Therapeutic complement inhibition – from experimental to clinical medicine.
Internationally, the use of the C5-inhibiting monoclonal antibody eculizumab has in the course of just a few years become the first choice of treatment of atypical haemolytic uraemic syndrome and the most severe phenotypes of paroxysmal nocturnal haemoglobinuria. At present eculizumab is the only complement inhibitor in ordinary clinical use. This despite the fact that there only exists one randomised, placebo-controlled trial of eculizumab for paroxysmal nocturnal haemoglobinuria and none for atypical haemolytic uraemic syndrome, and that the therapy is very costly. There is reason to believe that complement inhibition as therapy will increase in the future, and that other drugs will also prove to be effective.
Medisinsk divisjon Nordlandssykehuset Bodø og Institutt for klinisk medisin Universitetet i Tromsø
Knut Tore
KT
Lappegård
Barnemedisinsk avdeling Kvinne- og barneklinikken Oslo universitetssykehus.
Anna
A
Bjerre
Avdeling for blodsykdommer Oslo universitetssykehus og Institutt for klinisk medisin Universitetet i Oslo.
Geir Erland
GE
Tjønnfjord
Forskningslaboratoriet Nordlandssykehuset Bodø og Senter for molekylær inflammasjonsforskning (SFF-CEMIR) Norges teknisk-naturvitenskapelige universitet.
Tom Eirik
TE
Mollnes
D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D065766:Atypical Hemolytic Uremic Syndrome / Q000188:drug therapy; D003167:Complement Activation / Q000187:drug effects / Q000502:physiology; D051056:Complement Inactivating Agents / Q000494:pharmacology / Q000627:therapeutic use; D003165:Complement System Proteins / Q000187:drug effects / Q000502:physiology; D006457:Hemoglobinuria, Paroxysmal / Q000188:drug therapy; D006801:Humans; D007249:Inflammation / Q000503:physiopathology
D061067:Antibodies, Monoclonal, Humanized; D051056:Complement Inactivating Agents; D003165:Complement System Proteins