SUBOPTIMAL CLINICAL-RESPONSE TO ANTITUMOR NECROSIS FACTOR-ALPHA (TNF-ALPHA) ANTIBODY THERAPY IN A PATIENT WITH SEVERE RHEUMATOID-ARTHRITIS AND LYMPHADENOPATHY
Y. Saeki et al., SUBOPTIMAL CLINICAL-RESPONSE TO ANTITUMOR NECROSIS FACTOR-ALPHA (TNF-ALPHA) ANTIBODY THERAPY IN A PATIENT WITH SEVERE RHEUMATOID-ARTHRITIS AND LYMPHADENOPATHY, Scandinavian journal of rheumatology, 27(4), 1998, pp. 303-305
This concerns a patient with severe rheumatoid arthritis (RA) and lymp
hadenopathy (LA) who showed suboptimal clinical response to anti-tumor
necrosis factor alpha (TNF alpha) antibody (Ab), cA2 therapy. The ass
essment of TNF alpha and IL-6 mRNA expression in the swollen lymphnode
(LN) of the patient by reverse transcription, polymerase chain reacti
on (RT-PCR) before cA2 treatment, showed only enhanced IL-6 production
, but not TNF alpha Moreover, cA2 failed to inhibit in-vitro spontaneo
us IL-6 production in the LN block culture from the patient. Taken tog
ether, these results indicate that IL-6 production in the swollen LNs
of the patient might not depend on TNF alpha This might partly cause s
uboptimal clinical response to anti-TNF alpha Ab therapy in the patien
t.