Ra. Stuart et al., ELEVATED SERUM INTERLEUKIN-6 LEVELS ASSOCIATED WITH ACTIVE DISEASE INSYSTEMIC CONNECTIVE-TISSUE DISORDERS, Clinical and experimental rheumatology, 13(1), 1995, pp. 17-22
Objective. It is well established that connective tissue diseases such
as systemic lupus erythematosus (SLE) are associated with a weak or a
bsent acute phase response, although elevated serum interleukin 6 leve
ls have been described. In this study, we have sought to correlate ser
um levels of IL-6 with standard laboratory avid clinical assessments o
f disease activity in two connective tissue diseases, namely SLE and s
ystemic sclerosis (SSc), and, for comparative purposes, rheumatoid art
hritis (RA). Methods. Serum IL-6 levels were determined by bioassay an
d also, in some sera by immunoradiometric assay. They were compared wi
th two inflammatory parameters, serum C-reactive protein (CRP) and pla
sma viscosity (PV) and with appropriate clinical measurements in the v
arious patient groups, including BILAG in SLE, the skin score in SSC,
and the Ritchie index in RA. Results. Serum IL-6 (SeIL-6) levels were
elevated in active SLE, SSc, and RA. This was poorly correlated with t
he acute phase response in SLE and SSc, but there was a strong relatio
nship of SeIL-6 to disease activity in these conditions. In SLE, the B
ILAG disease activity index correlated best with SeIL-6 levels while t
here was only a weak relationship between CRP and IL-6, and no relatio
nship between CRP and disease activity, In SSc there was a relationshi
p disease activity to SeIL-6 but not between SeIL-6 and either CRP or
PV. In a small RA group there was a much stronger relationship of SeIL
-6 to CRP and PV, as has been previously described. Conclusion. The de
termination of SeIL-6 may be a useful indicator of disease activity in
those patients groups, including SLE and SSc, in which a normal acute
phase response by the liver is often lacking. The mechanism underlyin
g this hepatic impairment requires further investigation, but is clear
ly not dire to a failure to generate the appropriate cytokine signal.
Excessive local or systemic production of IL-6 in connective tissue di
seases could play an important pathogenic role in these conditions, fo
r example through stimulating autoantibody synthesis.