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High-molecular-weight kininogen is cleaved in active erythema multiforme
D M Lang1, S L Sugimoto, J G Curd
1Division of Allergy, Scripps Clinic, La Jolla, Calif.
The Journal of Allergy and Clinical Immunology
|April 1, 1989
Summary
Erythema multiforme (EM) involves kinin pathway activation, evidenced by cleaved high-molecular-weight kininogen (HMWK) in patients. These levels decrease during recovery, suggesting kinins contribute to EM inflammation.
Area of Science:
- Immunology
- Dermatology
- Biochemistry
Background:
- Erythema multiforme (EM) is an inflammatory skin condition with poorly understood pathogenesis.
- The specific mediators involved in EM inflammation require further characterization.
- This study investigates the role of kinins in EM pathophysiology.
Observation:
- Patients with active EM showed significantly elevated levels of cleaved high-molecular-weight kininogen (HMWK) in plasma.
- Cleaved HMWK levels decreased during disease remission.
- Active EM plasmas also contained elevated C1 inhibitor and C1 inhibitor-kallikrein complexes.
Findings:
- The findings indicate activation of the kinin system and contact system in active EM.
- Elevated cleaved HMWK suggests kinin generation plays a role in EM inflammation.
- These changes were specific to EM and not observed in serum sickness or chronic idiopathic urticaria/angioedema.
Implications:
- Kinins may contribute to the inflammatory manifestations of Erythema Multiforme in some patients.
- Further research is needed to identify the specific kininogenase responsible for HMWK cleavage in EM.
- Understanding kinin involvement could lead to new therapeutic strategies for EM.
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