Eczema
Pathology and epidemiology
The main pathology for Eczema is the epidermal alterations such as spongiosis or epidermal edema that present as epidermal vesicles. This epidermal change is usually accompanied by perivascular lymphohistiocytic infiltrate in the dermis, edema of dermal papillae, mast cell degranulation, acanthosis, and hyperkeratosis. The acute phase is dominated by spongiosis which is the intercellular epidermal fluid that stretches the intercellular bridges between the keratinocytes that eventually break and result in the development of vesicles (Weston & Howe, 2021).
Eczema is predominantly a disease of childhood. Worldwide it affects 15-30% of children. The prevalence of Eczema in the United States is 0.9% in adults and 10-12% in children. Approximately 95% of cases occur before the age of 5, and the disease usually starts to manifest within the first ear of life, as early as two months of age. Females have a greater risk of having Eczema than males. (Kim, 2021).
Diagnosis
Eczema is diagnosed when symptoms and signs elicited from the history and physical exam, respectively, meet specific clinical criteria. (Kapuraret. al., 2021). The American Academy of Dermatology Criteria will confirm the diagnosis of atopic dermatitis if a patient has 3 essential features (Pruritis, Eczema with specific morphology and distribution of skin lesions that are age-specific, and a chronic history), Important features (Early age of onset, family history of atopy or Eczema, xerosis and IgE reactivity) and Associated features such as periocular or periauricular skin lesions (Weston & Howe, 2021)
Laboratory tests are rarely necessary as there is no biomarker for Eczema, nor is there use for radiological investigation. However, various tests can be done to support the diagnosis or rule out other skin conditions. Some laboratory tests are; Serum IgE levels, potassium hydroxide preparation, patch testing, and genetic testing (Weston & Howe, 2021). A swab of infected skin for bacterial culture and sensitivity may be necessary in cases of superimposed infection on the skin vesicles. It may be necessary to do a complete blood count for thrombocytopenia to rule out the immune deficiency.
Skin biopsy can also be done, although pathology findings are not specific. A skin biopsy will help in differentiating acute, subacute, and chronic spongiosis and ruling out other conditions (Kim, 2021).
Clinical presentation and differential diagnosis
The most significant clinical feature of atopic dermatitis is severe pruritis and dry skin. The clinical presentation depends on the disease activity, age of presentation, and ethnicity (Weston & Howe, 2021). Pruritis and spongiotic dermatitis involve the trunk, face, and extensor extremities in children younger than 2 years, flexor surfaces such wrists or ankles in children over 2 years till puberty, and hands in adults (Siegfried et al., 2015).
Similar diseases that might get confused with Eczema and how to differentiate them are; seborrheic dermatitis, which lacks absence of family history with greasy, scaly lesions; psoriasis is characterized by patched lesions localized on extensor surfaces in all age groups and pitted nails; Contact dermatitis is characterized by a positive exposure history and family history is absent; Scabies is characterized by finger web involvement and positive skin scarping for infection and immunodeficiency diseases are characterized by a history of recurrent infection in addition to the skin lesions (Siegfried et al., 2015).
Genetics of Eczema
There is a genetic component to atopic Eczema in addition to the influence of environment and immune factors. Genetic risk factor for atopic dermatitis is mutations of the filaggrin (FLG) chromosome 1q21.3. The mutation results in a defective epidermal barrier due to the loss of function of the filaggrin protein. The heritability of atopic dermatitis is estimated at 75% in various twin studies (Loset et al., 2019).
Treatment
Treatment goals for atopic dermatitis are repairing the damaged skin, limiting itching, treating superinfection, and decreasing inflammation when necessary (Kapur et al., 2018). Treatment involves the use of antihistamines for inflammation, antidepressants to induce sleep and reduce pruritis, antibiotics to treat secondary infections, and systemic corticosteroids for severe cases. Some of the natural therapies for the treatment of mild to moderate atopic dermatitis include; bathing with warm water for 5-10 minutes every day, limiting the use of soap for genitalia and axilla, applying cream moisturizer immediately after bathing to retain moisture, using occlusion to retain moisture such as the use of plastic wraps and gloves, soaking in colloidal oatmeal and cutting fingernails short to avoid injury to the skin (Kapur et al., 2018).
Prognosis is good after treatment, with patients reporting improved skin conditions. Poor treatment outcomes or poor prognosis were associated with a family history of the condition, female gender, coexisting allergic rhinitis and asthma, and early infantile presentation of the disease (Kim, 2021).
References
Kim, S. B. (2021). Atopic dermatitis. Medscape. Retrieved December 02, 2021, from https://emedicine.medscape.com/article/1049085-overview#a2
Weston, W. L., & Howe, W. (2021). Uptodate. Retrieved December 02, 2021, from https://www.uptodate.com/contents/atopic-dermatitis-eczema-pathogenesis-clinical-manifestations-and-diagnosis?topicRef=1727&source=see_link#H1974708121
Loset, M., Brown, S. J., Saunes, M., & Hveem, K. (2019). Genetics of atopic dermatitis: From DNA sequence to clinical relevance. Karger, 235(5), 355-364.https://doi.org/10.1159/000500402
Kapur, S., Watson, W., & Carr, S. (2018). Atopic dermatitis. Allergy, Asthma and Clinical Immunology, 14(Suppl 2), 52. https://doi.org/10.1186/s13223-018-0281-6
Siegfried, E. C., & Hebert, A. A. (2015). Diagnosis of atopic dermatitis: Mimics, overlaps, and complications. Journal of Clinical Medicine, 4(5), 884-917. https://doi.org/10.3390/jcm4050884
