Atopic Dermatitis
Contributed by: Omar F. Merchant, Baylor College of Medicine, 1 Baylor Plaza, Houston, Tx 77030
Merchant OF “Atopic Dermatitis” in Pathway Medicine: An Introduction to Clinical Medicine", PathwayMedicine.org (2015).
| Overview |
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- Atopic Dermatitis is a chronic pruritic condition of the skin, with typical onset in childhood, characterized by the clinical appearance of eczematous lesions and histopathology showing spongiosis, or edema between keratinocytes. Patients often display a personal or family history of other atopic disorders such as asthma and allergic rhinitis.
| Pathogenesis |
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- Overview
- The pathogenesis of atopic dermatitis is unclear but appears to involve contributions from genetics, skin barrier dysfunction, immune dysregulation, microbes, and neurological pathways.
- Genetics
- Genetics clearly plays a role in atopic dermatitis with nearly a 70% concordance in monozygotic twins. As discussed, patients often have a family history of atopic diseases which includes atopic dermatitis, asthma, and allergic rhinitis
- Skin Barrier Dysfunction
- The skin of those with atopic dermatitis is often dry and appears to result from an altered skin barrier that is more prone to moisture-loss and penetration of environmental irritants, yielding inflammation. As a result, liberal application of emollients with moisturizers such as petrolatum is a key aspect of atopic dermatitis management.
- Immune Dysregulation
- The immune response of those with atopic dermatitis appears to dysregulated with a predilection to the Th2 over the Th1 system of T-cells. Additionally, keratinocytes appear to produce fewer antimicrobial peptides. Whatever the underlying defect, patients with atopic dermatitis display inflamed skin which is typically treated with topical corticosteroids.
- Microbes
- The overlying microbiome clearly plays an important role in skin homeostasis and flares of atopic dermatitis are often triggered by the presence of Staphylococcus aureus. Often patients are treated with oral antimicrobials to reduce S. aureus colonization.
- Neurological Pathways
- Increasing evidence has shown that pruritic neurological pathways in those with atopic dermatitis become trained to have a lower threshold for activation. Treatment of pruritus is a key aspect of disease as scratching leads to further inflammation and skin barrier dysfunction. Hence the “itch-scratch-itch” cycle is often references as a pathogenic mechanism by which pruritus and inflammation contribute to one another.
| Morphology |
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- Overview
- The clinical appearance of atopic dermatitis is shared by a number of different pathogenic entities including contact dermatitis. An umbrella term of 'eczema' is used to describe these lesions that typically evolve with time from acute lesions to chronic lesions as patients rub and scratch their skin.
- Acute Eczema
- Acute lesions manifest as poorly defined pink papules that coalesce into plaques and can be weepy due to serous crust overlying.
- Chronic Eczema
- As the patient rub and scratch acute eczematous lesions due to chronic pruritus, the lesions evolve by thickening and are thus described as “lichenified”, resembling lichen growing on rocks.
| Pathology |
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- The hallmark histological feature of any eczematous lesion, including atopic dermatitis, is spongiosis. Spongiosis refers to edema and thus increased space between keratinocytes of the spiny layer of the epidermis. The desmosomes between keratinocytes are typically preserved and thus the keratinocytes appear to be separated by a spongy layer. In more florid cases, frank vesicles can appear within the epidermis.
- In acute lesions, serous exudate can be seen in the top layers of the skin whereas in chronic lesions the entire epidermis appears thickened (acanthosis) and the corneal layer expands (hyperkeratosis) and corneocytes show retention of nuclei (parakeratosis). A perivascular infiltrate is sometimes seen beneath the epidermis.
| Treatment |
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- Treatment of atopic dermatitis revolves around improving the skin barrier with emolliation, reducing inflammation with topical corticosteroids, and eliminating super-infection with S. aureus when present. When severe, systemic immunosuppression may be required or the use of phototherapy is often employed.
| Further Reading |
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- Brown, Sara, and Nick J. Reynolds. “Atopic and non-atopic eczema.” British Medical Journal 7541 (2006): 584.
- Sehgal, Virendra N., et al. "Atopic dermatitis; Etio-pathogenesis, An overview." Indian journal of dermatology 60.4 (2015): 327.
- Marks, James G., and Jeffrey J. Miller. Lookingbill and Marks' principles of dermatology. Elsevier Health Sciences, 2013.
| To cite this article |
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