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Published on: May 15, 2019
In vitro thalidomide does not interfere with the activation of complement by M. leprae
Edward J Shannon1, Felipe G Sandoval, Melvyn J Morales
1National Hansen's Disease Programs, Laboratory Research Branch, Louisiana State University, Baton Rouge, LA, USA. eshannon@hrsa.gov
Journal of Drugs in Dermatology : JDD
|March 4, 2011
Summary
Thalidomide, the primary treatment for Erythema nodosum leprosum (ENL), does not inhibit complement activation by M. leprae or zymosan. This study investigated the mechanism of thalidomide
Area of Science:
- Immunology
- Dermatology
- Pharmacology
Background:
- Erythema nodosum leprosum (ENL) is a complication of multibacillary leprosy.
- Thalidomide is the standard treatment for ENL, but its mechanism of action is unknown.
- Immune complexes and complement activation are implicated in ENL pathogenesis.
Purpose of the Study:
- To investigate whether thalidomide inhibits complement activation.
- To determine if thalidomide's anti-inflammatory effect in ENL is mediated by complement inhibition.
Main Methods:
- Normal human serum was incubated with M. leprae or zymosan in the presence or absence of thalidomide.
- Complement activation was assessed by measuring residual functional complement activity using the CH50 assay.
- Hydrolyzed thalidomide and its metabolites were also tested.
Main Results:
- Both M. leprae and zymosan activated the complement system.
- Thalidomide, hydrolyzed thalidomide, and its metabolites did not inhibit complement activation by M. leprae or zymosan.
- Residual complement activity was similar whether thalidomide was present or absent during incubation.
Conclusions:
- Thalidomide does not suppress ENL by inhibiting complement activation.
- The mechanism by which thalidomide exerts its therapeutic effect in ENL remains to be elucidated.
- Further research is needed to understand thalidomide's action and alternative treatment strategies for ENL.
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