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On the other hand, these drugs increase the concentration of the vasoactive signaling substance bradykinin.

"Through further bioinformatic analyses, we were able to identify several candidate genes at the three risk loci indicating that genetic changes in the bradykinin, coagulation and fibrinolysis signaling play a role in the development of this type of angioedema," adds first author Carina Mathey, doctoral student at the Institute of Human Genetics at the UKB and the University of Bonn.

Drugs can help prevent these attacks by blocking a protein, kallikrein, that ramps up bradykinin levels—this essentially counteracts the effects of the loss of C1-esterase inhibitor.

In people with hereditary angioedema, stress, illness, or trauma can trigger high blood levels of bradykinin, producing severe swelling of limbs, the abdomen, or even the throat, which can suffocate a person.

That disease results from mutations that disable a protein called C1-esterase inhibitor that’s part of a signaling pathway controlling levels of bradykinin, a peptide hormone that causes blood vessels to leak fluid.