Lecture on eczema

2021-03-24 12:00 AM

Whether internal or external causes are related to a specific body's response to an allergic reaction, the patient may be a topic.

Eczema is a common skin disease, today and in the future, due to the need for industrialization, more use of occupational Eczema chemicals will increase.

Eczema can be defined as a superficial inflammatory state of the skin, acute or chronic, progressing intermittently or recurring, clinically manifested by a patch of erythema, blisters and pruritus, a complex internal cause, foreign world but always plays the role of "atopic body", histologically there is a spongiotic phenomenon (Spongiosis).

As typical, chronic or recurrent itchy skin disease, treatment is difficult.


Complicated causes are sometimes difficult or undetectable. May be due to:

Foreign causes

Physical, chemical, plant and biological factors that touch the skin induce dermatitis, eczema (these substances are known as metastases). For example light, topical medicine, oral injection, chemicals used in industry, in the home (rubber, nickel, chromium, cement, paint ...).

Some skin diseases that cause itching (fungus, scabies ...) due to rubbing, applying miscellaneous drugs ... can become secondary eczema.

Internal causes

Disorders of internal organs, neurological disorders, and endocrine disorders can be direct or indirect cause of eczema.

Whether the cause of internal or external causes is related to a specific reaction of the body to an allergic reaction, the patient may have a "atopic form".

According to Halpern, Coombs reacting to eczema is classified as "delayed cell hypersensitivity" in which the role of lymphocytes carrying antigen memory.



Of any nature, any area of ​​the skin can be eczema, but depending on the clinical form or the location (will be presented in the clinical section).

Basic damage: The primary lesion in eczema is a patch of red skin and blisters, blisters are typical of eczema, eczema develops in four stages:

Stage of erythema: the disease begins with red spots or patches on the skin, slight swelling, slight streaks, unclear boundaries, very itchy - on a congested red background there are speckled round papules (real Substances are blisters that are extruding from the bottom.

The blister stage (also known as the runny phase): the blisters grow more and more and appear on the surface of the lesion, eczema blisters have the following properties:

Small blisters with toothpick tip, needle tip 1 - 2 mm.

Shallow, self-breaking.

Close side by side tightly all over the wound surface.

Extrusion from bottom to layer.

The surface lesions are covered with blisters. The blisters are shallow, ruptured by themselves and scratched by itching, so the lesions are slippery and fluid, so it is also called a runny stage, this period lasts for days or weeks, the blisters burst, leaving a small spot like needles (also known as eczema wells of Devergie), many points suddenly linked into plaque, red oozing, and easy to infect secondary infections with pus, crust ..

Stage of young skin

In this stage, the lesions reduce inflammation, reduce congestion, reduce drainage, the lesions are suddenly dry, scaly, on the young skin into a smooth, shiny skin like onion peel, the skin is slightly stained, darker.

The stage of likenization, buffalo collar braking

Eczema progresses from time to time, the skin becomes darker, increased infection, rough surface, hard palpation, prominent papules, flat papules between the skin as in lichen, the process This is called lichenification. Contains are persistent.

The red, blister, or watery phase is also called the acute phase eczema.

The crusting phase, so young, drier skin is called subacute eczema.

The stage of lichenification and buffalo kinking is called chronic eczema.

Divided into 4 stages of eczema to easily understand the progression of eczema, but in fact the phases are not really divided so clearly, but often alternate, nested. For example, on regional lesions is a discharge phase, with an area that has already started on young skin, then it is necessary to evaluate which stage lesions prevail and diagnose acute, subacute, or chronic stage. chemical. Going to the later stage when for some reason (rubbing, applying inappropriate drugs) back to the previous stage.

Itching is the most frequent, persistent symptom, eczema is considered to be the typical itchy skin disease.

Progression: chronic or recurrent, multiple episodes of illness, periods of temporary relief alternating.

Clinical forms

Contact eczema: (contact eczema, contact dermatitis)

Location: the first appearance in the contact area is usually the open area, sometimes printing the image of the contact (for example, the strap of the sandals, the picture of the watch strap ...)

Basic damage: congestive red skin, sometimes strong congestive redness, slight swelling, blisters on the surface, sometimes blisters, acute wet slurry, drainage, edema. May have a chronic, dry, thick, and scaly appearance.

Contact discontinuation relieves, re-exposure to a relapse or worsening allergen.

Skin test (skin test) with contact material (allergen) is usually positive, usually skin pressure test, patch test (Patch test) but not when the disease is prosperous or on treatment for corticosteroids.

Some foreign allergens (Allergens) gay contact eczema such as: Nickel, potassium dichromate, fomaldehyte, cement, rubber, neomycin, Streptomycin ...

Nonallergic contact eczema commonly referred to as irritant contact dermatitis is absent. the allergic immune mechanism, usually by exposure to high concentrations of chemicals (such as strong acids and alkalis) and almost everyone who comes into contact is exposed to the exposed skin.


Detect contact allergen and avoid contact with the allergen.

Topical corticoids.

Oral corticoids when the disease spreads or damage to the face, genitals, drink in the morning.

Atopic dermatitis (AD)

Atopic dermatitis is a skin manifestation of Atopic state (Atopic state, Atopic diathesis), 70% of patients have a family history of asthma, allergic rhinitis, hay fever or eczema. About 10% of children experience some form of atopic dermatitis.

There is formation and elevation of IgE, also known as IgE hyper-dermatitis, a hypersensitivity reaction due to the release of a potent active substance from the Mastocytes or Basophils cells.
Pathogenesis and immunology of Atopy dermatitis (AD).

Clearly familial, if both parents are allergic, 79% of children with AD, 73 of children with AD have a family history of AD.

The recent genomic study found in AD patients found:

Chromosome 11913 has a high affinity for IgE.

Chromosome 5931 - 33 are genes for the cytokins IL4. IL5, 6MCSF.

Chromosome 14911 - 1 is a gene for the mastocyte Chymase (Mastocyte).

Chromosome 6q gene of HLA - DR.

Chromosome 16p 11-2-11.1 gene of the IL4 receptor.

The role of Reagin antibodies in the pathogenesis of AD is well thought out.

IgE is elevated in 80% of AD patients and the more severe the AD, the higher the IgE level in AD patients than in asthma and allergic rhinitis. However, in 20% of AD patients still have normal IgE levels. Explain this using the following mechanism:

On the one hand in AD disease, Histamine acts on the H2 receptor of leukocytes, making the function of leukocytes weakened, impaired lymphoid transformation (TTL loss). On the other hand, the decrease in TS number means that lymphocytes carry H2 receptors, these cells are responsible for producing a histamine-triggered IgE inhibitor, the production of IgE increases due to lack of weakness. this factor. In addition, the increase in IgE is also due to an increase in the level of AMP - Phosphodiesterase in the B cells / or T helper cells (T helper) in AD, causing an increase in IgE synthesis.

Elevated IgE is not a fundamental factor in the pathogenesis of AD.

According to Thomas Biefer, Langerhans cells in AD patients surface a receptor that is very effective for IgE, and Langerhans cells carrying this receptor will be able to fix IgE and antigen intrusion, after resistance introduction. is originally active in the production of cytokines, and chemokines will initiate an eczema reaction. In AD patients only a few airborne allergens are required to trigger an eczema reaction. This mechanism is found in 30-40% of patients with AD.

In cell-mediated immune AD disease, there is a decrease in reactivity in slow skin tests such as Tuberculine, Candidine ...

Lymphocytic transformation is most impaired, especially during an episode of AD, a decrease in circulating T lymphocytes, especially T, which inhibits the IgE-Fc receptor, which explains the overproduction of IgE in AD.

Decreased kinetic chemistry in patients with AD is susceptible to infection through trauma, abrasion or staph infection, 90% of AD patients have a Coagulase positive reaction to a staphylococcus. Staph is the predominant bacteria on the skin of AD patients and the frequent presence of staph on the skin of AD patients leads to the initiation of histamine release, which causes itching and dermatitis in AD.

AD patients have a high level of Acetylcholine in their skin, which partly explains the impact of the emotional factors of AD.

There is an increase in the activity of Nucleotide-Phosphodiesterase, which rapidly hydrolyzes the cyclic nucleotide, resulting in a decrease in cAMP, so the inhibitory effect of histamine production is ineffective, while cGMP strengthens, leading to histamine. overproduction in patients with AD.

Chronic progression - flare-ups alternating with remission, sometimes turning into asthma or hay fever.

Factors that exacerbate the disease are allergens or food, emotional stress, menstrual disorders, thyroid disease, staph infection, especially Staphylococcus aureus, which need some attention. Woolen substance increases disease.

As a recurrent or chronic illness, the main clinical lesions are: 

Dermatitis: red maculopapular with papular papules.

Buffalo neck collar.

Dry skin, scratches, secondary infection.

The disease is common in childhood from 2 months to 2 years old, in children, adolescents and adults.

Under 7 years old accounts for 80- 90%, about 10% of the disease extends to adulthood. 

Clinical manifestations by age:

Eczema in infancy and infancy, childhood:

(infantile Atopic dermatitis) (infancy) seen in children from 2 weeks to 2 years. Common in children with plump 2-3 months old, initially on the cheeks, forehead (horseshoe shape), around the mouth, head, later may be in the neck, face stretched, torso, groin. Lesions are red inlays, with many blisters on the surface, slippery, strong discharge, secondary infection with pus, scaly secretion.

May include laxative, otitis media.

Child type atopic dermatitis:

Children (childhood) or adolescents (Adolescent) 2-3 years old to 12-20 years old. Are lichenized plaques (buffalo neck) in disc form somewhere on the stretched sides, knees, elbows, then spread to the folds, in addition, itchy papules, dry skin, and buffalo neck kink.

Sometimes accompanied by cataracts, conjunctivitis.

Adult type atopic dermatitis:

In adults (Adult) are mainly buffalo neck, the special position is large folds and hands, in women can have nipple inflammation, cheilitis.

Progressive chronic, sometimes turning into asthma or hay fever.

Treatment of topical eczema should pay attention to the following points:

Avoid substances that irritate the skin.

Keep the skin hydrated to use cream, moisturizing grease (Lacticare ...) in stable episodes.

Take a warm, but not hot, bath, and limit soap.

Apply glucocorticoids.

Antibiotics against yellow staphylococci when superinfection should use erythromycin.

Synthetic antihistamines.

Systemic corticosteroids (oral) should be limited to use, only for the period of disease and use in short bursts.

UVA, UVB, PUVA are effective.

Eczema bacteria

Due to an allergy to staphylococcal toxin, streptococcus or Trichophyton's toxin, Epidermophyton. 

Often appear on skin abrasions infections, insect stings, burns, fistula, incisions ...

The location is usually on one or both sides of the leg, sometimes around the incision, around the stoma, or around the ear after a purulent middle ear infection.

The lesions are suddenly, draining fluid, pus, scaly secretion, relatively clear limit.

Surrounding the lesion maybe some "satellite" pustules or boils.

There are cases in addition to the major lesions of the face, body, limbs with small red patches, papular papules, blisters and itchiness called "secondary allergic rash".

Nummular eczema

Characterized by round, coinlike oval lesions, initially, red secretion, blisters, papules, a little bit, then scaly, scaly skin, lichenification is clearly limited. , usually localized in the trunk, extensor face of the limbs, before the bone, the back of the hand.

Common in middle-aged men, especially in autumn and winter.

There is an opinion that coinage eczema is a special form of bacterial eczema, which is an allergic rash with a localized infection in the body. Currently, coinfection eczema is a subdivision of Atopic eczema but IgE is normal, however, this issue is debated.

Histopathology has an increase in thorns, spongy cells. 

Treatment of corticosteroids, sometimes injecting corticoids under lesions can apply Coaltar.
Systemic antibiotics.

The PUVA is quite effective.

Seborrheic dermatitis, oily eczema

 A common chronic skin disease characterized by redness and scaling, fatty deposits in the active sebaceous glands such as the face, head and folds. Most common in people 20-50 years old, can be seen in children (the first months), childhood, adolescence. Men often suffer more. It is possible that "oily geomorphology" is possible.

The most common location is the head, the face is usually on the eyebrows, around the eyes, between the nose, the nasolabial folds. behind the ears, sometimes in the body, especially the skin of the thymus region, the fascia, the armpit folds, the groin under the breasts, and genitals. Lesions are red, scaly, fatty plaques, sometimes papules on the surface, relatively clear limit, dry, but microscopic with porous phenomenon.

Skin histopathology has non-specific keratosis, proliferation, spongiotic, non-specific inflammatory dermis.
Need differential diagnosis with psoriasis, rash, scalp fungus, facial fungus, thrush, lupus erythematosus.


Topical corticosteroid ointments are effective, but care should be taken to apply the facial corticosteroid, which can cause skin atrophy, vasodilation

UV irradiation.

You can use Shampoos with sulfur and coaltar or a solution of corticoids.

Shampoo ketoconazole 2% or cream.

Folds using castellani solution.


General treatment

With eczema in the acute phase need rest, limit stimulants (coffee, alcohol ...).

Avoid exposure to the allergen if found.

Avoid scratching and rubbing, avoid soap.

If there is a clear infection (fever, high leukocytes, swelling and pain, lymph nodes, and pus crust secreting), use antibiotics for 7-10 days (Tetracycline, erythromycin).

For antipruritic, antipruritic, antiallergic drugs: synthetic antihistamines. 
Prolonged eczema, with a secondary allergic rash, may require a single course of oral corticoids if there are no contraindications.

Local treatment

For acute, watery, erosive eczema, use skin-soothing, antiseptic, anti-itch, and dehydrated drugs such as gauze with 1/4000 diluted purple saline solution, 9% physiological saline, 0.25 silver nitrate. %, 1% Rivanol o, Yarish solution for the first 5 - 7 days then apply colourant with 1% Methin purple solution, Millian solution, combined with the lake.

When the lesions dry, apply zinc cream oil, corticoid ointment + antibiotics (Synalar cream, neomycin, cream celestoderm -neomycin ....).

With chronic eczema, you can use Gondron, coaltar, corticoids or corticoid + a.salicylic fat like diprosalic fat.