅Ρ, ΠΏΠΎΠ΄ΠΌΡΡΠ΅ΡΠ½ΡΠ΅ Π²ΠΏΠ°Π΄ΠΈΠ½Ρ, Π»ΠΎΠΊΡΠ΅Π²ΡΠ΅ ΠΈ ΠΏΠΎΠ΄ΠΊΠΎΠ»Π΅Π½Π½ΡΠ΅ ΡΠΌΠΊΠΈ, ΠΏΠ°Ρ ΠΎΠ²Π°Ρ ΠΎΠ±Π»Π°ΡΡΡ, Π²ΠΎΠ»ΠΎΡΠΈΡΡΠ°Ρ ΡΠ°ΡΡΡ Π³ΠΎΠ»ΠΎΠ²Ρ, ΠΏΠΎΠ΄ ΠΌΠΎΡΠΊΠ°ΠΌΠΈ ΡΡΠ΅ΠΉ)
- ΠΠ½Π΄ΠΈΠ²ΠΈΠ΄ΡΠ°Π»ΡΠ½Π°Ρ ΠΈΠ»ΠΈ ΡΠ΅ΠΌΠ΅ΠΉΠ½Π°Ρ ΠΈΡΡΠΎΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ
- Π₯ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΡΠ΅ΡΠΈΠ΄ΠΈΠ²ΠΈΡΡΡΡΠ΅Π΅ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅
ΠΠ°Π»ΡΠ΅ (Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅) ΠΊΡΠΈΡΠ΅ΡΠΈΠΈ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ
- ΠΠΎΠ²ΡΡΠ΅Π½Π½ΡΠΉ ΡΡΠΎΠ²Π΅Π½Ρ ΠΎΠ±ΡΠ΅Π³ΠΎ ΠΈ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΡ IgE-Π°Π½ΡΠΈΡΠ΅Π»
- ΠΠ°ΡΠ°Π»ΠΎ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ Π² ΡΠ°Π½Π½Π΅ΠΌ Π΄Π΅ΡΡΠΊΠΎΠΌ Π²ΠΎΠ·ΡΠ°ΡΡΠ΅ (Π΄ΠΎ 2-Ρ Π»Π΅Ρ)
- ΠΠΈΠΏΠ΅ΡΠ»ΠΈΠ½Π΅Π°ΡΠ½ΠΎΡΡΡ Π»Π°Π΄ΠΎΠ½Π΅ΠΉ («ΡΠΊΠ»Π°Π΄ΡΠ°ΡΡΠ΅») ΠΈ ΠΏΠΎΠ΄ΠΎΡΠ²
- Pityriasis alba (Π±Π΅Π»Π΅ΡΠΎΠ²Π°ΡΡΠ΅ ΠΏΡΡΠ½Π° Π½Π° ΠΊΠΎΠΆΠ΅ Π»ΠΈΡΠ°, ΠΏΠ»Π΅ΡΠ΅Π²ΠΎΠ³ΠΎ ΠΏΠΎΡΡΠ°)
- Π€ΠΎΠ»Π»ΠΈΠΊΡΠ»ΡΡΠ½ΡΠΉ Π³ΠΈΠΏΠ΅ΡΠΊΠ΅ΡΠ°ΡΠΎΠ· («ΡΠΎΠ³ΠΎΠ²ΡΠ΅» ΠΏΠ°ΠΏΡΠ»Ρ Π½Π° Π±ΠΎΠΊΠΎΠ²ΡΡ ΠΏΠΎΠ²Π΅ΡΡ Π½ΠΎΡΡΡΡ ΠΏΠ»Π΅Ρ, ΠΏΡΠ΅Π΄ΠΏΠ»Π΅ΡΠΈΠΉ, Π»ΠΎΠΊΡΠ΅ΠΉ)
- Π¨Π΅Π»ΡΡΠ΅Π½ΠΈΠ΅, ΠΊΡΠ΅ΡΠΎΠ·, ΠΈΡ ΡΠΈΠΎΠ·
- ΠΠ΅ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΡ ΡΡΠΊ ΠΈ Π½ΠΎΠ³
- Π§Π°ΡΡΡΠ΅ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½ΡΠ΅ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΡ ΠΊΠΎΠΆΠΈ (ΡΡΠ°ΡΠΈΠ»ΠΎΠΊΠΎΠΊΠΊΠΎΠ²ΠΎΠΉ, Π³ΡΠΈΠ±ΠΊΠΎΠ²ΠΎΠΉ, Π³Π΅ΡΠΏΠ΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΏΡΠΈΡΠΎΠ΄Ρ)
- ΠΠ΅Π»ΡΠΉ Π΄Π΅ΡΠΌΠΎΠ³ΡΠ°ΡΠΈΠ·ΠΌ
- ΠΡΠ΄ ΠΏΡΠΈ ΠΏΠΎΠ²ΡΡΠ΅Π½Π½ΠΎΠΌ ΠΏΠΎΡΠΎΠΎΡΠ΄Π΅Π»Π΅Π½ΠΈΠΈ
- Π‘ΠΊΠ»Π°Π΄ΠΊΠΈ Π½Π° ΠΏΠ΅ΡΠ΅Π΄Π½Π΅ΠΉ ΠΏΠΎΠ²Π΅ΡΡ Π½ΠΎΡΡΠΈ ΡΠ΅ΠΈ
- Π’ΡΠΌΠ½ΡΠ΅ ΠΊΡΡΠ³ΠΈ Π²ΠΎΠΊΡΡΠ³ Π³Π»Π°Π· (Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΡΠΈΡΠ½ΠΈΠ΅)
- Π¨Π΅Π»ΡΡΠ΅Π½ΠΈΠ΅, ΠΏΠΎΠΊΡΠ°ΡΠ½Π΅Π½ΠΈΠ΅, Π·ΡΠ΄ ΠΏΠΎΡΠ»Π΅ ΠΏΡΠΈΠ½ΡΡΠΈΡ Π²Π°Π½Π½ (Π½Π°Π±Π»ΡΠ΄Π°Π΅ΡΡΡ Ρ Π΄Π΅ΡΠ΅ΠΉ Π΄ΠΎ 2Ρ Π»Π΅Ρ).
ΠΠ»Ρ ΠΏΠΎΡΡΠ°Π½ΠΎΠ²ΠΊΠΈ Π΄ΠΈΠ°Π³Π½ΠΎΠ·Π° ΠΡΠ Π½Π΅ΠΎΠ±Ρ ΠΎΠ΄ΠΈΠΌΠΎ ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΠ΅ ΡΡΡΡ Π±ΠΎΠ»ΡΡΠΈΡ ΠΈ Π½Π΅ ΠΌΠ΅Π½Π΅Π΅ ΡΡΡΡ ΠΌΠ°Π»ΡΡ ΠΊΡΠΈΡΠ΅ΡΠΈΠ΅Π².
ΠΠ΅Ρ Π°Π½ΠΈΠ·ΠΌΡ ΡΠ°Π·Π²ΠΈΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
Π ΠΎΡΠ½ΠΎΠ²Π΅ ΠΡΠ Π»Π΅ΠΆΠΈΡ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠ΅. ΠΠ°ΡΠΎΠ³Π΅Π½Π΅Π· ΠΡΠ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΏΠΎΠ»ΠΈΡΠ°ΠΊΡΠΎΡΠ½ΡΠΌ ΠΏΡΠΈ Π²Π΅Π΄ΡΡΠ΅ΠΉ ΡΠΎΠ»ΠΈ ΠΈΠΌΠΌΡΠ½Π½ΡΡ Π½Π°ΡΡΡΠ΅Π½ΠΈΠΉ. ΠΠ΅Π΄ΡΡΠΈΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΌΠ΅Ρ Π°Π½ΠΈΠ·ΠΌΠΎΠΌ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΡΠ ΡΠ²Π»ΡΡΡΡΡ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ ΡΠΎΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΡ Th1/Th2 β Π»ΠΈΠΌΡΠΎΡΠΈΡΠΎΠ² Π² ΡΡΠΎΡΠΎΠ½Ρ Th2-Ρ Π΅Π»ΠΏΠ΅ΡΠΎΠ², ΡΡΠΎ ΠΏΡΠΈΠ²ΠΎΠ΄ΠΈΡ ΠΊ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΠΈΡΠΎΠΊΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠΈΠ»Ρ ΠΈ Π²ΡΡΠΎΠΊΠΎΠΉ ΠΏΡΠΎΠ΄ΡΠΊΡΠΈΠΈ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΡ IgE-Π°Π½ΡΠΈΡΠ΅Π». Π ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ ΠΈΠΌΠΌΡΠ½Π½ΠΎΠ³ΠΎ ΠΏΡΡΠΊΠΎΠ²ΠΎΠ³ΠΎ ΠΌΠ΅Ρ Π°Π½ΠΈΠ·ΠΌΠ° ΠΏΡΠΈ ΠΡΠ Π²ΡΡΡΡΠΏΠ°Π΅Ρ Π²Π·Π°ΠΈΠΌΠΎΠ΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ Π°Π»Π»Π΅ΡΠ³Π΅Π½ΠΎΠ² ΡΠΎ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ Π°Π½ΡΠΈΡΠ΅Π»Π°ΠΌΠΈ (ΡΠ΅Π°Π³ΠΈΠ½Π°ΠΌΠΈ) Π½Π° ΠΏΠΎΠ²Π΅ΡΡ Π½ΠΎΡΡΠΈ ΡΡΡΠ½ΡΡ ΠΊΠ»Π΅ΡΠΎΠΊ. ΠΠ΅ΠΈΠΌΠΌΡΠ½Π½ΡΠ΅ ΡΡΠΈΠ³Π³Π΅ΡΠ½ΡΠ΅ ΡΠ°ΠΊΡΠΎΡΡ ΡΡΠΈΠ»ΠΈΠ²Π°ΡΡ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠ΅ ΠΏΡΡΡΠΌ Π½Π΅ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΈΠ½ΠΈΡΠΈΠΈΡΠΎΠ²Π°Π½ΠΈΡ Π²ΡΡΠ²ΠΎΠ±ΠΎΠΆΠ΄Π΅Π½ΠΈΡ ΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΠΎΠ² Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ (Π³ΠΈΡΡΠ°ΠΌΠΈΠ½, Π½Π΅ΠΉΡΠΎΠΏΠ΅ΠΏΡΠΈΠ΄Ρ, ΡΠΈΡΠΎΠΊΠΈΠ½Ρ), ΠΊΠΎΡΠΎΡΡΠ΅ ΠΈΠΌΠ΅ΡΡ ΠΏΡΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ Ρ Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠΈ. ΠΠ°ΠΆΠ½ΡΡ ΡΠΎΠ»Ρ Π² ΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠ°Π½ΠΈΠΈ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ ΠΊΠΎΠΆΠΈ ΠΏΡΠΈ ΠΡΠ ΠΈΠ³ΡΠ°Π΅Ρ ΠΊΠ°ΠΊ ΡΠΎΠ±ΡΡΠ²Π΅Π½Π½ΠΎ Π³ΡΠΈΠ±ΠΊΠΎΠ²Π°Ρ ΠΈ ΠΊΠΎΠΊΠΊΠΎΠ²Π°Ρ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡ ΠΊΠΎΠΆΠΈ, ΡΠ°ΠΊ ΠΈ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΡΠ΅Π°ΠΊΡΠΈΠΈ Π½Π° ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΡ Π±Π°ΠΊΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΡΡ ΠΈ Π³ΡΠΈΠ±ΠΊΠΎΠ²ΡΡ ΠΊΠ»Π΅ΡΠΎΠΊ.
ΠΠΎΠ΄Ρ ΠΎΠ΄Ρ ΠΊ Π»Π΅ΡΠ΅Π½ΠΈΡ
ΠΠΎΠ΄ Π²ΠΎΠ·Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ΠΌ Π°Π»Π»Π΅ΡΠ³Π΅Π½Π° Π² ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌΠ΅ Π°ΡΠΎΠΏΠΈΠΊΠΎΠ² Π·Π°ΠΏΡΡΠΊΠ°Π΅ΡΡΡ ΡΠ΅Π»ΡΠΉ ΠΊΠ°ΡΠΊΠ°Π΄ Π²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΡ ΡΠ΅Π°ΠΊΡΠΈΠΉ. Π ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ΅ ΡΡΠΎΠ³ΠΎ Π² ΠΎΡΠ°Π³Π΅ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ ΠΎΠ±ΡΠ°Π·ΡΠ΅ΡΡΡ ΠΊΠ»Π΅ΡΠΎΡΠ½ΡΠΉ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°Ρ, ΠΎΡΠ½ΠΎΠ²Ρ ΠΊΠΎΡΠΎΡΠΎΠ³ΠΎ ΡΠΎΡΡΠ°Π²Π»ΡΡΡ ΠΊΠ»Π΅ΡΠΊΠΈ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ. ΠΡΠΈ ΠΊΠ»Π΅ΡΠΊΠΈ Π²ΡΠ΄Π΅Π»ΡΡΡ ΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΡ, ΡΠΈΡΠΎΠΊΠΈΠ½Ρ, IgE. ΠΠ°ΠΆΠ΅ ΠΏΡΠΈ ΡΡΡΡΠ°Π½Π΅Π½ΠΈΠΈ Π°Π»Π»Π΅ΡΠ³Π΅Π½Π° ΠΈΠ· ΠΎΠΊΡΡΠΆΠ΅Π½ΠΈΡ ΡΠ΅Π±ΡΠ½ΠΊΠ° Π²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠΉ ΠΏΡΠΎΡΠ΅ΡΡ ΠΏΡΠΎΠ΄ΠΎΠ»ΠΆΠ°Π΅ΡΡΡ. ΠΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠ΅ ΡΠ²Π»ΡΠ΅ΡΡΡ ΡΠ°ΠΌΠΎΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠΈΠ²Π°ΡΡΠΈΠΌΡΡ. ΠΠ°Π½Π½ΠΎΠ΅ ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ Π΄ΠΈΠΊΡΡΠ΅Ρ Π½Π΅ΠΎΠ±Ρ ΠΎΠ΄ΠΈΠΌΠΎΡΡΡ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΡ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π²ΡΠ΅ΠΌ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°ΠΌ Ρ ΠΡΠ. ΠΠΎΡΠΊΠΎΠ»ΡΠΊΡ ΠΊΠ»Π΅ΡΠΎΡΠ½ΡΠΉ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°Ρ Π΄Π°ΠΆΠ΅ ΠΏΡΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π½Π΅ ΠΌΠΎΠΆΠ΅Ρ ΠΈΡΡΠ΅Π·Π½ΡΡΡ Π² ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ Π½Π΅ΡΠΊΠΎΠ»ΡΠΊΠΈΡ Π΄Π½Π΅ΠΉ, Π½Π΅ΠΎΠ±Ρ ΠΎΠ΄ΠΈΠΌΠ° Π΄Π»ΠΈΡΠ΅Π»ΡΠ½Π°Ρ Π±Π°Π·ΠΈΡΠ½Π°Ρ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½Π°Ρ ΡΠ΅ΡΠ°ΠΏΠΈΡ β Π½Π΅ ΠΌΠ΅Π½Π΅Π΅ 2-3 ΠΌΠ΅ΡΡΡΠ΅Π² Π΄ΠΎ Π΄ΠΎΡΡΠΈΠΆΠ΅Π½ΠΈΡ ΠΏΠΎΠ»Π½ΠΎΠΉ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ΅ΠΌΠΈΡΡΠΈΠΈ.
ΠΠ°ΠΏΡΠ°Π²Π»Π΅Π½ΠΈΡ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΠΡΠ
- ΠΠΈΠ΅ΡΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ ΠΈ ΠΌΠ΅ΡΡ ΠΏΠΎ ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ Π²Π½Π΅ΡΠ½Π΅ΠΉ ΡΡΠ΅Π΄Ρ
- Π‘ΠΈΡΡΠ΅ΠΌΠ½Π°Ρ ΡΠ°ΡΠΌΠ°ΠΊΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ
- Π°Π½ΡΠΈΠ³ΠΈΡΡΠ°ΠΌΠΈΠ½Π½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ
- ΠΌΠ΅ΠΌΠ±ΡΠ°Π½ΠΎΡΡΠ°Π±ΠΈΠ»ΠΈΠ·ΠΈΡΡΡΡΠΈΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ
- ΠΈΠ½Π³ΠΈΠ±ΠΈΡΠΎΡΡ ΠΊΠ°Π»ΡΡΠΈΠ½Π΅Π²ΡΠΈΠ½Π° [ΠΈΡΡΠΎΡΠ½ΠΈΠΊ Π½Π΅ ΡΠΊΠ°Π·Π°Π½ 177 Π΄Π½Π΅ΠΉ]
- ΡΡΠ΅Π΄ΡΡΠ²Π° Π΄Π»Ρ Π»Π΅ΡΠ΅Π½ΠΈΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠ½ΠΎ-ΠΊΠΈΡΠ΅ΡΠ½ΠΎΠ³ΠΎ ΡΡΠ°ΠΊΡΠ°
- Π²ΠΈΡΠ°ΠΌΠΈΠ½Ρ
- ΠΈΠΌΠΌΡΠ½ΠΎΠΌΠΎΠ΄ΡΠ»ΠΈΡΡΡΡΠΈΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ
- ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ, ΡΠ΅Π³ΡΠ»ΠΈΡΡΡΡΠΈΠ΅ ΡΡΠ½ΠΊΡΠΈΡ Π½Π΅ΡΠ²Π½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ
- ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ, ΡΠΎΠ΄Π΅ΡΠΆΠ°ΡΠΈΠ΅ Π½Π΅Π½Π°ΡΡΡΠ΅Π½Π½ΡΠ΅ ΠΆΠΈΡΠ½ΡΠ΅ ΠΊΠΈΡΠ»ΠΎΡΡ
- Π°Π½ΡΠΈΠ±ΠΈΠΎΡΠΈΠΊΠΈ
- ΡΠΈΡΡΠ΅ΠΌΠ½ΡΠ΅ ΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠΈΠ΄Ρ (ΠΏΠΎ ΡΠΏΠ΅ΡΠΈΠ°Π»ΡΠ½ΡΠΌ ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΈΡΠΌ)
ΠΡΠ½ΠΎΠ²Π½ΡΠ΅ ΡΠ΅Π»ΠΈ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ
- Π£ΡΡΡΠ°Π½Π΅Π½ΠΈΠ΅ ΠΈΠ»ΠΈ ΡΠΌΠ΅Π½ΡΡΠ΅Π½ΠΈΠ΅ Π²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΡ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ ΠΈ ΠΊΠΎΠΆΠ½ΠΎΠ³ΠΎ Π·ΡΠ΄Π°
- ΠΠΎΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΈΠ΅ ΡΡΡΡΠΊΡΡΡΡ ΠΈ ΡΡΠ½ΠΊΡΠΈΠΈ ΠΊΠΎΠΆΠΈ (ΡΠ»ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΌΠΈΠΊΡΠΎΡΠΈΡΠΊΡΠ»ΡΡΠΈΠΈ ΠΈ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° Π² ΠΎΡΠ°Π³Π°Ρ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΡ, Π½ΠΎΡΠΌΠ°Π»ΠΈΠ·Π°ΡΠΈΡ Π²Π»Π°ΠΆΠ½ΠΎΡΡΠΈ ΠΊΠΎΠΆΠΈ)
- ΠΡΠ΅Π΄ΠΎΡΠ²ΡΠ°ΡΠ΅Π½ΠΈΠ΅ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΡΠΆΡΠ»ΡΡ ΡΠΎΡΠΌ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ, ΠΊΠΎΡΠΎΡΡΠ΅ ΠΏΡΠΈΠ²ΠΎΠ΄ΡΡ ΠΊ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΡ ΠΊΠ°ΡΠ΅ΡΡΠ²Π° ΠΆΠΈΠ·Π½ΠΈ Π±ΠΎΠ»ΡΠ½ΡΡ ΠΈ ΠΈΠ½Π²Π°Π»ΠΈΠ΄ΠΈΠ·Π°ΡΠΈΠΈ
- ΠΠ΅ΡΠ΅Π½ΠΈΠ΅ ΡΠΎΠΏΡΡΡΡΠ²ΡΡΡΠΈΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ, ΠΊΠΎΡΠΎΡΡΠ΅ ΡΡΡΠΆΠ΅Π»ΡΡΡ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ ΠΡΠ.
Π ΠΎΡΠ½ΠΎΠ²Π΅ ΠΡΠ Π»Π΅ΠΆΠΈΡ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΠ΅, ΠΏΠΎΡΡΠΎΠΌΡ ΠΎΡΠ½ΠΎΠ²Ρ Π»Π΅ΡΠ΅Π½ΠΈΡ ΡΠΎΡΡΠ°Π²Π»ΡΡΡ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ.
ΠΠΎΠ»ΠΈΠΎΡΠ³Π°Π½Π½ΠΎΡΡΡ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠΉ ΠΏΡΠΈ ΠΡΠ ΡΡΠ΅Π±ΡΠ΅Ρ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΡ ΡΠΈΡΡΠ΅ΠΌΠ½ΠΎΠΉ Π±Π°Π·ΠΈΡΠ½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌΠΈ. ΠΠ°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ ΠΈΠΌΠ΅Π΅Ρ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ β Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Π΄ΠΎΠ»ΠΆΠ½ΠΎ Π±ΡΡΡ ΡΡΠ°ΠΏΠ½ΡΠΌ ΠΈ ΠΏΡΠΎΠ΄ΠΎΠ»ΠΆΠΈΡΠ΅Π»ΡΠ½ΡΠΌ.
ΠΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½Π°Ρ ΡΠ΅ΡΠ°ΠΏΠΈΡ ΠΏΡΠΈ ΠΡΠ
ΠΡΡΡΠ°Ρ ΡΠ°Π·Π°
- ΠΠ½ΡΠΈΠ³ΠΈΡΡΠ°ΠΌΠΈΠ½Π½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ 2-Π³ΠΎ ΠΏΠΎΠΊΠΎΠ»Π΅Π½ΠΈΡ (Ρ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΠΌΠΈ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΡΠ²ΠΎΠΉΡΡΠ²Π°ΠΌΠΈ β Π°Π½ΡΠΈΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΠ½ΡΠΌΠΈ ΠΈ ΠΌΠ΅ΠΌΠ±ΡΠ°Π½ΠΎΡΡΠ°Π±ΠΈΠ»ΠΈΠ·ΠΈΡΡΡΡΠΈΠΌΠΈ (Π»ΠΎΡΠ°ΡΠ°Π΄ΠΈΠ½)) β 4-6 Π½Π΅Π΄Π΅Π»Ρ. (ΠΡΠ²Π°Π΅Ρ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠ΅ Π½Π° ΡΠ°ΠΊΠΎΠ³ΠΎ ΡΠΎΠ΄Π° ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ ΠΈ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠ΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² ΡΡΠΈΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°Ρ ).
- ΠΠ½ΡΠΈΠ³ΠΈΡΡΠ°ΠΌΠΈΠ½Π½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ 1-Π³ΠΎ ΠΏΠΎΠΊΠΎΠ»Π΅Π½ΠΈΡ Π½Π° Π½ΠΎΡΡ (Π΅ΡΠ»ΠΈ Π½Π΅ΠΎΠ±Ρ ΠΎΠ΄ΠΈΠΌ ΡΠ΅Π΄Π°ΡΠΈΠ²Π½ΡΠΉ ΡΡΡΠ΅ΠΊΡ) β 4-6 Π½Π΅Π΄Π΅Π»Ρ. (ΠΡΠ²Π°Π΅Ρ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠ΅ Π½Π° ΡΠ°ΠΊΠΎΠ³ΠΎ ΡΠΎΠ΄Π° ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ ΠΈ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠ΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² ΡΡΠΈΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°Ρ ).
- ΠΡΠΈΠΌΠΎΡΠΊΠΈ (Π½Π°ΡΡΠΎΠΉΠΊΠΈ ΠΊΠΎΡΡ Π΄ΡΠ±Π°, 1 % Ρ-Ρ ΡΠ°Π½ΠΈΠ½Π°, Ρ-Ρ ΡΠΈΠ²Π°Π½ΠΎΠ»Π° 1:1000 ΠΈ Π΄Ρ.), ΠΊΡΠ°ΡΠΈΡΠ΅Π»ΠΈ (ΡΡΠΊΠΎΡΡΠΈΠ½, ΠΆΠΈΠ΄ΠΊΠΎΡΡΡ ΠΠ°ΡΡΠ΅Π»Π°Π½ΠΈ, 1-2 % Ρ-Ρ ΠΌΠ΅ΡΠΈΠ»Π΅Π½ΠΎΠ²ΠΎΠ³ΠΎ ΡΠΈΠ½Π΅Π³ΠΎ ΠΈ Π΄Ρ.) β ΠΏΡΠΈ Π½Π°Π»ΠΈΡΠΈΠΈ ΡΠΊΡΡΡΠ΄Π°ΡΠΈΠΈ.
- ΠΠ°ΡΡΠΆΠ½ΡΠ΅ Π³Π»ΡΠΊΠΎΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠΈΠ΄Ρ (ΠΠΎΠΌΠ΅ΡΠ°Π·ΠΎΠ½ (Mometasone) ΠΊΡΠ΅ΠΌ, Π»ΠΎΡΡΠΎΠ½) β 3-7 Π΄Π½Π΅ΠΉ ΠΈ Π½Π΅Π³ΠΎΡΠΌΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ Π½Π°ΡΡΠΆΠ½ΡΠ΅ ΡΡΠ΅Π΄ΡΡΠ²Π°, ΠΏΠΎΡΠ΅Π½ΡΠΈΡΡΡΡΠΈΠ΅ Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΡ Π³Π»ΡΠΊΠΎΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠΈΠ΄ΠΎΠ² (Π Π΅Π³Π»ΠΈΡΠ°ΠΌ Π³Π΅Π»Ρ).
- Π‘ΠΈΡΡΠ΅ΠΌΠ½ΡΠ΅ Π³Π»ΡΠΊΠΎΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠΈΠ΄Ρ (ΠΏΡΠΈ ΠΎΡΡΡΡΡΡΠ²ΠΈΠΈ ΡΡΡΠ΅ΠΊΡΠ° ΠΎΡ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠΌΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ).
Π₯ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠ°Ρ ΡΠ°Π·Π°
- ΠΠ½ΡΠΈΠ³ΠΈΡΡΠ°ΠΌΠΈΠ½Π½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ 2-Π³ΠΎ ΠΏΠΎΠΊΠΎΠ»Π΅Π½ΠΈΡ β 3-4 ΠΌΠ΅ΡΡΡΠ° (ΠΡΠ²Π°Π΅Ρ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠ΅ Π½Π° ΡΠ°ΠΊΠΎΠ³ΠΎ ΡΠΎΠ΄Π° ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ ΠΈ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠ΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² ΡΡΠΈΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°Ρ )
- ΠΠ°ΡΡΠΆΠ½ΡΠ΅ Π³Π»ΡΠΊΠΎΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠΈΠ΄Ρ (ΠΠΎΠΌΠ΅ΡΠ°Π·ΠΎΠ½ (Mometasone) ΠΌΠ°Π·Ρ)
- ΠΠΎΠΌΠ±ΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΡΠ΅ ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π³Π»ΡΠΊΠΎΠΊΠΎΡΡΠΈΠΊΠΎΡΡΠ΅ΡΠΎΠΈΠ΄Ρ Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΠ΅ΡΠ°ΠΌΠ΅ΡΠ°Π·ΠΎΠ½Π°(Betamethasone), ΡΠΎΠ΄Π΅ΡΠΆΠ°ΡΠΈΠ΅ Π°Π½ΡΠΈΠ±Π°ΠΊΡΠ΅ΠΈΡΠ°Π»ΡΠ½ΡΠ΅ ΠΈ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ³ΡΠΈΠ±ΠΊΠΎΠ²ΡΠ΅ ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΡ, Π½Π°ΠΏΡΠΈΠΌΠ΅Ρ: ΡΡΠΈΠ΄Π΅ΡΠΌ(Gentamycin+Betamethasone+Clotrimazole), Π΄ΠΈΠΏΡΠΎΠ³Π΅Π½Ρ(Gentamycin+Betamethasone), Π΄ΠΈΠΏΡΠΎΡΠ°Π»ΠΈΠΊ(Betamethasone+Salicylic ac > ΠΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠ° ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠΉ
- ΠΠ½ΡΠΈΠ³ΠΈΡΡΠ°ΠΌΠΈΠ½Π½ΡΠ΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ 3-Π³ΠΎ ΠΏΠΎΠΊΠΎΠ»Π΅Π½ΠΈΡ β 6 ΠΌΠ΅ΡΡΡΠ΅Π² ΠΈ Π±ΠΎΠ»Π΅Π΅. (ΠΡΠ²Π°Π΅Ρ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠ΅ Π½Π° ΡΠ°ΠΊΠΎΠ³ΠΎ ΡΠΎΠ΄Π° ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ ΠΈ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠ΅ Π΄ΠΎΠ±Π°Π²ΠΊΠΈ Π² ΡΡΠΈΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°Ρ ).
- ΠΠΌΠΌΡΠ½ΠΎΠΌΠΎΠ΄ΡΠ»ΡΡΠΎΡΡ (ΠΈΠ½Π΄ΠΈΠ²ΠΈΠ΄ΡΠ°Π»ΡΠ½ΠΎ).
- Π‘ΠΏΠ΅ΡΠΈΡΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅ΡΠ°ΠΏΠΈΡ Π°Π»Π»Π΅ΡΠ³Π΅Π½Π°ΠΌΠΈ (Π‘ΠΠ’).
- ΠΠ°ΡΡΠΆΠ½Π°Ρ ΡΠ΅ΡΠ°ΠΏΠΈΡ ΠΈ ΡΠ°ΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΠΉ ΡΡ ΠΎΠ΄ Π·Π° ΠΊΠΎΠΆΠ΅ΠΉ (ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅, ΠΊΠ΅ΡΠ°ΡΠΎΠΏΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ ΡΠ»ΡΡΡΠ°ΡΡΠΈΠ΅ ΠΌΠΈΠΊΡΠΎΡΠΈΡΠΊΡΠ»ΡΡΠΈΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ, ΡΡΠ΅Π΄ΡΡΠ²Π° Ρ ΠΏΠΎΠ»ΠΈΠ½Π΅Π½Π°ΡΡΡΠ΅Π½Π½ΡΠΌΠΈ ΠΆΠΈΡΠ½ΡΠΌΠΈ ΠΊΠΈΡΠ»ΠΎΡΠ°ΠΌΠΈ).
ΠΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΠΎΠ΅ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ ΠΠ΅ΠΌΠΎΠ»ΠΈΠ·ΡΠΌΠ°Π±ΠΎΠΌ
ΠΠ»Ρ Π»Π΅ΡΠ΅Π½ΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ° ΡΠ°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°Π΅ΡΡΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°Ρ ΠΠ΅ΠΌΠΎΠ»ΠΈΠ·ΡΠΌΠ°Π± (nemolizumab) β Π³ΡΠΌΠ°Π½ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠ΅ ΠΌΠΎΠ½ΠΎΠΊΠ»ΠΎΠ½Π°Π»ΡΠ½ΠΎΠ΅ Π°Π½ΡΠΈΡΠ΅Π»ΠΎ, ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ½ΠΎΠ΅ ΠΊ ΠΈΠ½ΡΠ΅ΡΠ»Π΅ΠΉΠΊΠΈΠ½Ρ-31. Π ΠΆΡΡΠ½Π°Π»Π΅ The New England Journal of Medicine Π² 2017 Π³ΠΎΠ΄Ρ Π±ΡΠ»ΠΈ ΠΎΠΏΡΠ±Π»ΠΈΠΊΠΎΠ²Π°Π½Ρ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ II ΡΠ°Π·Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΠΠ΅ΠΌΠΎΠ»ΠΈΠ·ΡΠΌΠ°Π±Π° Π΄Π»Ρ Π»Π΅ΡΠ΅Π½ΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ° ΡΡΠ΅Π΄Π½Π΅ΠΉ ΠΈ ΡΡΠΆΡΠ»ΠΎΠΉ ΡΠΎΡΠΌΡ. [3] Π ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ 12 Π½Π΅Π΄Π΅Π»Ρ 264 Π²Π·ΡΠΎΡΠ»ΡΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°, Π΄Π»Ρ ΠΊΠΎΡΠΎΡΡΡ ΡΡΠ°Π½Π΄Π°ΡΡΠ½Π°Ρ ΡΠ΅ΡΠ°ΠΏΠΈΡ ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°ΠΌΠΈ Π½Π΅ ΠΏΡΠΈΠ½Π΅ΡΠ»Π° ΡΡΠΏΠ΅Ρ Π°, ΠΏΠΎΠ»ΡΡΠ°Π»ΠΈ Π΄ΠΎΠ·Ρ ΠΠ΅ΠΌΠΎΠ»ΠΈΠ·ΡΠΌΠ°Π±Π° Π² ΡΠ°Π·Π½ΡΡ Π΄ΠΎΠ·ΠΈΡΠΎΠ²ΠΊΠ°Ρ (0,1 ΠΌΠ³; 0,5 ΠΌΠ³; 2 ΠΌΠ³/ΠΊΠ³) ΠΈΠ»ΠΈ ΠΏΠ»Π°ΡΠ΅Π±ΠΎ. ΠΡΠ΅Π½ΠΊΠ° ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎΡΡΠΈ Π·ΡΠ΄Π° ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»Π°ΡΡ ΠΏΠΎ Π²ΠΈΠ·ΡΠ°Π»ΡΠ½ΠΎ-Π°Π½Π°Π»ΠΎΠ³ΠΎΠ²ΠΎΠΉ ΡΠΊΠ°Π»Π΅, ΠΈΠ·ΠΌΠ΅ΡΡΠ»Π°ΡΡ ΠΏΠ»ΠΎΡΠ°Π΄Ρ ΠΏΠΎΡΠ°ΠΆΡΠ½Π½ΠΎΠ³ΠΎ ΡΡΠ°ΡΡΠΊΠ°. ΠΠ°ΠΈΠ»ΡΡΡΠΈΠ΅ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π΄Π°Π½Π½ΡΠΌ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠΌ Π±ΡΠ»ΠΈ ΠΎΡΠΌΠ΅ΡΠ΅Π½Ρ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ², ΠΏΠΎΠ»ΡΡΠ°Π²ΡΠΈΡ Π΄ΠΎΠ·Ρ ΠΏΠΎ 0,5 ΠΌΠ³/ΠΊΠ³. Π‘ΡΠ΅Π΄ΠΈ Π½ΠΈΡ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎΡΡΠΈ Π·ΡΠ΄Π° ΡΠΎΡΡΠ°Π²ΠΈΠ»ΠΎ 60 % , Π² Π³ΡΡΠΏΠΏΠ΅ ΠΏΠ»Π°ΡΠ΅Π±ΠΎ β 21 %; ΡΠΎΠΊΡΠ°ΡΠ΅Π½ΠΈΠ΅ ΠΏΠ»ΠΎΡΠ°Π΄ΠΈ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΡ β 42 %, Π² ΠΏΠ»Π°ΡΠ΅Π±ΠΎ Π³ΡΡΠΏΠΏΠ΅ β 27 %.
ΠΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠ° Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ°
- ΠΠ΅ΡΠ²ΠΈΡΠ½Π°Ρ ΠΏΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠ° ΠΡΠ ΡΠΎΡΡΠΎΠΈΡ Π² ΠΏΡΠ΅Π΄ΡΠΏΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠΈ ΡΠ΅Π½ΡΠΈΠ±ΠΈΠ»ΠΈΠ·Π°ΡΠΈΠΈ ΡΠ΅Π±ΡΠ½ΠΊΠ°, ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎ Π² ΡΠ΅ΠΌΡΡΡ , Π³Π΄Π΅ Π΅ΡΡΡ Π½Π°ΡΠ»Π΅Π΄ΡΡΠ²Π΅Π½Π½Π°Ρ ΠΏΡΠ΅Π΄ΡΠ°ΡΠΏΠΎΠ»ΠΎΠΆΠ΅Π½Π½ΠΎΡΡΡ ΠΊ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΠΌ
- ΠΡΠΎΡΠΈΡΠ½Π°Ρ ΠΏΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠ° ΠΎΡΠ½ΠΎΠ²ΡΠ²Π°Π΅ΡΡΡ Π½Π° ΠΏΡΠ΅Π΄ΡΠΏΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠΈ ΠΌΠ°Π½ΠΈΡΠ΅ΡΡΠ°ΡΠΈΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΈ/ΠΈΠ»ΠΈ Π΅Π³ΠΎ ΠΎΠ±ΠΎΡΡΡΠ΅Π½ΠΈΠΉ Ρ ΡΠ΅Π½ΡΠΈΠ±ΠΈΠ»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠ³ΠΎ ΡΠ΅Π±ΡΠ½ΠΊΠ°. Π§Π΅ΠΌ Π²ΡΡΠ΅ ΡΠΈΡΠΊ Π°ΡΠΎΠΏΠΈΠΈ Ρ ΡΠ΅Π±ΡΠ½ΠΊΠ°, ΡΠ΅ΠΌ Π±ΠΎΠ»Π΅Π΅ ΠΆΡΡΡΠΊΠΈΠΌΠΈ Π΄ΠΎΠ»ΠΆΠ½Ρ Π±ΡΡΡ ΡΠ»ΠΈΠΌΠΈΠ½Π°ΡΠΈΠΎΠ½Π½ΡΠ΅ ΠΌΠ΅ΡΡ.
- ΠΡΠΎΡΠΈΠ»Π°ΠΊΡΠΈΠΊΠ° ΠΡΠ ΡΠΎΡΡΠΎΠΈΡ ΡΠ°ΠΊΠΆΠ΅ Π² Π°Π΄Π΅ΠΊΠ²Π°ΡΠ½ΠΎΠΌ Π»Π΅ΡΠ΅Π½ΠΈΠΈ Π΄Π΅ΡΠ΅ΠΉ Ρ Π½Π°ΡΠ°Π»ΡΠ½ΡΠΌΠΈ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡΠΌΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ.
ΠΠΈΠ΅ΡΠ°
Π‘Π»Π΅Π΄ΡΠ΅Ρ ΠΈΡΠΊΠ»ΡΡΠΈΡΡ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ (Ρ ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΠ΅) ΡΡΠΈΠ³Π³Π΅ΡΡ. ΠΠΈΠ΅ΡΠ° ΠΎΡΠ½ΠΎΡΠΈΡΡΡ ΠΊΠ°ΠΊ ΠΊ Π΄Π΅ΡΡΠΌ, ΡΠ°ΠΊ ΠΈ ΠΊ Π±Π΅ΡΠ΅ΠΌΠ΅Π½Π½ΡΠΌ ΠΈ ΠΊΠΎΡΠΌΡΡΠΈΠΌ ΠΆΠ΅Π½ΡΠΈΠ½Π°ΠΌ.
ΠΡΠΎΠ³Π½ΠΎΠ·
ΠΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΉ Π΄Π΅ΡΠΌΠ°ΡΠΈΡ ΠΈΠΌΠ΅Π΅Ρ Π²ΠΎΠ»Π½ΠΎΠΎΠ±ΡΠ°Π·Π½ΠΎΠ΅ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅: Ρ 60 % Π΄Π΅ΡΠ΅ΠΉ ΡΠΈΠΌΠΏΡΠΎΠΌΡ ΡΠΎ Π²ΡΠ΅ΠΌΠ΅Π½Π΅ΠΌ ΠΏΠΎΠ»Π½ΠΎΡΡΡΡ ΠΈΡΡΠ΅Π·Π°ΡΡ, Π° Ρ ΠΎΡΡΠ°Π»ΡΠ½ΡΡ ΡΠΎΡ ΡΠ°Π½ΡΡΡΡΡ ΠΈΠ»ΠΈ ΡΠ΅ΡΠΈΠ΄ΠΈΠ²ΠΈΡΡΡΡ Π² ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ Π²ΡΠ΅ΠΉ ΠΆΠΈΠ·Π½ΠΈ. Π§Π΅ΠΌ ΡΠ°Π½ΡΡΠ΅ Π΄Π΅Π±ΡΡ ΠΈ ΡΠ΅ΠΌ ΡΡΠΆΠ΅Π»Π΅Π΅ ΠΏΡΠΎΡΠ΅ΠΊΠ°Π΅Ρ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅, ΡΠ΅ΠΌ Π²ΡΡΠ΅ ΡΠ°Π½Ρ Π΅Π³ΠΎ ΠΏΠ΅ΡΡΠΈΡΡΠΈΡΡΡΡΠ΅Π³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ, ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎ Π² ΡΠ»ΡΡΠ°ΡΡ ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΡ Ρ Π΄ΡΡΠ³ΠΎΠΉ Π°Π»Π»Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΏΠ°ΡΠΎΠ»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. Inβ¦ β¦ Medical dictionary
atopic dermatitis β noun a severe form of dermatitis characterized by atopy β’ Syn: βatopic eczema β’ Hypernyms: βdermatitis β¦ 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 β¦ Wiktionary
atopic dermatitis β a type of dermatitis (q.v.). * * * β¦ 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 siteβ¦ β¦ 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 β¦ Medical dictionary
atopic eczema β noun a severe form of dermatitis characterized by atopy β’ Syn: βatopic dermatitis β’ Hypernyms: βdermatitis β¦ Useful english dictionary
atopic β (Λ)Δ|tΓ€pik, (Λ)a| , ΙΛ , Δk 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 β¦ Useful english dictionary