Plasma levels of soluble CD30 are increased in children with chronic renalfailure and with primary growth deficiency and decrease during treatment with recombination human growth hormone
G. Barbano et al., Plasma levels of soluble CD30 are increased in children with chronic renalfailure and with primary growth deficiency and decrease during treatment with recombination human growth hormone, NEPH DIAL T, 16(9), 2001, pp. 1807-1813
Background. Previous studies have suggested that in vivo Th2 lymphocyte act
ivation is related to increased soluble CD30 (sCD30) plasma levels. As vari
ous hormones (dehydroepiandrosterone, glucocorticoids, progesterone) can re
gulate the Th1/Th2 balance, and because growth hormone (GH) enhances lympho
cyte function, we measured sCD30 plasma levels, before and after treatment
with recombinant human GH (rhGH), in children with growth failure due to ch
ronic renal failure (CRF) or to isolated GH deficiency in order to evaluate
the potential effects of rhGH treatment on Th1/Th2 balance.
Methods. sCD30 plasma levels were determined by ELISA assay in 30 children
with CRF (mean age 10.7 +/- 3.7 years), in five children with isolated GH d
eficiency (mean age 11.4 +/- 2.6 years), and in 10 normal controls (mean ag
e 10.1 +/- 3.5 years).
Results. sCD30 levels were higher in the 30 children with CRF than in the 1
0 controls (179.8 +/- 79.4 vs 11.3 +/- 10.9 U/ml, P < 0.001) exhibiting an
inverse correlation with glomerular filtration rate (GFR) (r=-0.7860, P < 0
.001). In 11 children with CRF, after 19.9 +/- 16.7 months of rhGH treatmen
t, a decrease of sCD30 plasma level (170 +/- 50 vs 134 +/- 49 U/ml, P < 0.0
1) was observed. The five children with primary GH deficiency had higher sC
D30 plasma level than controls (mean 147 +/- 105 vs 11 +/- 10U/ml, P < 0.00
4) and sCD30 plasma levels decreased to 95.2 +/- 109.6 U/ml after rhGH trea
tment.
Conclusions. The finding that rhGH treatment decreased sCD30 plasma levels
in children with CRF, and that children with primary GH deficiency had high
er sCD30 plasma levels than controls, suggest that GH may regulate CD30 exp
ression and possibly the balance of Th1/Th2. Whether the uraemia-induced in
crease in sCD30 is due to decreased renal excretion, to overproduction or b
oth, remains to be determined.