Wa. Hanekom et al., Plasma-soluble CD30 in childhood tuberculosis: Effects of disease severity, nutritional status, and vitamin A therapy, CL DIAG LAB, 6(2), 1999, pp. 204-208
Plasma-soluble CD30 (sCD30) is the result of proteolytic splicing from the
membrane-bound form of CD30, a putative marker of type 2 cytokine-producing
cells. We measured sCD30 levels in children with tuberculosis, a disease c
haracterized by prominent type 1 lymphocyte cytokine responses. We postulat
ed that disease severity and nutritional status would alter cytokine respon
ses and therefore sCD30 levels. Samples from South African children enrolle
d prospectively at the time of diagnosis of tuberculosis were analyzed, (Pa
tients were originally enrolled in a randomized, double-blind placebo-contr
olled study of the effects of oral vitamin A supplementation on prognosis o
f tuberculosis.) Plasma samples collected at the time of diagnosis and 6 an
d 12 weeks later (during antituberculosis therapy) were analyzed. sCD30 lev
els were measured by enzyme immunoassay, The 91 children included in the st
udy demonstrated high levels of sCD30 at diagnosis (median, 98 U/liter; ran
ge, 11 to 1,569 U/liter), Although there was a trend toward higher sCD30 le
vels in more severe disease (e.g., culture-positive disease or miliary dise
ase), this was not statistically significant, Significantly higher sCD30 le
vels were demonstrated in the presence of nutritional compromise: the sCD30
level was higher in patients with a weight below the third percentile for
age, in those with clinical signs of kwashiorkor, and in those with a low h
emoglobin content. There was minimal change in the sCD30 level after 12 wee
ks of therapy, even though patients improved clinically. However, changes i
n sCD30 after 12 weeks differed significantly when 16 patients (51%) who re
ceived vitamin A were compared with those who had received a placebo. Vitam
in A-supplemented children demonstrated a mean (+/- standard error of the m
ean) decrease in sCD30 by a factor of 0.99 +/- 0.02 over 12 weeks, whereas
a factor increase of 1.05 +/- 0.02 was demonstrated in the placebo group (P
= 0.02). We conclude that children with tuberculosis had high sCD30 le, el
s, which may reflect the presence of a type 2 cytokine response. Nutritiona
l compromise was associated with higher sCD30 levels. Vitamin A therapy res
ulted in modulation of sCD30 levels over time.