D. Kaldennemeth et al., NMR MONITORING OF RHEUMATOID-ARTHRITIS PATIENTS RECEIVING ANTI-TNF-ALPHA MONOCLONAL-ANTIBODY THERAPY, Rheumatology international, 16(6), 1997, pp. 249-255
The aim of this study was to investigate if dynamic gadolinium-DTPA-su
pported magnetic resonance (MR) imaging can monitor the therapeutic ef
fect of a fast-acting immune-modulating drug like anti-tumour necrosis
factor alpha (anti-TNF-alpha) monoclonal antibody (moab) in patients
with rheumatoid arthritis (RA). Dynamic MR imaging was performed on 64
joints in a total of 18 patients before and after infusion with eithe
r a placebo or 1 or 10 mg/kg of anti-TNF-alpha moab. Additionally, tre
ating the placebo group and reinfusing the verum group with either 3 o
r 10 mg/kg was monitored by quantitative nuclear magnetic resonance (N
MR). Time-dependent signal intensity changes were then correlated with
a total of five Paulus criteria and with ESR and C-reactive protein (
CRP). No changes in either the gadolinium uptake or clinical parameter
s were seen after the infusion of a placebo. Therapy with 1 mg/kg anti
-TNF-alpha moab resulted in a significant decrease in clinical disease
activity, as well as in gadolinium-DTPA uptake in dynamic NMR studies
. However, correlations between signal intensity changes and Paulus cr
iteria were only demonstrated for the variable ''doctor's evaluation o
f disease activity''. Patients given 10 mg/kg moab demonstrated a very
significant improvement in all clinical manifestations of their disea
se, as well as a high significant reduction in gadolinium uptake (P =
0.004). In addition, the latter group showed significant correlations
between time-dependent signal intensity changes and five Paulus criter
ia: ''number of swollen joints'', ''number of painful joints'', ''dura
tion of morning stiffness'', ''doctor's evaluation of disease activity
'' and ''patient's evaluation of disease activity''. No differences an
d correlations were seen for ESR and CRP. We concluded that dynamic NM
R studies are suitable to monitor inflammatory activity in RA patients
under therapy with biological response modifiers such as anti-TNF-alp
ha moab.