Vulvar contact dermatitis

Introduction to vulvar contact dermatitis Vulvar contact dermatitis is an inflammatory reaction that occurs at the contact site after exposure of the skin or mucous membrane to exogenous substances, manifested as erythema, swelling, papules, blisters and even bullae. According to the etiology, the pathogenesis can be divided into two categories: primary stimulant dermatitis (IRD) and allergic contact dermatitis (ACD). basic knowledge The proportion of illness: the incidence rate is about 0.007%-0.009% Susceptible people: women Mode of infection: non-infectious Complications: genital pruritus, allergic dermatitis

Causes of vulvar contact dermatitis

Materialization factor (60%):

Irritant by acid or alkali or other substances that can strongly irritate the skin, such as strong disinfectant, potassium permanganate that is not completely dissolved during vaginal washing, allergic contact dermatitis, because some people are exposed to sensitive substances, such as vulva Contact with deodorant sprays, contraceptives (condoms, contraceptives), dyed clothing, anesthetics or topical antibiotic preparations (especially penicillin) can cause dermatitis. Chemical: a wide variety, mainly including metal products such as nickel and chromium. Daily necessities such as detergents, brighteners, leather, plastics and rubber products, cosmetics such as rouge, perfume, hair dye, etc., external medicine.

Biological factors (35%):

Animal: animal toxins, fur, down products, etc. Botanical: the leaves, stems, flowers, seeds, juices of plants, common lacquer, ramie, fig, ginkgo, mango and so on. Contact between husband and wife can also lead to mutual allergies.

Pathogenesis

1. Acute dermatitis histopathology

Epidermal cell and intracellular edema, even sponge formation, epidermal blistering, bullae, intraepithelial lymphocytes, neutrophil infiltration, cells are mainly concentrated in the vesicles, connective tissue edema in the superficial dermis, vasodilation, small blood vessels around Focal lymphocytic infiltration, sometimes with a small number of neutrophils and eosinophils.

2. Subacute dermatitis histopathology

Epidermal cell edema, sponge formation and a few blisters, mild epidermal thickening and varying degrees of parakeratosis, more lymphocytic infiltration around the dermis.

3. Chronic dermatitis histopathology

The acanthosis is thickened, the epidermis is prolonged, and there are hyperkeratosis and parakeratosis. There may be mild intercellular edema in the epidermis, mild perivascular lymphocytic infiltration in the superficial dermis, and a small amount of eosinophils and fibroblasts. The number of capillaries increases, and endothelial cells swell and proliferate.

Primary irritation contact dermatitis (ICD): The contact itself is very irritating to the skin. Anyone who comes into contact with a certain concentration of the substance can develop a non-immune skin inflammatory response. The primary stimulus can be divided into two. Species: one is very irritating, short-term exposure after exposure, such as dermatitis caused by strong acid and alkali, and the other is weak irritant, caused by long-term exposure, such as detergents, organic solvents, etc. Dermatitis, the common cause of ICD in the vulva is a high concentration of disinfectant preservatives, such as potassium permanganate or some irritating external drugs, such as edulis, retinoic acid, lactic acid, salicylic acid, etc., factors affecting ICD In addition to the physical and chemical properties, concentration, amount, time and method of exposure, it is also related to host factors such as age, gender, ethnicity, genetic background, location, and local environmental factors such as temperature, humidity, friction, and pressure. Aallele and AA genotypes were significantly increased in people who were susceptible to ICD.

Some aspects of the pathogenesis of ICD are not fully understood.

Allergic contact dermatitis (ACD): The contact itself is non-irritating and toxic. Most people do not develop after exposure. Only a few sensitive individuals have a certain incubation period after contact, and allergic inflammation occurs in the skin at the contact site. .

ACD belongs to T cell-mediated delayed type hypersensitivity. T cells, keratinocytes, Langerhans cells, macrophages, vascular endothelial cells, and mast cells all participate in the reaction. The pathogenesis is complex and is summarized as follows:

(1) Induction period: Most of the allergens causing ACD are haptens, which bind to the carrier protein on the epidermal cell membrane to form a whole antigen to obtain immunogenicity. The whole antigen is recognized and swallowed by Langerhans cells (LC) in the epidermis. Drinking and digesting into peptide fragments, and then combining with the MHC class II antigen molecules on the surface of the LC to form an antigen MHC complex. The LC carrying the antigen flows back to the local lymph nodes through the lymph, and is presented to the CD 4T cells, which migrates from the epidermis to the local part with the LC. Lymph node, its antigen processing activity is gradually lost and the immune irritancy is gradually strengthened. The maturation process of LC is considered to be the key to effectively induce skin allergic reaction. This process is affected by TNF-, IL-1, GM-CSF, in LC direction. CD 4T cells present antigenic processes. The T cell receptors of CD 4T cells must simultaneously recognize antigens and MHC class II antigen molecule complexes to be activated by LC-present antigens, ie MHC-restricted. In this process, LC is also simultaneously The adhesion molecules such as ICAM-1, LFA-3 and B7t were expressed and combined with LFA-1, CD2 and CD28 on the lymphocyte membrane to form a second signal to complete the sensitization reaction.

(2) Excitation period: After sensitization, when the body is exposed to the same antigen again, the antigen is transferred to the specific CD4 T-sensitive cells through the induction period. After the CD4 T cells recognize the antigen, the cells can differentiate and proliferate. Releases a series of cytokines: IL-2, IFN-, GM-CSF, IL-3, IL-4, TNF, promotes T cell proliferation, expands immune response, activates cytotoxic T cells, naturally kills cells and macrophages The cells, as a result, cause epidermal sponge formation and inflammatory cell infiltration of the dermis, telangiectasia and permeability increase, and epidermal cells are destroyed, resulting in acute dermatitis of papules, blisters and even bullae.

Vulvar contact dermatitis prevention

Timely diagnosis, search for allergens, remove the cause, avoid re-exposure to known allergens and similar drugs, avoid scratching, hot water, soap and other stimuli.

Vulvar contact dermatitis complications Complications vulvar pruritus allergic dermatitis

The genital area is exposed to some irritating substances and feels burning, pain, and itching at the contact area. The skin redness, rash, and blisters appear in the skin. In severe cases, necrosis and ulceration may occur. Allergic dermatitis occurs in areas exposed to allergic substances. If the cause can be removed early and treated properly, it can be cured quickly, otherwise it may be converted into co-infection and eczema-like dermatitis.

Vulvar contact dermatitis symptoms Common symptoms Itching papules Eczema edema Swelling pain Herpes skin blisters or bullae damage the skin rough vulva swelling

Because the skin of the genital area is loose, the skin is thin and tender, the nerve endings are rich, and it is not easy to be exposed to ventilation. The rash of the same substance in the genital area is more serious than that occurring in other parts of the body. The affected part is often obviously swollen, and it is violently itchy or burning, and it is painful.

1. Irritant contact dermatitis (ICD)

(1) Acute irritant contact dermatitis: caused by strong irritants, common irritants causing acute ICD in the vulva are: high concentration of disinfectant, dimethyl sulfoxide, amphipidin, retinoic acid, etc., local performance For erythema, edema, blisters, bullae and even necrosis, vulva, labia minora, clitoris showed localized edema, without obvious edges, skin lines disappeared, conscious pain or burning sensation.

(2) Stimulating reaction: slight skin damage has not reached the level of dermatitis. It is a stimulating reaction. The skin lesions are single. It can be expressed as vulva, labia majora, rough skin, dry desquamation, long-term skin thickening, and occasionally develop into Cumulative ICD, such irritants are hygiene products, soaps, external washing drugs, ethanol, hydrogen peroxide, and the like.

(3) Subjective stimuli: refers to some chemical-induced genital sensation, burning sensation, pain, no erythema, edema and other skin lesions, histological examination is usually unchanged, subjective symptoms vary from person to person, common stimuli There are sanitary articles, external medicines, suppository drugs, perfumes, urinary sputum, etc., and chemical fiber underwear with poor gas permeability can increase local moist heat and cause itching.

(4) Cumulative dermatitis: multiple repeated subthreshold stimulation of various weak stimuli can lead to cumulative ICD. At the beginning, only genital itching, pain, dryness, erythema, desquamation, repeated exposure to irritants and certain After the stimulation threshold, there may be clear skin lesions of irritating dermatitis, long-term itching, scratching can cause vulva, the labia majora becomes obvious, the clitoris and labia minora can be hypertrophied, and histological examination can find skin thickening and inflammatory cells. Infiltration, the intensity of the reaction varies with the skin sensitivity of the individual patient. Due to repeated exposure to the irritant, the skin barrier function cannot be repaired in time, the healing time is longer, and the prognosis can be various. The stimulants are mostly detergents and chemical solvents. .

(5) dry eczema-like dermatitis: long-term use of potassium permanganate solution, benzalkonium bromide solution or excessive soap cleaning can cause dryness and itching of the vulva.

(6) post-traumatic irritant dermatitis: irritated dermatitis occurs in the genital area after immersion, rubbing erythema or acute ICD, resulting in erythema, papules, blisters, herpes and desquamation, which can later develop into a disc shape An eczema-like reaction is more complicated and slower to heal if there is a secondary infection.

2. Allergic contact dermatitis

Lighter genital contact areas appear clear red spots, erythema slightly edema, may have papules, herpes, blister, bullae, erosion, exudate, crusting, size labia, clitoris with localized edema, Without obvious edges, the skin is bright and the skin lines disappear. Acute ACD is usually cured within 1 to 2 weeks after removal of allergens, but if it continues to contact allergens, the skin lesions are recurrent and chronically hypertrophic. Pigmentation, prolonged and difficult to heal, common allergens original sanitary napkins, suppository drugs, topical drugs, contraceptives, perfumes, nail polish, metal nickel on clothing.

Examination of vulvar contact dermatitis

The patch test is an auxiliary diagnostic method for determining the body's allergic reaction. According to the nature of the test substance, prepare an appropriate concentration of the infusion solution, solution, ointment or directly use the original as a reagent, soak the test solution with 4 layers of 1 cm2 gauze, or place the test object on the gauze, and place the forearm flexion side. Covered with slightly larger transparent cellophane, surrounded by adhesive plaster, removed after 48 hours, can induce local skin reaction, and the results were judged according to local skin performance at 72 hours.

Diagnosis and differentiation of vulvar contact dermatitis

diagnosis

According to the history of exposure to foreign substances, the acute dermatitis with clear boundary at the contact site, the rash is mostly in a single shape, and the lesion is quickly resolved after the cause is removed. The patch test is helpful to find the cause.

Differential diagnosis

1. Candida sex female vaginitis: vulva, vaginal mucosa congestive erythema, mild swelling, impregnation, mucosal surface of the mucous membrane, subcutaneous basal red, micro-osmotic, conscious pruritus, curd-like leukorrhea, vagina The secretion fungus was microscopically examined for hyphae and spores, and cultured with Candida albicans.

2. Female genital eczema: According to polymorphic skin lesions, it is easy to have exudation, the boundary is unclear, and repeated episodes are chronically identifiable. When the condition is difficult to distinguish from eczema, a patch test is needed to determine the cause.

3. Fixed drug: According to the clear history of medication, edematous erythema of the vulva, central blisters, erosion, and the same lesions can be identified in the original drug site.

4. Seborrheic dermatitis: In addition to the crease of the sinus, the disease is often accompanied by other sebum overflow sites, the lesions are follicular erythema, maculopapular rash, covered with greasy scales, suede or erosion, can There are varying degrees of itching.

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