What is eczema? A general term that describes an inflammation of the skin. What are the characteristics of eczema? There are several types of eczema, although the term “eczema” is usually used to refer to different variants of the disease. What are the main types of eczema? Discover six (6).
This is the most common form of chronic eczema. Atopy is the tendency to react by allergic reactions mediated by antibodies called IgE in contact with allergens normally harmless to the rest of the population (dust, pollen, animal hair, etc.). Atopic people often present, simultaneously or alternately, various allergic reactions, such as hay fever, urticaria, asthma, or food allergies. These allergies often have a hereditary component since they are observed in many cases in families where at least 1 member suffers.
Atopic dermatitis affects 10 to 20% of children and 2 to 3% of adults in Europe. The disease starts most often in the infant and persists most often during childhood up to 5-6 years, but it persists sometimes in adulthood in about 15% of patients.
Here is what is known about the causes of atopic dermatitis which is a multifactorial disease involving genetic and environmental factors:
Atopic dermatitis is a disease with a genetic factor since 50 to 70% of parents of atopic children have a sign of atopy (eczema in childhood for example) and 70% of identical twins both have atopic eczema. This genetic factor is polygenic because it affects at least 2 types of genes:
*** Genes of the Superficial Cutaneous Barrier
The skin has a very thin and very resistant superficial barrier, yet patients with atopic dermatitis carry genetic mutations, especially on the gene encoding filaggrin, a structural protein of the epidermis that plays a role in the structure of the skin. cutaneous barrier and now an optimal level of skin hydration. As the skin plays less of a barrier role, antigens and chemical irritants can, therefore, penetrate more easily …
*** Genes of the Cutaneous Immune System
Thus, atopic react more to their environment, and trigger skin inflammatory reactions in the presence of antigens, notably involving Langherans cells (antigen-presenting cells), lymphocytes (antibody-producing white blood cells), etc.
Atopic dermatitis is a disease in which environmental factors are involved, including:
*** The Digestive Flora
For some years, we have been discovering how the microbiota or composition of the digestive bacterial flora plays a role in many diseases and in the individual response to treatments. Atopic dermatitis is no exception to this rule since it has been discovered that the microbiota is a complex ecosystem involved in the maturation of the immune system. Anomalies of early diversification of the gut microbiota have been observed in children at risk of atopic and neonates at risk of atopy.
*** The Cutaneous Flora
The cutaneous microbiome of the newborn is gradually formed after birth from the mother’s microbiome and the environment. As for the intestinal microbiota, there are differences between the cutaneous microbiome of atopic children and that of non-atopic children, especially during outbreaks of atopic dermatitis, during which there is a proliferation of strains of staphylococci (Staphylococcus aureus) in 90% of patients. case and Staphylococcus epidermidis), related to skin immunity deficiency through a deficit in “natural antibiotics” of the skin: beta-defensins.
Thus, local treatments for atopic dermatitis tend to favor natural bacterial diversity on the surface of the skin to limit the role of Staphylococcus aureus. Thus, it is necessary to avoid antiseptics in atopic dermatitis and the local steroids feared by the mothers tend to favor bacterial diversity, to the detriment of Staphylococcus aureus.
“Western Urban” Type of Lifestyle Poses an Increased Risk of Atopic Diseases
The increase in the frequency of atopic dermatitis has been regular for several decades in developing countries, suggesting that environmental factors play a major role in the pathophysiology of the disease, including the reduction of exposure. Infectious agents in early childhood: recent studies confirm that the “western urban” type of lifestyle poses an increased risk of atopic diseases compared to the “rural” type of lifestyle (exposure to bacteria and parasites early childhood), especially in populations predisposed genetically and in the same geographical areas. This also raises other factors more present in the “western urban” lifestyle (role of abandonment of breastfeeding? Milk allergy? Greater concentration of pollutants and allergens in the environment? ), but this remains to be proven scientifically.
Finally, it should be noted that there is more of a child’s eczema in the countries of Northern Europe than in the countries of southern Europe: it is, therefore, questionable whether there are factors that can lead to children’s eczema in northern countries (is the meticulous hygiene of young children in the northern countries responsible for the increase in children’s eczema in these countries? Are northern children more allergenic than in the South? Can the colder climate explain the greater frequency of children’s eczema in northern countries?
All of this data has made it possible to develop a “biodiversity theory” that protects atopic dermatitis, which combines environmental biodiversity with the biodiversity of the various cutaneous and digestive microbiomes.
*** How Is Atopic Dermatitis Manifested?
In infants lesions start on the cheeks or even the forehead and scalp, then they extend on the extension of the arms and legs and the trunk. It is dry and rough redness or oozing and crusting, which always itch (the infant tends to carry their hands, which can cause scratches.
After 2 years, atopic dermatitis lesions will predominate in the bending folds of the elbows and knees or wrists.
In adolescents and adults, the lesions are located mainly on the face and the neck (the Anglo-Saxons speak of “head and neck dermatitis”) and the members. They are often thickened (we talk about lichenification of the skin).
*** Complications of Atopic Dermatitis
– Superinfection with staphylococcus aureus or “impetiginisation”, responsible for the purulent discharge, sometimes with yellow bubbles and crusts like honey.
– Superinfection with the herpes virus (especially HSV-1). It is rare (5% of children with atopic dermatitis) but formidable, it results in a sudden worsening of the disease and the appearance of small multiple vesicular lesions evoking those of chickenpox, giving wounds. We are talking about Kaposi-Juliusberg syndrome.
The management of the atopic dermatitis of the child thus resorts to the limitation of the favoring factors and in particular the elements accentuating the cutaneous drought by applying moisturizing creams, avoiding the too hot and prolonged baths, and by using soft soaps (of type bath oil or sugars for example). Hydrotherapy is one of the therapeutic weapons to fight against atopic eczema but it is generally used only in conjunction with conventional corticosterone cream treatments during outbreaks in particular.
So these are the characteristics of eczema named Atopic dermatitis. Let’s continue with the characteristics of eczema called contact dermatitis.
2. The Characteristics of Eczema or Contact Dermatitis
Allergic contact dermatitis is characterized by eczema lesions appearing on average 3 days after contact of the skin with certain substances called allergens (this delay can be increased to 10 days if it is the first contact of the skin with the allergens). This is an allergic reaction to the substance. This allergic reaction does not necessarily occur at first contact and may occur after several months or years of tolerance to the allergen (one becomes allergic to a substance that was tolerated, for example, nickel jewelry or coins ).
Depending on the type of eczema, the symptoms may last 1 or 2 weeks, or continue for several years.
When scraped off, the plates ooze and become more irritated. Sometimes these areas can become infected. It is possible in particular to contract;
– impetiginization, which is a bacterial superinfection, especially with Staphylococcus aureus, of eczema, characterized by the appearance of meliceric crusts (like crystallized honey),
– cellulite This complication is characterized by the sudden appearance of swelling on the skin of a limb, which becomes sensitive, red, and hot.
In these cases, it is important to consult quickly.
3. Seborrheic Dermatitis
Seborrheic dermatitis refers to a benign skin disease that is characterized by the formation of red patches accompanied by dander, a kind of dandruff on the surface of the skin. This disease evolves by outbreaks and can last several years.
It is called “seborrheic” because it mainly affects the fatty parts of the skin, such as the face, trunk, and hair. It has no character of gravity and entails no complication but is inconvenient aesthetically. The proliferation of yeast would be responsible for red plaques. The treatments are based on the use of antimycotics (shampoos, creams, lotions).
It affects between 3% and 5% of the population and is manifested by the creation of red patches and scales of white or yellowish coloring.
*** Causes of Seborrheic Dermatitis
At present, it is not known with certainty the origin of seborrheic dermatitis.
Two elements are involved: the area of oily skin and a fungus (yeast) type Malassezia furfur (formerly pitysporum). But it does not seem that sufferers suffer from an excess of sebum production. Malassezia yeasts are present on all skins, but some people seem to react inappropriately, which may lead to seborrheic dermatitis. Another hypothesis is that yeasts transform sebum into free fatty acids, which themselves would be a source of inflammation.
Visible manifestations are enough for the doctor to make a diagnosis, although the lesions presented are sometimes similar to those of psoriasis. It is not always easy to differentiate between these two diseases. Sebopsoriasis is also mentioned in profuse forms of seborrheic dermatitis associated with psoriasis plaques on the body.
*** Symptoms of Seborrheic Dermatitis
Symptoms vary slightly depending on the area (s) affected:
– On the scalp (the most common): white scales, kinds of dandruff visible on clothes or shoulders when the person is combing, red scalp, itching.
– On the skin, it is red patches that peel. They are preferential:
– On the face: in the nasolabial folds (furrows between the nose and both ends of the mouth), the wings of the nose, the eyebrows, the eyelids, behind the ears, and in the external auditory canal. Plates are generally symmetrical.
– On the trunk, the back: on a median vertical line between the breasts (intermuscular zone), or on the back a median zone between the shoulders (interscapular zone).
On the genital areas, hairy areas, and folds, for example, folds of the groin.
– Itching: they are relatively frequent, but not systematic and may be accompanied by burning sensations.
– The lesions are very inconstant: they come and go, often triggered by stress, fatigue, or overwork. And they are improved by the sun.
*** Risk Factors for Seborrheic Dermatitis
It can also affect infants (so-called “milk crusts”), and about 70% of them are concerned before the age of 3 months. There is an extended form of Leiner-Moussous erythrodermia that usually cures itself. It remains common in children (10% of them up to 5 years). About 4% of adults have seborrheic dermatitis. In the over 65 years, a quarter of the population is affected.
This disease is, therefore, more common at both ends of life, just after birth or after 65 years.
People over 65 years old, those with oily skin, Parkinson’s disease, who are HIV positive or with a declared AIDS stage, people with trisomy 21, cancers of the upper aerodigestive tract, alcoholism, or neuroleptic drugs. Also, stress and fatigue are factors of seizures (not of the disease).
*** Prevention of Seborrheic Dermatitis
Prevention of seborrheic dermatitis is difficult. It goes through the reduction of the contributing factors in lifestyle such as fatigue, overwork, alcohol …
Therapeutically, prevention consists of
– the reduction of residual sebum by a daily toilet of the affected areas with mild products
– the reduction of fungal colonization by the use at the first signs of antifungal products
– the fight against inflammation by not scratching its lesions and using moisturizing cosmetics and gentle care.
4. Nummular Eczema or Discoid Dermatitis
Nummular eczema is an inflammation of the skin characterized by coin-shaped lesions or discoid eczematous lesions. The diagnosis is clinical. Treatment includes local corticosteroids and ultraviolet phototherapy.
Nummular eczema is very common in middle-aged and older patients and is often associated with dry skin, especially during the winter. Dermatophytidic reactions (identity, or id) can be manifested by nummular dermatitis. The cause is unknown.
Discoid lesions often begin as spots, papules, and confluent vesicles, which eventually seep and crust. Later, they become dry, scaly, lichenified and sometimes annular (central healing). The lesions are often intensely itchy. We can count between 1 and up to about 50 and their diameter is generally between 2 and 10 cm. They are often in the foreground on the extremities of the limbs and on the buttocks, but also on the trunk. The aggravations and the remissions can alternate, in this case, the lesions tend to reappear in the already healed parts.
Clinical assessment: The diagnosis is clinical, and based on the appearance and the characteristic distribution of the cutaneous lesions. Research examinations of bacteria and fungi can be performed to exclude an infection.
– Support care
– Corticosteroids (most often topical but sometimes intralesional or oral)
– Ultraviolet light therapy
No treatment is always effective. Po antibiotics (eg, dicloxacillin or cefalexin 250 mg QID) and wet compresses may be prescribed for oozing and purulent lesions. Medium to high potency corticosteroids in cream or ointment should be applied 2 times/day. An occlusive dressing comprising a corticosteroid cream under a polyethylene film or a dressing impregnated with flurandrenolide may be set up at bedtime. Intralesional infiltrations of corticosteroids may be proposed for the few lesions that are not sensitive to treatment.
In the most frequent, resistant, and recurrent cases, only ultraviolet B or oral psoralen plus ultraviolet A (PUVA) may be useful. Sometimes oral corticosteroids are needed, but their long-term use should be avoided; a reasonable starting dose is prednisone 40 mg 1 day / 2. Alternatives to corticosteroids for recalcitrant diseases include cyclosporine and methotrexate.
5. Stasis Dermatitis or Variceal Eczema
Stasis dermatitis is inflammation of the lower limbs caused by stagnation of the blood (venous insufficiency) and fluid retention.
Stasis dermatitis occurs in people with chronic venous insufficiency of the lower legs, that is, lesions in the veins of the leg that prevent the blood from circulating normally. Affected individuals develop swelling (edema), rarely varicose veins (dilation and torsion of the veins), and finally a stasis dermatitis. Stasis dermatitis usually appears around the ankles, but can go up to the knees.
At first, the skin blushes and peels slightly. In a few weeks or months, it is pigmented in dark brown. Finally, lesions of certain skin areas can worsen and an ulcer (open wound), usually in the ankle. Ulcerative lesions are sometimes infected by bacteria. Stasis dermatitis causes itching and swelling of the legs but is not painful. Pressure ulcers are usually painful.
The skin can become hard, thick, painful, and sensitive. In case of complications, we talk about lipodermatosclerosis.
– The appearance of the skin and presence of chronic venous insufficiency
– Possibly, ultrasound
Doctors diagnose stasis dermatitis in people who have typical skin changes and chronic venous insufficiency, but sometimes a more complete assessment and imaging tests (such as an ultrasound) are needed.
– Measures to prevent blood pooling in the legs
– Measures to relieve dermatitis
– For ulcers, special dressings, or Unna’s boot
– In case of infection, antibiotics
– Treatment of chronic venous insufficiency
Long-term treatment aims to treat chronic venous insufficiency by preventing the accumulation of venous blood in the lower limbs, especially in the ankle. When people sit, they must raise their legs at the level of the heart plan. The prescription of compression stockings to the person’s measurements also avoids blood stasis and reduces edema. The relief of mass distribution relief is generally not appropriate.
– Treatment of dermatitis
In the case of recent dermatitis, moist compresses, such as compresses moistened with tap water or soaked with aluminum acetate (Burow’s solution), relieve the symptoms and prevent infection by preserving the cleanliness of the skin. skin. When the disorders worsen, as evidenced by an increase in body temperature, redness, oozing or small ulcerations, a more absorbent dressing may be used, for example, a hydrocolloid dressing.
Corticosteroid creams or ointments are also useful, and are often associated with a zinc oxide paste and applied in a thin layer. Corticosteroids should not be applied directly to the ulcerated lesion because they delay healing.
– Treatment of ulcers
When individuals have large ulcerated lesions or extensive lesions, special absorbent dressings containing hydrocolloid or hydrogel dressings may be used. Antibiotics are prescribed only if the skin is already infected. Sometimes the skin of another area of the body is removed and grafted to cover the very large ulcerated lesions.
Some people have to be treated with an Unna boot, an elastic bandage containing zinc gelatin. The band is applied at the level of the ankle and the lower part of the leg where it hardens like plaster but is lighter. The boot limits swelling and protect the skin from irritation while the dough promotes healing. In the first phase, the boot is changed every 2 or 3 days, then it is left in place for a week before the change. After healing the eschar, an elastic band should be applied before people get up. Regardless of the bandage used, a decrease in edema (usually with compression) is essential for healing.
During stasis dermatitis, the skin is easily irritated. Antibiotic creams, anesthetics (first aid creams), alcohol, witch hazel, lanolin, or other chemicals should not be applied as they can make the condition worse.
6. Dermatitis Herpetiformis or Duhring-Brocq Disease
Dermatitis herpetiformis is an autoimmune disease leading to the formation of small blisters with severe itching, and swelling as in urticaria in people with celiac disease.
– In this autoimmune disease, gluten from wheat, rye, and barley products causes the immune system to attack the skin.
– People have small blisters with itching and swelling as in hives on various areas of the body.
– Doctors diagnose dermatitis herpetiformis by examining skin samples under a microscope.
– People usually respond to treatment with dapsone or sulfapyridine and a gluten-free diet.
Dermatitis herpetiformis often affects young adults but can also affect children and the elderly. It is rare in black and Asian populations.
Despite its name, dermatitis herpetiformis has no relation to the herpes virus. The term herpetiformis is used to describe how blisters cluster together (similar to a rash caused by herpesvirus).
In people with dermatitis herpetiformis, glutens, proteins in foods made from wheat, rye, or barley, activate the immune system that attacks the skin, causing a rash and itching. People with dermatitis herpetiformis have celiac disease, which is an intestinal disorder due to sensitivity to gluten, but they do not necessarily have symptoms of celiac disease. There is also a high incidence of other autoimmune diseases in these individuals, such as thyroiditis, systemic lupus erythematosus, sarcoidosis, pernicious anemia, and diabetes. Dermatitis herpetiformis is sometimes associated with intestinal lymphoma.
Small blisters and hives usually develop gradually, mainly at the elbows, knees, buttocks, lumbar region, and neck, but may develop suddenly. Sometimes, blisters appear on the face and neck. Because the itching is intense and the skin is fragile, the blisters usually rupture quickly, and only a few remain intact, which is helpful for the doctor’s examination. Blisters can develop in the mouth, but they usually do not cause symptoms. The itching and burning are often severe. Iodine and iodine preparations (such as laminar and seaweed products, and some skin soaps) can aggravate the rash. Some specialists also suggest avoiding iodized salt.
Cutaneous biopsy: The diagnosis is based on skin biopsy, in which there are certain types of antibodies, with a particular disposition in the skin. Doctors are screening for celiac disease in all people with dermatitis herpetiformis.
– Gluten-free diet
– Dapsone, and sometimes other drugs
Blisters do not heal spontaneously. People generally follow a gluten-free diet (a diet without wheat, barley, or rye), which is the main treatment for celiac disease.
Dapsone, taken orally, almost always provides relief in 1 to 3 days but requires regular blood count because it can cause anemia. Sulfapyridine (or sulfasalazine) is also given orally and may be prescribed to persons with dapsone intolerance. However, sulfapyridine can cause anemia and a decrease in white blood cell counts (increasing the risk of infection), and also requires regular blood cell counts.
After gaining control of the disease with the drugs and a strict gluten-free diet for at least 6 months, it is usually possible to discontinue drug therapy. However, some people can never stop the medication. In most people, even minimal re-exposure to gluten leads to a new episode. A gluten-free diet followed literally for 5 to 10 years reduces the risk of intestinal lymphoma.