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  • Eczema is an inflammatory dermatitis, erythemato-vesicle, pruriginous
  • It is the most common of dermatoses
  • The predominant histological lesion is Malpighi mucous body spongiosis
  • This group of eczema has two well-defined entities: allergic contact eczema and constitutional eczema (atopic dermatitis)

Clinical study:

  • Acute eczema: the eczema flare-up develops in 4 stages:

Erythematous phase: erythematous, oedium, hot, wiping, crumbled edges

Blister phase: after a few hours, the vesicles appear on the surface of the erythema, contain a clear serosity

Oozing phase: the vesicles break and allow a yellowish serous liquid to flow, the closet is then covered with yellowish crusts (serosity clotting)

Repair phase (peeling phase): at the fall of the crusts appears a pink, wrinkled, highly descising epidermis

  • Chronic eczema:

Lichenified eczema: appearance of a greyish, thickened, gridded and very pruriginous plaque

Chronic eczema of palms and plants: appearance of palmoplantar keratodermy

Note: The edges of eczema lesions are usually crumbled, the pruritus is constant


Useful for diagnosis in atypical forms

  • At the skin level:

Spongiosis: oedematous distension of intercellular spaces, making small vesicles

Exocytosis: inflammatory cells (lymphocytics) from the dermis

  • At the level of the dermis: edema, hair dilation and inflammatory infiltrator

Contact Eczema:

  • Definition: a major cause of adult eczema is acquired inflammatory dermatosis, due to percutaneous sensitization to untolerated or allergenic molecules
  • Pathophysiology: this is a delayed hypersensitivity reaction to cell mediation, in 2 phases:

Awareness phase: from a few days to several years, the exogenous sensitizing product is most often a haptene (small substance, non-immunogenic by itself) that enters the skin and combines with a protein to form a couple " "haptene-protein" (allergen) that will be picked up by epidermal Langerhans cells and presented to LT and lymph nodes.  These activated LTs proliferate under the action of IL2 and then differentiate into circulating "memory" lymphocytes

Revelation phase: 24-48h, after further contact with the allergen, the allergen-specific Tm lymphocytes recognize the allergen presented by Langerhans cells, proliferate and secrete cytokines (IL2, TNF) that recruit inflammatory mononucleated cells responsible for the clinical and histological response of eczema

  • Etiological diagnosis:

Interrogation: a very important element of the etiological investigation, it is necessary to look for:

Initial Topography: The lesions are initially located at the contact area with the allergen, they can then diffuse remotely

Trigger circumstances: specify activities that may have led to contact with a particular allergen 24 hours to a few days before: occupation, gardening, application of a cosmetic…

Timeline: Changes in injuries over time (holidays, work stoppages)

Local Treatments Used: Before and After Dermatosis

Clinical examination: will specify the elementary lesions and the evolution in 4 stages – pruritus, some locations have a referral value:

▪ Lobule of the ear, wrist and umbilical – Nickel awareness

▪ Face, eyelids or neck – cosmetic allergy, nail polish, perfumes

▪ Feet: Allergy to a Shoe Constituent (Leather Chrome)

Skin tests (patch tests): these tests reproduce the same lesions as those of eczema

Technique: on the skin of the back, apart from an eczema flare-up and at a distance from a local corticosteroid therapy, the substance is applied to be tested and covered with a non-allergenic medium (cellulose lozenges).  Standard European batteries are usually produced (25 substances most frequently involved), sometimes specialized batteries oriented

Reading: is done at 48 hours, 15 minutes after removing the tests, a second reading is done at 72-96h, sometimes 7 days for certain allergens (corticosteroids)

Negative test: normal skin

Positive test: reproducing the eczema lesion: () – erythema, papule, () erythema, papule, vesicle, erythema, papule, numerous confluent vesicles (bubbles)

Main causes:

Occupational Allergens: The occupations most often involved are:

Building trades: cement, paint, glue, varnish, carpentry, rubber

Hairdressers: dyes, preservatives and foaming agents, Nickel (instruments)

Health profession: antiseptic, antibiotics, NSAIDs, Neomycin, sparadrap

Cosmetics: perfumes, preservatives, excipients, nail polish, deodorants, shampoos, lacquers, Peruvian balm (lipstick, creams)

Clothing products: textile dyes, leather, shoe glue, rubber, costume jewellery, accessories (watch, belt buckle, jeans buttons): Nickel

Photo-allergens: Some allergens induce contact eczema only after UV irradiation – photo-exposed areas (NSINs, some plants)

  • Differential diagnosis:

Irritation dermatitis: secondary to direct physical or chemical (non-immunological) aggressions, may take on the appearance of acute or chronic eczema, occurs during the first contact

Dermatitis (or eczema) atopic

Facial edema: erysipelas, angioedema (Quincke edema), shingles

Constitutional Eczema (Atopic Dermatitis):

  • Definition: is a chronic and pruriginous inflammatory dermatosis, occurring on atopic terrain, frequent (10-20% of children). Atopy refers to a particular condition characterized by a genetic predisposition to increased synthesis of IgE and allergic diseases (allergic rhinitis, conjunctivitis, asthma, eczema)
  • Pathophysiology: multifactorial pathology, results from the interaction between:

Genetic factors: This is a complex polygenic disease, two types of genes appear to be involved: epidermal barrier genes located in the region of the 1q21 epidermal differentiation complex (including the filagragin gene) and genes regulating the specific and innate immune system. The disease is 80% consistent in monozygotic twins and 30% in dizygotes, 50-70% of patients with DA have a first-degree relative with DA, asthma or allergic rhinitis

Immunological factors: the delayed hypersensitivity reaction that involves T cells and antigen-presenting cells, the release of cytokines into the skin by activated lymphocytes eczema lesions

Innate abnormalities of the epidermal barrier: abnormalities of the corneal layer and skin lipids explain skin dryness, mutations in a corneal layer protein (filaggrine) increase in the amount of water lost and facilitate the a penetration of allergens

Epidemiology/environmental factors: it is high prevalence (10-20%) children in industrialized countries with a high socio-economic level. Hygienic theory: decreased exposure to infectious agents – changes in the regulation of the innate immune system allergy

  • Clinical:

Infant and young child (up to 2 years old):

Start: usually around 3 months, sometimes earlier

Clinic: lesions are type of acute eczema (4 stages), important pruritus, in the very small, in the form of rubbing the cheeks against the sheets, agitation

Associated signs: skin xerosis, palmoplantar hyperlinearity, cheilitis…

Topography of lesions: symmetrically touches the convex areas of the face (cheeks, forehead, chin), fairly clear respect for the mid-facial region (nose, peribuccal) and limbs, can extend to the neck, scalp, retro-ear region, folds of bending, trunk

Children over 2 years of age:

Clinic: the predominant lesions are chronic, the skin xerosis is almost constant, more pronounced in winter

Topography of lesions: lesions are more localized: folds (elbows, hollow poplities, neck and sub-ear), in certain bastion areas (hands and wrists, ankles, nipples)

Teenagers and adults:

Start: Late onset to adulthood is possible but rare

Clinic: lichenified eczema appearance with a prurigo table, predominant to the limbs or nummular eczema or erythrodermia

Topography of lesions: folds, retro-ear furrow, back of hands, peribuccal region, sometimes lower limbs

  • Evolution:

In the short term: the evolution is chronic, made of alternations between relapses and remissions according to different aggravating factors, with the possibility of complications. The most common triggers are: dental flare-ups, infections, vaccinations, changes in environment or diet, heat, untimely use of soaps and antiseptics, wearing wool or textile clothing synthetic, emotions, stress and annoyance of the child

In the long term: in infants, most often spontaneously supportive (total remission within a few years), persistent forms in childhood are often more localized, resurgence or persistence in adolescence or in young adults is Possible

  • Complications: extension of lesions to erythrodermia, stunted growth, contact hermits

Overinfections: bacterial (Staphylococcus), viral (herpes virus: kaposi Juliusberg varioliform pustulosis that may have severe evolution, vulgar wart, molluscum contagiosum)

  • Diagnosis: clinical, given the personal and family history of atopy, age of onset of lesions, appearance and topography of lesions. Biological explorations: increase in serum IgE and blood hypereosinophilia


  • Local means:

Antiseptic: permanganaté bath (KMnO4): 1 250 mg tablet in 5 litres of water where the affected part will be immersed for 15 minutes

Local antibiotics: Fucidine®: cream (oozing lesion), ointment (dry lesion)

Dermocorticoids: their level of action and galenic presentation are depending on the seat, appearance, extent of lesions and age of the patient

Emollient and moisturizer: simple vaseline, ureal-based preparation (Xeal®: 10, 30, 50), moisturizer (Avène Xeracalm®, Xemosse uriage®, Atoderm®…)

Topical calcineurine inhibitors: Tacrolimus (Protopic®): ointment at 0.03% for 2 to 16 year olds, 0.1% for adults

  • General means:

Antibiotics: avoid lactamines (allergenic character), macrolides will be used mainly: Erythromycin (500 mg tablet, 2-3 g/d), Rovamycin® (tablet, syrup in children), anti-staphylococcal: Fucidine® (250 mg tablet and Pyostacin syrup® (50mg/g)g.

Antihistamines: Polaramine (syrup, 2 and 6 mg tablet), Méquitazine (Primalan®)

Corticosteroids: Cortancyl® (5, 10 and 20 mg tablet) prescribed only in generalized severe eczema

  • Indications:

Treatment of allergic contact eczema:

Etiological treatment: allergen removal (fundamental therapeutic measure), but the ubiquity of some allergens makes it difficult to remove them

Symptomatic treatment:

Local corticosteroid therapy (Diprosone®, Locoid®, Efficort®…): for 1-2 weeks

General corticosteroid therapy: if over-stressed and/or diffuse impairment (15-30 mg/d for 3-7 days)

Antiseptic baths and general antibiotic therapy: indicated in case of overinfection

Prevention and follow-up: in a professional setting, relies on the wearing of gloves, protective clothing, in occupations at high risk of awareness, the layout of the workstation in collaboration with the occupational doctor, there is no possibility desensitization in contact eczema

Treatment of atopic eczema:

Treatment of relapses: dermocorticoids (no general corticosteroid therapy in AD), topical calcineurine inhibitors, oral antihistamines (H1 anti-h1), local or systemic antibiotics (in case of obvious infection)

Maintenance treatment: emollients, hygiene measures (avoid irritating textiles: wool, synthetics with large fibers, prefer cotton and linen, avoid exposure to tobacco, maintain a cool temperature in the room and do not cover too much at night , physical exercises, sports to advise (shower and emollients after), daily short bath, with a warm temperature and loaves or gels without soap), attention: herpetic contage! vaccination allowed outside of flare-ups

Therapeutic Education: from the patient or parents, aims to learn to live optimally with a chronic illness, to know the aggravating factors, to understand and to see practical demonstrations of local care…

Other treatments: phototherapy, Ciclosporin, Azathioprine

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