Plasma-soluble CD30 in childhood tuberculosis: Effects of disease severity, nutritional status, and vitamin A therapy

Citation
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
Citations number
24
Categorie Soggetti
Immunology
Journal title
CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY
ISSN journal
1071412X → ACNP
Volume
6
Issue
2
Year of publication
1999
Pages
204 - 208
Database
ISI
SICI code
1071-412X(199903)6:2<204:PCICTE>2.0.ZU;2-G
Abstract
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.