A study by Dr Leung showed that children with food allergy related eczema differ from those eczema patients without food allergy by changes in uninvolved skin. Those with food allergy were shown to have increased water loss, increased Staph colonization, and changes consistent with a immature skin barrier (as determined by gene expression studies).
The study was done by sampling the upper layer of the skin by removing cells with scotch tape. The food allergy involved was peanut allergy, in those considered food allergic. It should be noted that peanuts are far more active as lectins than other food allergens, that this study was done in a dry elevated city of Denver, and that it may or may not be applicable to all eczema patients with food sensitivities. The implication of the study is that a defective skin barrier plays a role in food allergy related eczema. We are still far from being certain that this is a as good a way to determine if food allergies are involved in an eczema patient’s outbreaks, compared to history of flares. Also, the tests used are mostly not clinically available. Nevertheless, it is an important advance, and supports the notion that a sub-population of a topic dermatitis patients do have food allergies related to their condition.
New Studies in Eczema, medically termed Atopic dermatitis, extend our understanding, and verify what we already know.
Early eczema, and according to some, the majority of eczema is caused by reactions from the branch of the immune system related to antibody production known as TH2 immunity. One of the popular biologics for eczema targets this system. We might expect that people with this kind of immunity would cause reactions very shortly after exposure to allergens to which they are sensitive. But although some academic proponents of eczema being a result of immediate sensitivity, testing for IgE sensitivity, while useful for pollen, dander, and dust, is often not very helpful in identifying allergic triggers, especially if food allergy is involved.
A recent study by Dr Emma Guttman-Yassky showed that in a subgroup of Eczema patients , substances secreted by white blood cells called lymphocytes called cytokines, had characteristics of a delayed hypersensitivity or TH1 response instead. These cytokines were of the types IL 22 and IL 17, both related to delayed reactions.
Using a biologic antibody that blocked IL-22, she demonstrated that eczema patients with high IL-22 had greater improvement than eczema patients with low IL-22. She claimed this as the first example of personalized medicine for Atopic Dermatitis. While it is an important finding for drug blockade of immune reactivity, those using holistic, integrative, natural, or nutritional dermatology know that tailoring diet, food elimination, and appropriate digestive and other supplements to control the underlying causes such as microbiome imbalances or digestive disturbances to calm down the inflammation, have been practicing personalized medicine long before this study.