NICE (CG57, 2007) diagnostic criteria: itchy skin plus 3+ :
- visible flexural dermatitis (or visible dermatitis on the cheeks and/or extensor areas in children <18/12) – can look like dirt where darkened esp neck
- personal history of flexural dermatitis (or dermatitis on the cheeks and/or extensor areas in children <18/12)
- personal history of dry skin (xerosis) in the last 12 months
- personal history of asthma or allergic rhinitis (or history of atopic disease in a first-degree relative of children aged <4yr)
- onset of signs and symptoms under the age of 2 years (do not use this criterion in children under 4 years).
On examination, may also see lichenification (increased skin markings due to chronic rubbing), excoriations caused by scratching, and hyperlinear palms (look at thenar eminence).
Babies tend to get eczema on the face. Older infants get it on extensor surfaces. From walking age, antecubital and popliteal fossae. In children of Asian, black Caribbean and black African ethnic groups, extensor surfaces tend to be affected rather than flexures, and discoid or follicular patterns may be more common.
Severe (NICE criteria): widespread areas of dry skin, incessant itching, redness (with or without excoriation, extensive skin thickening, bleeding, oozing, cracking and alteration of pigmentation).
Cf Moderate: frequent itching, redness (with or without excoriation and localised skin thickening)
Eczema (or atopic dermatitis, same thing) associated with parental allergies (OR 1.94), parent-reported infection after birth (OR 1.45), parent-reported jaundice (OR 1.27). Being a migrant (OR 0.63) and keeping a dog (OR 0.78) are protective. Prenatal probiotics did not reduce risk (Lactobacillus rhamnosus GG, LGG). Respiratory viral infections in pregnancy associated with wheezing illness in infants (mothers with asthma) and eczema. [Australia, Ped All Imm 2014:25:151]. Febrile and gynae infections in pregnancy associated with eczema in child (Italy, Ped All Imm 2014:25:159]. Children of Japanese mothers with higher anxiety scores during pregnancy were more likely to be affected by eczema!
Many roads lead to Rome! Can be seen as combination of impaired innate and distorted adaptive immunity, interacting in framework of cutaneous immune system with suboptimal barrier function. Epidermal barrier can be genetically disturbed, but gene expression (eg of filaggrin) is also influenced by microenvironment eg Th2 cells. Some genetic structural abnormalities can be seen to induce nonspecific inflammatory reaction (eg SPINK5 defects). And almost certainly, epigenetic regulation will affect gene expression in both keratinocytes and immune cells.
Facilitated antigen presentation mediated by IgE bound to high affinity IgE receptor FcEpsilonRI, on dendritic cells, is an important part of it. Vitamin D plays a key roll, stimulates Toll like receptors, increasing pro-inflammatory cytokines but studies equivocal whether low (or indeed high) levels increase risk.
Eczema can exist without IgE against aeroallergens and food allergens, so is primarily a non IgE mediated disease, although both IgE and non-IgE hypersensitivity can co-exist, particularly in babies.
Still not understood how eczema and Staph aureus interact. Colonization appears to amplify local inflammatory reaction, but also increases IgE against a large spectrum of other things (possibly including self proteins). It is as if there is something specifically different about how immune cells handle Staph. Toll like receptors esp TLR-2 recognize Staph aureus cell wall. Overgrowth of staph during flares is associated (preceded?) by loss of diversity of skin microbiome.
Unmasking of the HSV entry receptor Nectin-1 in adherence junctions, among other things, contribute to eczema herpeticum. See Flares, below.
Atopy patch test (using intact protein allergens) can prove type IV reactions. Correlates with oral food challenge. Hyper IgE syndromes are important differential for AD, STAT3 mutations, skin (and other) abscesses, recurrent pneumonia (and pneumatocoele), connective tissue and skeletal abnormalities, mucocutaneous candidiasis. DOCK8 type Hyper IgE syndrome show sensitization predominantly against food allergens, which is a clue (STAT3 and AD show predominantly sensitization to aeroallergens).
Normal looking skin is not immunobiologically normal! Invisible inflammation, hence still needs treatment. Pimecrolimus and betamethasone both normalize expression of filaggrin, the later is perhaps a better anti-inflammatory but steroids reduce expression of enzymes for lipid and protein synthesis, so may impair skin barrier restoration.
Stress, humidity, extremes of temperature can cause flares of atopic eczema. But what causes a flare in some can apparently help in others! Any factors causing flares should be avoided where possible.
UVB causes sunburn. UVA (longer wavelength) more relevant to photosensitivity reactions. Both cause long term skin damage. EU commission recommends UVA protection making up at least 1/3 of total suncream SPF. A few available on prescription for photodermatosis (incl vitiligo) but not for eczema per se. Lipscreen (Uvistat) available for chronic/rec HSV labialis. Sunsense is lotion.
Avoid wool in contact with skin. No evidence that bio detergent or fabric softener a major problem. Avoiding excessive product and not overloading machine (so disperses fully) prob more important.
See eczema management.
National eczema society, British Association of Dermatologists, Eczema Outreach Scotland.