CHILDREN'S PHASE

 In most patients, the first symptoms of atopic dermatitis appear in the first year of life and persist for several years, then improve during adolescence.

A very small percentage of people develop a severe form of atopic dermatitis, which often has a major impact on the quality of life of the patient and their loved ones.

However, the recurrent and often seasonal nature of AD makes epidemiological assessment difficult. Over the last 30 years, the incidence of atopic dermatitis has increased 2-3 times worldwide, currently affecting 18% of children and 5% of adults, either as dermatitis in adults or as persistent dermatitis in children or adolescents. In the United States, the incidence is slightly higher.

Symptoms
“ ... This disease currently affects 18% of children and 5% of adults '

Atopic dermatitis is characterized by a wide variety of clinical manifestations covering a wide spectrum of lesions and degrees of severity. Atopic dermatitis manifests itself with pruritus, dry skin, erythema and itching. In the absence of standardized assessment methods and specific tests to assess the severity of the disease as well as the benefits of treatment, patient management is currently based on visual observation of the skin and assessment scales such as EASI or SCORAD, which allow for the determination of disease points.

The Hanifin and Rajka criteria, described in 1980, remain valid and widely used. (HANIFIN JM et al.) Diagnostic features of atopic dermatitis Acta Derm Venerol 1980; 92:44-47). Hanifin and Rajka developed a list of primary and secondary diagnostic criteria for atopic dermatitis. The main criteria include pruritus, typical appearance and topography of lesions depending on age, chronic or chronically recurrent course, and personal and family history of atopy. Secondary criteria include xerosis, ichthyosis and hyperlinearity of the hands, perifollicular keratosis, increased serum IgE concentration, early age of onset, dermatitis of the hands and feet, cheilitis, dermatitis of the palate, lower subdigital fold (Dennie-Morgan sign), pityriasis alba.

The diagnosis of atopic dermatitis in adolescents or adults may be more complex, especially when its symptoms differ from typical forms of atopic dermatitis in children. Some symptoms are more specific in adults. These include eczema on the head and neck, eczema on the arms, nummular eczema with multiple lichenoid areas, or nodular prurigo lesions. In such cases, the diagnosis is usually eliminative and requires further tests to exclude other diseases (patch test, biopsy).

Recent research conducted by C. Roduit (RODUIT C. et al. Phenotypes of Atopic Dermatitis Depending on the Timing of Onset and Progression in Childhood JAMA Pediatr. 2017 Jul; 171(7): 655-662), covering 1038 patients followed for a period six years, identified 4 subtypes of AD defined on the basis of the onset of the clinical picture and its evolutionary course. Specifically, this classification includes an early transient phenotype with onset before age 2 years and the absence of other signs and symptoms, an early persistent phenotype with onset before age 2 years and symptoms persisting until age 6 years, a late phenotype with onset after age 2 years, and finally an absent phenotype. . The study found a stronger correlation between early-onset atopic dermatitis and the onset of asthma and allergic rhinitis compared with late-onset cases, but also a stronger correlation between persistent early onset and sensitization to food allergens. Atopic dermatitis can therefore be seen as a possible gateway to the "atopic march", i.e. the typical progression of atopic diathesis in childhood from food allergy to allergic rhinoconjunctivitis and asthma. Atopic dermatitis can develop after the first month of life. Let us now analyze the different phases of onset and their associated clinical features.

NEWBORN AND INFANT PHASE

From the second month to the second year of life, most children initially present with a seborrheic appearance with persistent scales, often greasy and yellowish, on the scalp (cradle cap); the initial inflammatory involvement affects the cheeks with a quite clear and characteristic involvement of the central part of the face, lesions on the limbs are located on the protrusions. On the trunk, the changes usually stop at the edge of the diaper, although sometimes they may affect the folds. The perineum and buttocks area usually remains asymptomatic. In the second year of life, xerosis appears, which is more visible and lasting. At this stage, clinical symptoms include erythema, exudate and crusts. Chronic lesions may have the appearance of well-circumscribed coin-shaped nucleated plaques or, less commonly, an annular appearance with a central scar. Acute lesions are initially exudative, then crusted and often lichenified.

CHILDREN'S PHASE

Over two years of age, inflammation is characterized by elective

topography corresponding to the folds of the upper and lower limbs, but also to the creases behind the ears, wrists and ankles; eyelid involvement is also possible. At this stage, acute exudative lesions subside. Minor clinical signs such as perioral pigmentation and infraorbital folds may occur. Unlike infants, dry skin is a permanent feature. Pityriasis alba, i.e. dry patchy achromatic lesions, may also occur.

ADOLESCENT AND ADULT PHASE

It is characterized by intense xerosis and local changes on the face, neck and bends of the limbs. Signs of lichenization are visible.

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Atopic dermatitis can therefore be seen as a possible precursor to the "atopic march", i.e. the typical progression of atopic diathesis in childhood through food allergy and allergic rhinitis, conjunctivitis and asthma.

Pathogenesis
From the defect of the epithelial barrier function to the reversal of the immune response.

The pathogenesis of atopic dermatitis is complex and involves the existence of interactions between genetic mutations, skin barrier dysfunction, immune deficiencies, changes in lipid composition, microbial imbalances and the neuroimmune system.

Many environmental factors should also be taken into account, such as increased exposure to inhalant or food allergens, pollution, infections, taking antibiotics, breastfeeding time, diet, use of cosmetics or aggressive detergents.

GENETIC PREDISPOSITIONS

A family history of atopy, or more precisely atopic dermatitis, is a risk factor for the development of the disease. It was observed that children of parents with a history of allergic diseases had an increased risk of developing atopic dermatitis, while children of parents suffering from asthma, allergic rhinitis or food allergies had a 1.5-fold increased risk of developing atopic dermatitis. Therefore, the hypothesis of a predisposing genetic basis has been widely analyzed, paying attention to specific genetic mutations. Multiple predisposition genes located on different chromosomes appear to be involved. So far, over 34 locus have been identified in the genetic predisposition to atopic dermatitis, which are associated with epidermal barrier dysfunction, dysregulation of the immune response and abnormalities in the microbiome.

The stratum corneum plays an important role as an epidermal barrier. The keratinized cells that constitute it can be compared to "bricks" forming a hydrophilic wall surrounded by lipophilic "mortar" composed of hydrophobic lipid lamellas filling the extracellular space. Corneocytes are non-nucleated, flattened cells filled with keratin fibers resulting from the differentiation of keratinocytes at the level of the outer surface of the granular layer.

During keratinocyte differentiation, the plasma membrane of the cells is replaced by a rigid and insoluble protein envelope, the cornified envelope, consisting of structural proteins such as loricrin, involucrin, filaggrin, and small proline-rich proteins. Lamellar bodies will then form in the stratum corneum and secrete lipids (ceramides and free fatty acids), responsible for creating an additional protective barrier of the intercellular space. Tight junctions that maintain strong cohesion between corneal cells enhance the protective function and block the penetration of exogenous factors.

The epidermal barrier as a whole prevents the penetration of allergens, irritants and microorganisms. The genes that play a major role in atopic dermatitis include genes encoding structural and functional proteins of the epidermis and genes encoding proteins that regulate the innate and adaptive immune response. Genetic mutations in structural and functional proteins lead to impaired epidermal barrier function.

In patients with atopic dermatitis, the process of epidermal cell differentiation is disturbed. Many barrier changes originate from primary genetic mutations in a group known as the epidermal differentiation complex (EDC), identified on chromosome 1q21. This complex includes the filaggrin gene (FLG), which encodes profilaggrin, which is then cleaved to yield filaggrin subunits, intercellular structural proteins that bind to keratin intermediate filaments in corneocytes and attract water in the stratum corneum, promoting epidermal differentiation and hydration. Changing these proteins cause increased water loss, skin dryness, and infiltration and presentation of antigen to Langerhans cells.

Studies have shown a correlation between filaggrin mutations and a severe early-onset phenotype associated with the development of asthma.

It should be emphasized that the mutation can also be detected in asymptomatic patients, and the lack of the mutated gene does not protect against the disease.

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The hypothesis of a predisposing genetic basis has therefore been extensively investigated, revealing some genetic mutations.

It was observed that children born

People with a history of allergic diseases have an increased risk of developing atopic dermatitis.

Genetic mutations alone cannot explain the pathogenesis of atopic dermatitis. In fact, genetic mutations encoding filaggrin occur in only 10-50% of patients with atopic dermatitis. In the development of atopic dermatitis, we take into account the polymorphism of the FLG gene and genes related to the immune system and the skin barrier, but it is equally important to investigate the epigenetic regulatory mechanism, which is another key to understanding this disease. Epigenetics is the study of the regulation of gene expression, which does not involve changes in the DNA sequence. These modifications activate or inhibit the transcription of specific genes, causing the new mRNA to be translated into a polypeptide chain. They therefore influence the functioning of cells, their activation and polarization, as well as the ability to produce cytokines. The main epigenetic modifications are DNA and/or histone methylation and acetylation. Changes in the epigenome may be persistent across generations, while environmental changes may impact both the postnatal and prenatal periods.

Differences in the epigenome of patients with atopic dermatitis with skin lesions and healthy people have been confirmed by research. In atopic dermatitis, epigenetic changes concern genes regulating the immune response, genes of innate immunity and genes encoding structural proteins of the epidermis. It can be argued that epigenetic regulation is the link between changes in the environment around us (Western lifestyle, industrialization, air pollution, dietary changes, obesity, increased use of antibiotics and tobacco smoking) and genetic changes.

BARRIER DYSFUNCTION

The impairment of barrier function in atopic dermatitis is multifactorial, as it is caused by genetic factors as well as physical factors such as exposure to lower average temperatures, lower humidity and UV index, and changes induced by scratching. Alteration of the bacterial flora, in particular colonization of Staphylococcus aureus and Malassezia yeasts, may also have functional repercussions on the barrier.

DISREGULATION OF THE IMMUNOLOGICAL RESPONSE

Loss of skin barrier function promotes percutaneous penetration of irritants, pathogens and allergens. Moreover, the weakening of the epithelium caused by scratching stimulates the release of pro-inflammatory cytokines (alarms), which activate epidermal dendritic cells (Langerhans cells) and trigger a second type of inflammatory immune response. Due to increased barrier permeability and weakened tight junctions in the granular layer, dendrites are able to penetrate beyond the barrier to detect and present antigens. Activation of Th2 cells releases IL-4 and IL13, which contribute to the release of specific IgE by B cells.

Th2 cells are involved in the immune response, but they are not the only ones, as mast cells, basophils and eosinophils also produce IL-4, IL-13 and IL-5. IL-4 and IL-13 are involved in the pathophysiology of itch, but also promote the colonization of Staphyloccocus aureus in the skin and contribute to the activation of dendritic cells and the activation and survival of Th2 lymphocytes.

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Barrier dysfunction and impaired antimicrobial immunity lead to increased skin susceptibility to bacterial infections in patients with atopic dermatitis.

MICROBIOME

The skin microbiome refers to all the microorganisms present on the surface of the epidermis. The human microbiota varies quantitatively and qualitatively from person to person. This variability is influenced by a number of factors, such as skin thickness, exposure to ultraviolet rays, temperature, humidity, sebum production, skin pH, and the natural folds and recesses of body cavities, resulting in areas of high humidity, oily areas, and dry areas on the body. . Skin microorganisms form a system of diverse interactions that benefit the host, a phenomenon known as commensalism. They participate in metabolic processes, maintain an appropriate immune response by influencing the innate and adaptive immune system, prevent the development of pathogenic microorganisms and contribute to the proper functioning of the epidermal barrier. Unfavorable conditions for the development of certain microorganisms or their incorrect functioning cause diseases such as atopic dermatitis.

It has been shown that there is a difference in the composition and diversity of microorganisms found on the skin of people suffering from eczema and healthy people. In the case of atopic skin, a reduction in the number of commensal bacteria of the genus Streptococcus, Corynebacterium, Cutibacterium and Proteobacteria and an increase in the total number of bacteria of the Staphylococcus genus (in particular S. aureus) were observed. Changes in the microbiota, both quantitative and qualitative, may occur before the clinical manifestation of the disease. Moreover

o treatment with moisturizers and emollients in patients with atopic eczema can restore the barrier function and normalize the skin microbiota. A reduction in microbiome diversity is correlated with disease severity and promotes the colonization of pathogenic bacteria.

Research on the microbiome and the development of atopic dermatitis focuses mainly on Staphylococcus aureus. This Gram-positive bacterium is found in the upper respiratory tract and on the skin. S. aureus is present on the skin of people with eczema, with a higher incidence of lesions than on healthy skin. It is also the most common pathogen responsible for the clinical symptoms of skin infections. A correlation was established between a higher colonization rate and pathogen density and the severity of skin lesions and disease severity. This may be related to the adaptation of S. aureus to the inflammatory response. Colonization by pathogenic staphylococci is promoted by reduced filaggrin levels and structural collapse of corneocytes, higher than normal skin pH, and decreased production of antimicrobial peptides.

In patients with atopic dermatitis, barrier dysfunction and impaired antimicrobial immunity lead to increased skin susceptibility to bacterial infections. Staphylococcus aureus colonizes the skin of AD patients in 60-100% of cases, compared with 5-30% in healthy controls.

ITCHING AND THE NEUROIMMUNE SYSTEM

Pruritus has been defined as "an unpleasant feeling that causes the urge to scratch." Itching is one of the main diagnostic criteria for atopic dermatitis. It can significantly impact patients' quality of life, so much so that when not treated appropriately, it can limit daily activities, reduce productivity and disrupt sleep. Interference between keratinocytes, the immune system and non-histaminergic sensory nerves is believed to be responsible for itch. Additionally, emotional stress, lack of sleep, and alcohol consumption may worsen pruritus in patients.

Itch pathways are complex, not fully established, and may overlap with pain pathways. Specific itch receptors (pruriceptors) are located mainly in the epidermis and at the dermal-epidermal junction.

Itch is expressed and transmitted to the brain through specific pathways, including:

TWO BASIC POPULATIONS OF C FIBERS (C fibers insensitive to mechanical stimuli and C fibers sensitive to mechanical stimuli)
FINE MYELINIZED Aδ FIBERS
Sensory neurons whose cell bodies are located in the spinal ganglion transmit primary afferents to the skin and send projections to the dorsal horn of the spinal cord, where they form connections or synapses with the second and third neurons, forming part of the spinothalamic pathway, which then ascends to the thalamus and travels to the somatosensory cortex and anterior cingulate cortex. The second and third neurons have excitatory and inhibitory functions.

Pruriceptors are divided into histaminergic and non-histaminergic receptors, depending on their reactivity to histamine. Activation of nonhistaminergic pruritus receptors seems to be important in the pathogenesis of atopic pruritus. These receptors are activated by substances such as substances released during mast cell degranulation, proteins synthesized in keratinocytes, exogenous chemicals, cytokines and pathogen molecules. Common immunodeficiencies associated with the pathogenesis of AD are also implicated in atopic pruritus. Th2 cells, eosinophils, neutrophils and mast cells release pro-inflammatory cytokines and peptides that activate pruriceptor pathways.

One of the best-known mediators of itch is IL31, produced by Th2 cells. Studies have shown increased levels of IL-31 in the skin of patients with atopic dermatitis. IL-31 also stimulates the elongation and branching of nerve fibers, which may increase the feeling of itching.

Other cytokines, particularly IL-4 and IL-13, may be responsible for pruritus. Furthermore, IL-4 may trigger a potential increase in itch by sensitizing neurons to other stimuli. Keratinocytes can release certain factors that also cause itching. For example, scratching the skin damages epithelial keratinocytes, leading to the release of inflammatory cytokines, direct and indirect activation of the Th2 axis, and the production of itch-promoting cytokines by both keratinocytes and immune cells. The feedback loops in atopic dermatitis are known as “recurrent itch-scratch-itch.” The role of histamine in AD-related pruritus is unclear. Patients generally respond poorly to non-addictive antihistamines used to relieve pruritus, suggesting the involvement of a non-histaminergic mechanism.

It has also been observed that patients with atopic dermatitis have an increased sensitivity to itching caused by insensible stimuli in healthy people. This phenomenon, called neuronal sensitization, results from increased sensitivity to stimuli. Itching may persist after the initial trigger.

Treatment
Conventional treatments for atopic dermatitis may include both no

major treatments such as oil baths and emollients, as well as the use of topical treatments (dermocorticoids, topical calcineurin inhibitors), as well as systemic treatments (such as steroids, cyclosporine, methotrexate, azathioprine, dupilumab). New conventional treatments are based on the action of specific molecules involved in the pathophysiology of eczema.

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Atopic dermatitis presents a wide range of clinical manifestations.

EMOLIENTS

Regular daily use of moisturizing creams and emollients is an essential complement to the treatment of atopic dermatitis. Third-generation emollients containing physiological lipids (ceramides, cholesterol and polyunsaturated fatty acids) should be chosen. These emollients stimulate epidermal differentiation and correct the defect of lipid cement between corneocytes. The choice of cleanser is also important to maintain the skin barrier. Its pH should be ideally acidic, because a low pH in the stratum corneum will reduce the activity of proteases involved in corneocyte exfoliation, increase the activity of ceramidases, accelerate the maturation of the lamellar lipid layers of the stratum corneum, and neutralize bacterial proliferation. In addition to using appropriate topical products, it is also recommended that especially young children be given several quick baths in lukewarm water each day, and that the body should be dried by simply wiping the wet skin without rubbing.

TOPIC IMMUNOSUPPRESSIVE AGENTS

in conventional treatment, they are recommended as first-line treatment.

Dermocorticoids have anti-inflammatory, antiproliferative, immunosuppressive and vasoconstrictor effects. Topical calcineurin inhibitors: their therapeutic effect is due to their ability to inhibit calcium-dependent calcineurin phosphatase, an enzyme particularly expressed in T cells and responsible for the synthesis of pro-inflammatory mediators such as inflammatory cytokines, thereby inducing a significant reduction in the inflammatory response.

Crisaborole is a phosphodiesterase type 4 (PDE4) inhibitor and an antagonist of two interleukins (IL-12 and IL-23) and a TNF-alpha inhibitor. Although the mechanism of its therapeutic action is not yet clearly established, its action on the inflammatory network that triggers atopic dermatitis is known.

Janus kinase (JAK) inhibitors are a class of drugs that block the activity of one or more members of a family of enzymes known as Janus kinases ("just another kinase") and are non-receptor tyrosine kinases that activate signals transmitted by inflammatory pro-cytokines (TNF-α , IL-1, IL-6 and IFN-γ).

PHOTOTHERAPY

In summer, improvement is observed in many patients suffering from atopic dermatitis. Phototherapy, i.e. treatment with UV rays, is often used for therapeutic purposes, especially in adults, and less often in children.

GENERAL TREATMENT

Oral systemic corticosteroids
Cyclosporine
Azathioprine
Mycophenolate mofetil
Methotrexate
Dupilumab,
a fully human monoclonal antibody that targets and inhibits the alpha chain common to IL-4 and IL-13 receptors. Scientific research focuses on new and increasingly innovative therapeutic strategies, including those targeting the polarized immune pathways occurring in AD.

HOMEOPATHIC TREATMENT

In the treatment of atopic dermatitis and other dermatological diseases, the most important thing is to examine the appearance of skin lesions and their topography. In atopic dermatitis, as in all forms of eczema, skin symptoms occur in different phases. Some medications are more common in patients with atopic dermatitis.

erythematous changes:

APIS MELLFICA

inflammatory swelling with intense itching, which disappears with cold

BELLADONNA

intense erythematous scar rash

MAGNAMM ACETICUM

small erythematous moles with pain and intense itching

RHUS TOXICODENDRUM

"leopard skin" appearance, itching does not go away after scratching, but goes away after applying warm water

SULFUR

light red, hot, foul-smelling rash that worsens with heat, washing and contact with wool

SULFUR IODATUM

dark red erythema, intense itching worsened by heat

URTICA URENS

pinkish swelling on pale pink skin, intense itching that is worsened by cold and relieved by rubbing

VESCULAR PATHOLOGICAL CHANGES

ANACARDIUM ORIENTALIS

vesicles containing lemon or purulent fluid, intense itching worsened by heat

CATHARSIS

Cantharis: blisters on healthy skin

CROTON TIGLIUM

liquid or purulent vesicles, intense and painful itching that worsens when scratched

RHUS TOXICODENDRON

transparent vesicles containing lemon fluid on an erythematous base, painful and itchy

PURULUS LESIONS

ANTIMONIUM CRUDUM

involvement of the face, mouth area and scalp, characteristic progression from a vesicle to a pustule, then to a scab, and finally to a ruptured lesion

GRAPHITES

Involvement of the flexion folds

h, fire feathers that transform into yellowish scabs, itching disappears with cold

PETROLEUM

dry skin, appearing dirty, thickened and cracked with serous exudate, irritating and foul-smelling, frequent superinfections, worsening in winter

PSORINUM

unhealthy-looking skin, foul-smelling eruptions, violent itching and frequent superinfections, worsened by the heat of the bed

SULFUR

oozing, foul-smelling erythema, burning itch worsened by heat, washing, contact with wool, tendency to infection

TUBERCULINUM

Eczema of the skin folds, especially in the retroauricular groove

PURULUS LESIONS AND INFECTIONS

CALCAREA SULFURICA

suppuration, thick, lumpy yellow pus

HEPAR SULFUR

yellow, very foul-smelling pus and swelling of the skin, worse with cold, stinging pain

MEZEREUM

scabs hiding the thick pus that flows from the ulcer

VIOLA TRICOLOR

oozing lesions on the scalp, thick exudate sticking the hair into strands

Psoriatic lesions

ARSENICUM ALBUM

Arsenicum album: atonic, thickened and dry skin, violent desquamation, burning itch, even if improved by heat, worsened by cold

ARSENICUM IODATUM

Peeling in the form of small scales, on the order of a millimeter on the skin with a striated appearance, signs of lichenization due to scratching, itching disappears at low temperatures

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Symptoms express a chorus of voices that together express a person's existence.

BERBERIS VULGARIS

dry and moving nodular lesions with a tendency to scar the central area, itching

HYDROCOTYLE ASIATICA

numerous large scales on dry scleroderma-like skin, lichenification due to scratching, variable itching

KALIUM ARSENIICOSUM

dry rash, cracks, especially in the folds of the elbows and knees, burning itching, worsened by heat

NATRUM SULFURICUM

large, thin, yellowish scales, skin is red and looks wet (false moisture), worsened by moisture and washing

CRACKING SKIN

ALUMINUM

very thin, dry skin, wrinkled, rough and parchment-like, itchy and improved with cold water

ANTIMONIUM CRUDUM

Hyperkeratosis of the hands and feet

ARSENICUM IODATUM

lichenization, dry scales

GRAPHITES

Cracks in skin folds, honey-like exudate

KALIUM ARSENICOSUM

cracks in the folds of elbows and knees, burning itch

NITRICUM ACIDUM

sharp edges of cracks in the mucocutaneous junction that are intensified by heat, adherent skin with a characteristic golden yellow color, bleeding easily on contact, very painful lesions that disappear with heat

PETROLEUM

dry, dirty-looking, cracked skin with a noticeable, itchy, foul-smelling discharge

TUBERCULINUM

cracking eruptions of skin folds, especially in the fold behind the ears, with obvious exudate

ANTIITRIC DRUGS

CHAMOMILLA VULGARIS

behavioral disturbances with agitation and anger, improving with passive movement, worsening in the context of teething episodes

CISTUS CANADENSIS

red, oozing, crusty lesions, located on the cheeks and wrists, worsening with cold, tingling sensation

DOLICHOS PRURIENS

intense itching, with or without lesions, worsening at night due to the warmth of the bed

MANGANUM ACETICUM

itching of joint folds

RADIUM BROMATUM

itching and burning on thickened skin

STAPHYSAGRIA

irregular itching, increased sensitivity, sensitivity to adversity

cradle cap

CALCAREA CARBONICA OTRARUM

dry and thick cradle cap, keratinizing, very sticky, wide fontanel, intense sweating of the neck

VIOLA TRICOLOR

oozing cradle cap, hair sticking to the scalp, itching is burning and worsens at night

ANTIMONIUM CRUDUM

cradle cap with pustular and oozing eruptions, yellowish exudate

ETIOLOGICAL DRUGS

STAPHYLOCOCCINUM

Staph infections

CANDIDA ALBICANS

Candida albicans infections

STREPTOCOCCINUM

streptococcal infections

SILICEA

tendency to suppuration and poor tolerance to vaccines

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Lycopodium clavatum is a symptomatic treatment for eczema, intense itching with itchy lesions leading to bleeding, and is also a primary treatment for seborrheic dermatitis

In the neonatal and infant phase, the examination of characteristic clinical symptoms depending on the age of onset allows us to emphasize the importance of drugs indicated in the treatment of cradle cap (Viola tricolor, Graphites, Antimonium crudum and Calcarea carbonica). Also in this phase, facial dermatitis with involvement of the mouth area corresponds to Antimonium crudum, while the expression of changes at the level of the protrusions of the limbs brings to mind Rhus toxicodendron, Lycopodium, Arsenicum album and Manganum aceticum.

In the second year, when xerosis and its accompanying erythema become more severe, other drugs will be used, such as Sulfur, Sulfur iodatum, Belladonna, Rhus toxicodendron associated with Arsenicum iodatum and Berberis vulgaris. Medications will play an important role in the lichenization phase in adolescents and adults

such as Lycopodium or Tuberculinum.

To complete our homeopathic offer, it is necessary to systematically search for sensitive and chronic type drugs. Only by prescribing complete treatment will it be possible to control relapses and stabilize the patient's general condition.

THE MOST COMMON SENSITIVE TYPES ARE

ARSENICUM ALBUM

in all acne that improves with heat

CALCAREA CARBONICA

the main drug for atopic dermatitis in children, especially in the case of cradle cap

LYCOPODIUM CLAVATUM

intense scratching of the lesions leading to bleeding, improved by cold

NATRUM MURIATICUM

coexistence of areas of dry and oily skin with recurrent herpes outbreaks aggravated by sun exposure, locations on the periphery of the scalp, eyelids, folds and fingers

PSORINUM

eczema on the skin giving off an unpleasant odor, which is made worse by heat and washing

SILICEA

exudative eczema of the furrows and mouth area, which easily turns into superinfection, worsens after vaccinations

SULFUR

all forms of pruritic erythematous eczema worsened by heat

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The choice of a homeopathic approach must be based primarily on the choice of a complete treatment, in which the manifestation of the disease is not perceived as a set of symptoms to be treated, but is recognized as a whole.

SULFUR IODATUM

Eczema with a red and intense color, irritating exudate that disappears after cooling, tendency to superinfection

THE MOST COMMONLY USED CHRONIC REACTION DRUGS ARE:

METHOD OF PSORIC REACTION

ARSENICUM ALBUM

dry and flaky skin, whitish scales, especially in people sensitive to cold

LYCOPODIUM CLAVATUM

Symptomatic treatment for eczema, intense itching with itchy lesions that bleed, main treatment for seborrheic dermatitis

PSORINUM

The person is thin and sensitive to cold, the skin has an unhealthy appearance, itching is aggravated by heat and worsens in winter

SULFUR

For use in dermatological diseases, recommended for people with dry and irritated skin, does not tolerate water, which intensifies itching, redness of the skin openings, profuse sweating, does not tolerate hot weather.

SEPIA OFFICINALIS

A drug with a psoric and sycotic reaction; indicated for atopic dermatitis in children with easily bleeding and cracking lesions

CALCAREA CARBONICA

A very good drug for atopic dermatitis in children with a number of fissure dermatitis and cradle cap, excessive sweating of the head, with a still open fontanelle

METHOD OF PSOR-TUBERCULIN REACTION

NATRUM MURIATICUM

to be considered in cases of skin fold eczema in children and seborrheic dermatosis, especially when the edges of the scalp are affected. Important feature: alternating dry skin on the body and seborrheic skin on the face.

SULFUR IODATUM

Patient similar to patient Sulfur, but agitated and with greater adenopathy

SILICEA

A drug with a tendency to cause tuberculin and sycotic reactions, characteristic elements: profuse sweating of the feet, strong odor, tendency to secondary infections and parasites

TUBERCULINUM

profuse sweating despite the cool temperature, characteristic feature: intertriginous eczema of the retroauricular area

METHOD OF SYCOTIC REACTION

MEDORRHINUM

an important medicine, especially in the case of diaper rash (urogenital system); stimulation

THUYA OCCIDENTALIS

medicine for oily skin with itchy papules and pustules

CALCEARA CARBONICA

very interesting in atopic dermatitis in children with fissure dermatitis and cradle cap, in case of sweating of the head, still open fontanel, child with a calm temperament

SEPIA OFFICINALIS

inflammation and lesions of the mucous membranes of the urogenital system, persistent dermatoses

SILICEA

a drug for chronic suppuration and poor tolerance to vaccinations

LUETICAL WAY OF REACTING

LUESINUM

indicated for all ulcers with indurated edges, dry, cracked dermatoses and those associated with ichthyosis

MERCURIUS SOLUBILIS

mercury stomatitis, exacerbation at night, ulcerative lesions of both skin and mucous membranes