Hereditary angioedema results from deficiency of which regulatory protein?

• A. C1 esterase
• B. C3
• C. DAF
• D. C5

Answer: (A)

Hereditary angioedema arises from a deficiency of C1 esterase inhibitor, a regulator of both the complement system and the kallikrein–kinin (contact) pathway. C1 esterase inhibitor keeps C1 activity in check and also inhibits kallikrein and factor XIIa. When this inhibitor is deficient, unregulated kallikrein activity increases production of bradykinin, a potent mediator of vascular permeability, leading to episodic, non-itchy swelling of the skin and mucosal tissues.

This explains the characteristic clinical picture: swelling without urticaria and often low C4 levels due to consumption from uncontrolled complement activation. The other options don’t fit because deficiencies in C3, DAF (CD55), or C5 disrupt other aspects of the complement system and do not produce the bradykinin-mediated angioedema seen in hereditary angioedema.