Eczema

What is Atopic Dermatitis/Eczema?

Atopic dermatitis or more commonly known as eczema is a longstanding recurring pruritic (itchy) skin condition which usually starts at a young age (some patients start in adulthood).

Eczema is characterized by xerosis (dry skin), lichenification (thickened skin with skin markings), excoriations and eczematous dermatitis skin changes. It can be complicated with herpes co-infection resulting in a condition called eczema herpeticum which will be described below. 

Eczema is associated with other atopic diseases (immunoglobulin E mediated) like asthma, Urticaria, allergic rhinitis and acute allergy to food. These conditions often run in the family.

The prevalence of eczema in developing is about 2-3% whereas in developed countries it is higher about 15-30%. Majority of eczema cases occur before the age of 5 with about 85% in the first year of life. 

What causes eczema?

Currently there is no definite theory to explain the cause of atopic dermatitis/eczema. There are current 2 hypotheses for the development of eczema as a result of the inflammatory process. The 2 theories are:

1.Primary immune dysfunction resulting in IgE sensitization:

• Usually there will be a balance of the subsets of T cells i.e. Th1, Th2 and Th17. However in patients prone to eczema there will be primary immune dysfunction with an imbalance in the T cells subsets which result in more interleukins which in turn results in immunoglobulin G.
  

2.Epidermal Barrier dysfunction

• It is hypothesized the patients with eczema has defects in the skin barriers which allows antigens to enter and trigger the stimulation of inflammatory cytokines.
  
• Inherited abnormality in the filaggrin expression will result in the skin barrier dysfunction resulting in more allergens to enter and inflammation process. Filaggrin is important to maintain the epithelial integrity. This may explain why atopic dermatitis may be inherited and run in families.
  

Clinical presentation of eczema

Eczema is a skin condition characterized by periods of flares and periods of remission. The rash is often very itchy resulting in recurrent scratching forming the itch-scratch cycle. Excoriations, lichenification (thickening and darkening of skin) and secondary bacterial infection may result from chronic scratching.

The skin is often dry (xerosis) and the rash is red, eczematous (inflamed, weepy blistered skin) and crusts may form on skin surface.  The distribution of the rash depends on the age of the patient.

During infancy under 1 year old, the rash often is generalized with sparing of nappy area as the skin there is moist. The skin in general is dry, red, scaly, inflamed and crusted patches and plaques can be seen first starting from antecubital (anterior part of elbow) and popliteal fossae (posterior part of knee) to face, scalp, extensors of limbs and then to whole body. Lichenification is not common.

In childhood, the skin is generally dry (xerosis), scaly, rough and lichenification of skin (thickened skin) due to constant rubbing and scratching can be seen. The younger kids will have rash over at the extensor surfaces of joints like knees, ankles, elbows and wrists. Genitalia may also be involved.

As the child grows older, the skin rash distribution changes to the flexor surfaces of joints (elbow and knee creases) and buttock and thigh creases. The rash seen during childhood is red, inflamed, exudative with crusts and excoriated.

In adults, the rash can be localized to hands, eyelids, flexures or it can be diffuse throughout the body. The skin is much drier and lichenified compared to childhood eczema. Recurrent secondary skin infection may also be present. Some eczema patients may have characteristic brown macular ring around their necks due to deposition of amyloid. 

Diagnostic Tests for Eczema

Diagnosis is made by clinical history and presentation. There no specific chemical marker to be tested to diagnose eczema. Investigations are usually done to exclude other conditions.

Allergy and radioallergosorbent testing (RAST) is of little clinical value. These tests are done to observe IgE mediated reactions. They have good negative predictive value but even if positive it is not confirmative, other challenge test is necessary. Skin patch test is only useful in identifying allergen in allergic contact dermatitis.

Skin culture can be sent to rule out skin infections caused by bacteria, virus or fungal. Blood tests result like raised eosinophil levels are seen in patients with eczema but not definitive. The total serum Immunoglobulin E is raised in patients with atopic dermatitis but not definitive also.

Skin biopsy will only show histological findings of acute, sub-acute or chronic dermatitis and no other definitive findings.

Treatment of Atopic Dermatitis

Patients must understand that atopic dermatitis/ eczema is a chronic long standing condition which will have periods of relapses and remissions. There is no specific food restriction diet that will improve eczema.

General management is to avoid triggering factors that precipitate eczema such as temperature changes, rough tight clothing and sweat. As the skin is generally dry in eczema patients, moisturizing the skin is important to restore the skin composition. Shower with gentle cleansers are also recommended.

Topical steroids are the mainstay treatment. Low potency steroids like hydrocortisone can be used for face, neck, groin and flexures area where the skin is thinner. For moderate lesions, mild to moderate strength steroids (e.g. betamethasone 0.025%, fluocinolone 0.0625%) can be used. For severe lichenified areas, moderate to potent steroids (e.g. betamethasone 0.05%-0.1%, clobetasol, fluocinolone 0.0125- 0.025 %) can be used.

Topical Immunomodulators like pimecrolimus and tacrolimus can be used if topical steroids are contraindicated or if steroid therapy has failed. There   slight burning sensation post application.

Oral antihistamines can help control the itch. Sedative antihistamine can be used if sleep is disturbed because of the itch.

Antibiotics and Antivirals can be given if suspected to have secondary bacterial infection or secondary herpes infection (eczema herpeticum).

Oral probiotics like lactobacillus may induce the Th1series instead of the Th2 immune series and hence inhibit the production of IgE antibodies.

Phototherapy like UV-A and narrowband UV-B bands are used as second line of therapy for moderate to severe eczema patients. However long term side effect is the increased risk of skin cancer especially in the fair-skinned people.

Immunosuppressive drugs like cyclosporine and azathioprine are used as third line of therapy for those with severe recalcitrant cases. Oral cyclosporine is effective treatment but it has adverse effects on the liver and kidneys hence only used for short term. Oral azathioprine is also effective but has liver and hematological side effects which make it unsuitable for long term treatment. Blood tests must be done regularly for monitor and stopped if adverse organ effects take place.

Oral steroids can also be used but it has adverse side effects like increased risk of diabetes, hypertension, glaucoma, skin striae, moon-like facies, osteoporosis and immunosuppression. 

Discoid Eczema

Discoid eczema is also known as nummular eczema is a form of eczema. In discoid eczema the lesions are round shaped which resembles coins hence the name nummular/discoid eczema. The prevalence is about 2 in 1000 people. It is common among the 20-30 years old or the 60-70 years old. It is also commoner in females. It is uncommon in children. The cause of it is similar to that of eczema.

The lesions are commonly found symmetrically on the arms and legs. It does not affect the face or scalp area. The rash is often very itchy. The lesions may start of as red to purple papules/vesicles which then will coalesce into plaques. Secondary bacterial infections with staphylococci may occur and result in crusting.  Post-inflammation brown hyperpigmentation may remain after the inflammation settles.

The diagnosis is often by clinical history and clinical features. Skin swab culture can be done to rule out bacterial or fungal infection of the skin. Treatment is same as that of eczema. 

Eczema Herpeticum

Eczema Herpeticum is a complication of patients who has an eczema flare and co-existing herpes simplex virus. It was previously known as Kaposi varicelliform eruption as it resembles chickenpox. It is more common in infants and young children with underlying eczema condition.

Certain conditions that cause breakdown of skin barrier can also precipitate eczema Herpeticum. The conditions include ichthyosis, cutaneous T cell lymphoma, mycosis fungoides, darier disease, thermal burn injuries, pemphigus vulgaris and viruses like coxsackievirus A16.

Clinical presentation: Patient will be unwell, having fever and sudden onset of clusters of itchy painful blisters. New lesions will occur and spread over a period of 7-10 days. The blisters may be filled with yellow purulent fluid or blood. The blisters may form crusts, erosions and ulcers. It will take about 2-6 weeks for the lesion to totally heal.

Secondary bacterial infection with streptococcus and staphylococcus will lead to impetigo and cellulitis described above. Post infection, lesions may heal with remnant scars. Very severe infection that has spread throughout the body (disseminated infection) in the immune compromised patients can be very serious.

Diagnosis: can be confirmed by a viral swab from a blister/vesicle that is sent for tests like Direct Fluorescent Antibody (DFA) stain, PCR (Polymerase Chain Reaction) sequencing and Tzank smear (reveal epithelial multinucleated giant cells and acantholysis) to identify the HSV virus.

Bacterial swabs can be taken for bacterial culture to identify any pathogen that could have caused secondary bacterial infections. If diagnosis is in doubt, biopsy of the lesion and histological examination will confirm the diagnosis.

Treatment of eczema Herpeticum: Eczema Herpeticum is a dermatology emergency, early administering anti-viral medication may reduce the need for hospitalization, complications and reduce morbidity.

Antiviral drugs: For adults, Oral aciclovir 400 to 800 mg 5 times daily or valaciclovir 1 g twice daily for 10 to 14 days can be given until lesions heal. In children, suspension form of antiviral medications with dosage according to the child's age can be given. Intravenous aciclovir is necessary in severe infection or infection that does not respond to oral tablets.

Antibiotics like penicillin, cephalosporin and erythromycin are prescribed if there is secondary skin bacterial infection.

Ophthalmologist consult is warranted if there is eye involvement as keratitis may cause scarring and other eye complications include optic neuritis which may affect vision. 

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