CIRCULATING TRANSFORMING-GROWTH-FACTOR-BETA 1 (TGF-BETA-1) IN GUILLAIN-BARRE-SYNDROME - DECREASED CONCENTRATIONS IN THE EARLY COURSE AND INCREASE WITH MOTOR FUNCTION
A. Creange et al., CIRCULATING TRANSFORMING-GROWTH-FACTOR-BETA 1 (TGF-BETA-1) IN GUILLAIN-BARRE-SYNDROME - DECREASED CONCENTRATIONS IN THE EARLY COURSE AND INCREASE WITH MOTOR FUNCTION, Journal of Neurology, Neurosurgery and Psychiatry, 64(2), 1998, pp. 162-165
Objective-To delineate the possible implication of the immunosuppressi
ve cytokine transforming growth factor beta 1 (TGF-beta 1) in the path
ogenesis of Guillain-Barre syndrome. Guillain-Barre syndrome is a diso
rder that may implicate cytokines in its pathogenesis. TGF-beta 1 is a
potent anti-inflammatory cytokine occasionally shown to be regulated
in the course of demyelinating disorders. Methods-The study measured c
irculating proinflammatory and anti-inflammatory cytokines from the pr
ogressing phase to early recovery in patients with Guillain-Barre synd
rome. Plasma concentrations of TNF-alpha, IL-1 beta, IL-2, IL-4, IL-6,
IL-10, and TGF-beta 1 were prospectively evaluated in 15 patients wit
h Guillain-Barre syndrome every three days for the first 15 days after
admission to hospital, and in 15 controls with non-inflammatory neuro
logical diseases. Results-Concentrations of TGF-beta 1 in plasma were
decreased in 13/15 patients (87 %) at day 1, remained low during progr
ession and the plateau of paralysis (days 1-10), and then progressivel
y increased up to control concentrations during early recovery (days 1
2-15). Concentrations of plasma TGF-beta 1 correlated positively with
motor function, the lowest values being in the most disabled patients.
Concentrations of plasma TGF-beta 1 were decreased before any treatme
nt, and during treatment by either plasma exchange or intravenous immu
noglobulins, plasma exchange being associated with a more pronounced d
ecrease in TGF-beta 1 at day 7, Circulating TNF-alpha concentrations w
ere raised, as previously reported, when other cytokines were either r
andomly increased (IL-2, IL-6), or undetectable (IL-1, IL-4, IL-7, IL-
10). Conclusions-Down regulation of TGF-beta 1 in the early course of
Guillain-Barre syndrome could participate in neural inflammation.