Atopic dermatitis, more commonly known as eczema, is a chronic, dry skin condition seen in infants, children, and adults.  In a typical pediatric scenario, parents schedule a doctor visit because their child has an irritated, itchy rash that fails to improve despite at-home treatment measures.  Upon examination, the child’s skin has a rough, sandpaper-like texture, and there are areas of redness with evidence of scratching.  Throughout the visit, the child repeatedly scratches the skin, sometimes to the point of bleeding.  This cycle of itching, scratching, and worsening irritation is what classifies atopic dermatitis as one of the most frustrating skin conditions, both for children and their parents.

There are some aspects of atopic dermatitis that mimic other skin problems.  Contact dermatitis may have a similar dry, irritated appearance.  It differs, however, because it can be attributed to a specific cause.  For example, a rash that develops after wearing a piece of jewelry is due to skin contact with the metal.  Infantile seborrhea is often confused with atopic dermatitis, particularly when it affects the forehead.  This type of rash may be seen as young as two weeks old, and it most commonly affects the scalp, forehead, and diaper area.  Itching is less common, and the skin has an oily rather than a dry appearance.

Cases of atopic dermatitis continue to increase among those in developed nations.  The incidence in infants and children is approximately 20 percent.  Genetics plays a role, and a family history of eczema, allergies, or asthma is common.  Most childhood develop symptoms prior to the age of five, with initial signs detected as young as three months old.  Whether or not symptoms persist or resolve can vary.  Some infants “outgrow” their eczema by age two, while others experience flares until the teen years.  In 70 to 90 percent of cases, however, atopic dermatitis resolves before adulthood.

Atopic dermatitis is influenced by both genetic and epigenetic factors. The primary reason it occurs is because of an ineffective skin barrier mechanism.  The skin consists of three layers: the outer epidermis with keratin and pigment, a middle dermis with oil and sweat glands, and an inner subcutaneous fat layer.  A fully functioning epidermis acts a waterproof barrier that retains skin moisture, and repels the sun’s UV-B radiation.  A protein called filaggrin is one of the “building blocks” of keratin which provides strength and integrity to the epidermis.  If a genetic mutation occurs, a defective version of filaggrin forms.  This results in skin that easily loses moisture, and that is prone to irritation.  10 percent of the northern European population and up to six percent of Asians have this mutation.  A few variants of mutated filaggrin have been noted among African Americans, but the overall prevalence is unknown.  Additional mutations of skin structural components have been observed which can increase the severity of this disease.

Over the past few decades, a “hygiene hypothesis” has been proposed to explain why atopic dermatitis occurs.  It is common for infants and toddlers to repeatedly put their fingers into their mouths.  The gut microbiome develops as they touch objects, and then ingest whatever microbes are present.  This stimulates the growth of bacterial flora within the gastrointestinal tract, and potentially protects against future atopy.  Maintaining a living environment that is “too clean” can prevent this from occurring.

Atopic skin has a different balance of normal flora than healthy skin.  Millions of bacteria, fungi, and viruses live on the skin and play an important role in its immune functions.  If exposed to a pathogen, normal skin flora protects against the development of an infection.  This becomes more difficult in the presence of atopic dermatitis.  Because the mutated filaggrin protein creates an abnormal epidermis, it is easier for harmful organisms attach to the skin.  These pathogens then multiply, and may colonize the skin surface.  As a result, the skin microbiome becomes overwhelmed, and cannot suppress infections.  Staphylococcus aureus, for example, commonly infects eczematous skin.

Flares of atopic dermatitis tend to occur during the colder months of the year.   The skin becomes dry due to in-home heat and cold outdoor air.  This is the case for the majority of infants and children with eczema.  A smaller percentage, however, experience worsening of their symptoms in warm, humid environments.

Certain skin exposures can contribute to atopic dermatitis.  Harsh soaps and detergents often irritate the skin, and impair its protective function.  Recent studies have indicated a link between tobacco smoke exposure and eczema.  Increased white blood cells, fibrinogen, and other inflammatory mediators at the subcutaneous level are felt to increase the skin’s permeability, therefore limiting its barrier function.

The classic signs and symptoms of atopic dermatitis are skin dryness with itching, redness, and irritation of the affected areas.  Recent studies indicate that pain is also a common symptom due to the severity of skin irritation.  Persistent scratching worsens the condition of the skin, and is associated with poor sleep quality in children.  Areas with repeated flares may develop a scaly appearance as well as pigmentary changes.  Different areas of the body are affected depending on the age of the child.  The face, trunk, and extensor surfaces of the arms and legs are common locations for infants with atopic dermatitis.  They often “squirm” or rub against surfaces to scratch and relieve the itching.  In contrast, children and teens acquire lesions in the folds of the elbows, behind the knees, and in the creases of the wrists and ankles.  Facial eczema may persist in older children, particularly on the lower eyelids.  Skin areas that are free of atopic lesions typically remain dry and prone to pruritus.

Dyshydrotic eczema differs from classic atopic dermatitis.  This type specifically affects areas of excessive sweating such as the hands and feet.  Despite the increased moisture, the palms and soles become dry and itchy.  The skin in these areas may blister and peel, exposing a raw and irritated inner skin layer.

This concept refers to the progression of allergy-related symptoms that begin during infancy, and progress throughout the childhood years.  The “march” begins with atopic dermatitis, and is followed by the development of asthma and allergic rhinitis.  For example, a four month old with eczema may experience an allergic reaction when a new food is introduced months later.  By the age of two, he or she may develop sneezing and watery eyes during the spring or summer.  Although no direct causal relationship has been identified between eczema and allergies, some studies suggest that inadvertent skin exposure may be a trigger because of permeability of the epidermis.

The link between atopic dermatitis and asthma is felt to be the result of different genetic mutation than the filaggrin one.  60% of children with severe atopic dermatitis later develop asthma.  Hereditary and environmental factors contribute to atopy, but it is also triggered by immune responses.  The antibody IgE is a key mediator of allergic reactions.  This antibody differs from those that fight infections.  In addition to IgE activity, cytokines released by specific components of the blood called T Helper cells promote itching and inflammation.

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