Suboptimal clinical response to anti-tumor necrosis factor alpha (TNFalpha) antibody therapy in a patient with severe rheumatoid arthritis and lymphadenopathy.
This concerns a patient with severe rheumatoid arthritis (RA) and lymphadenopathy (LA) who showed suboptimal clinical response to antitumor necrosis factor alpha (TNFalpha) antibody (Ab), cA2 therapy. The assessment of TNFalpha and IL-6 mRNA expression in the swollen lymph-node (LN) of the patient by reverse transcription, polymerase chain reaction (RT-PCR) before cA2 treatment, showed only enhanced IL-6 production, but not TNFalpha. Moreover, cA2 failed to inhibit in-vitro spontaneous IL-6 production in the LN block culture from the patient. Taken together, these results indicate that IL-6 production in the swollen LNs of the patient might not depend on TNFalpha. This might partly cause suboptimal clinical response to anti-TNFalpha Ab therapy in the patient.
Saeki
Y
Y
Department of Medicine III, Osaka University Medical School, Suita City, Japan.
Ohshima
S
S
Mima
T
T
Sasai
M
M
Nishioka
K
K
Shimizu
M
M
Suemura
M
M
McCloskey
R
R
Kishimoto
T
T
D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000628:therapy*; D002097:C-Reactive Protein / Q000032:analysis; D006801:Humans; D000069285:Infliximab; D015850:Interleukin-6 / Q000378:metabolism; D008198:Lymph Nodes / Q000378:metabolism; D008206:Lymphatic Diseases / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology* / Q000378:metabolism
D000911:Antibodies, Monoclonal; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069285:Infliximab