New developments in atopic dermatitis, urticaria, anaphylaxis, food, drug and insect allergy

Food allergy

Several westernized countries report that more than 1% of children have peanut allergy, environmental exposure to peanut may be a risk factor.

The role of regulatory T cells, complement, and platelet-activating factor in the development of food allergy were explored.

Oral immunotherapy showed some promise for the treatment of food allergy in 2009. We still do not know if treatment causes tolerance (cure) or temporary desensitization.

Drug hypersensitivity

Delayed anaphylaxis to mammalian meats may be related to IgE binding to the carbohydrate galactose-α-1,3-galactose. Murine (mouse) mAb drugs contain the same oligosaccharide which may explain patient hypersensitivity to mAb. mAb: If it ends in -mumab, it's a fully human protein, -zumab is humanized (10% mouse), -ximab is chimeric (33% mouse). ACP blog, 2012.

Venom anaphylaxis

Increased baseline serum tryptase levels may be a risk factor for venom anaphylaxis. Elevated tryptase may also be a risk factor for mast cell disorders in people with episodes of venom anaphylaxis.

Atopic dermatitis

Reduced skin barrier function in atopic dermatitis leads to allergen sensitization and increased infections.

Loss-of-function mutations in filaggrin gene are associated with atopic dermatitis, and now with peanut allergy too. JACI, 2011.

Chronic urticaria

Chronic urticaria can be controlled with increased doses of nonsedating antihistamines (double to quadrable the recommended dose) and omalizumab.

References:
Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects in 2009. Scott H. Sicherer et al. Journal of Allergy and Clinical Immunology, Volume 125, Issue 1, January 2010, Pages 85-97.
Image source: OpenClipArt.org, public domain.