Angioedema without urticaria is made up of a growing number of subtypes and offers a difficult diagnosis. This study sums up the current subtypes and new results that have been identified in recent years. The possible biochemical tests to classify bradykinin-mediated angioedeme were developed as new methods to quantify cleaved high molecular weight kininogen and active plasma kallikrein. In the past two years three novel subtypes have been identified of hereditary angioedema (HAE) with natural C1 inhibitor: Plasminogen mutation, kininogenic genes and angiopoietin 1 genes; involvement of the fibrinolytic and touch processes, and vasculature regulations respectively. In addition, an increased activation of truncated F12 mutants by plasma kallikrein and a declining bond of angiopoietin 1 to its receptor has been strengthened, consistent with the dominant negative for certain variants of C1 inhibitors.
The validation of biomarkers for the activation of the touch system may be useful to differentiate bradykinin from histaminergic angioedema. Currently, available laboratory testing is now somewhat limited to the assessment of supplementary activation and an angioedema mediator is still identifiable.
