Bradykinin Angioedema Explained

When you hear Bradykinin Angioedema, a rapid swelling of the skin and mucous membranes caused by excess bradykinin. Also known as BK‑mediated angioedema, it often shows up after taking certain medicines or due to genetic factors. The condition bradykinin angioedema is triggered when the body’s kallikrein‑kinin system goes haywire, allowing bradykinin to leak into tissues and cause fluid buildup. A common trigger is the class of blood‑pressure pills called ACE inhibitors, which block the enzyme that normally breaks down bradykinin, leading to sudden facial, lip or airway swelling.

Beyond drug‑induced cases, there are hereditary forms that stem from a missing or defective C1 esterase inhibitor. Without enough of this protein, the complement cascade stays active and more kallikrein is produced, flooding the system with bradykinin. This hereditary angioedema (HAE) can appear at any age and often runs in families. Another key player is kallikrein itself, the enzyme that converts high‑molecular‑weight kininogen into bradykinin. When kallikrein is overactive, even a small trigger can cause a big swell. Understanding these relationships—ACE inhibitors block breakdown, C1 esterase inhibitor deficiency removes the brake, and kallikrein supplies the gas—helps clinicians pinpoint why a patient is swelling.

How to Recognize and Treat the Swell

Clinically, bradykinin angioedema feels different from allergic swelling. It’s usually painless, doesn’t itch, and histamine blockers like antihistamines or steroids often don’t help. Quick recognition is vital because airway involvement can become life‑threatening within minutes. Diagnostic clues include a recent start of an ACE inhibitor, a family history of HAE, or low C4 complement levels. Once identified, the treatment path splits. For drug‑induced cases, stopping the offending medication is the first step. Acute attacks often respond to a bradykinin receptor antagonist such as icatibant, which blocks the B2 receptor and halts swelling. In hereditary cases, plasma‑derived or recombinant C1 esterase inhibitor concentrate or a kallikrein inhibitor like ecallantide can be given. Long‑term prevention may involve avoiding ACE inhibitors, using angiotensin‑II receptor blockers instead, or prophylactic C1‑esterase therapy for HAE patients.

Below you’ll find a curated set of articles that dig deeper into the drugs, mechanisms and real‑world management tips for bradykinin‑mediated swelling. Whether you’re a patient trying to understand why a new medication caused a flare, or a clinician looking for quick‑reference treatment options, the posts below break down each piece of the puzzle in plain language and practical steps.