Inflammatory mediators in umbilical plasma from neonates who develop early-onset sepsis.

OBJECTIVES: To study whether early-onset neonatal sepsis is associated with a prenatal immune response with elevated umbilical plasma levels of inflammatory mediators, and to study whether mediator levels may be helpful in identifying infected neonates. SETTING: Nested case-control study. METHODS: Cord blood was sampled from 7,073 consecutively delivered neonates. After review of the medical records, neonates suspected to suffer from infection were classified as infected (n = 52) or noninfected but sick controls (n = 33). We also included a group of healthy controls (n = 99). Umbilical plasma levels of tumour necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, IL-6, IL-8, soluble TNF receptors (p55 and p75), IL-1 receptor antagonist (IL-1RA) and C-reactive protein were measured by immunoassays. RESULTS: Infected neonates had higher levels of TNFalpha, IL-1beta, IL-6, IL-8, p55, p75 and IL-1RA than healthy controls (all p < 0.01). Among preterm infants (GA <37 weeks), those with infection (n = 11) had higher levels of IL-1beta, IL-6, IL-8, p55 and p75 than noninfected sick controls (n = 13) (all p < 0.05), but among term infants, the infected did not differ from the noninfected sick controls. Receiver operator characteristic plots showed that IL-1beta, IL-6 and IL-8 identified preterm infected neonates accurately. CONCLUSIONS: Early-onset neonatal sepsis is associated with a prenatal immune response with increased TNFalpha, IL-1beta, IL-6, IL-8, p55, p75 and IL-1RA levels in umbilical plasma. Among neonates who present symptoms suggestive of infection, cytokine levels may be helpful in identifying preterm, but not term infected individuals.

Cyclosporine in steroid-resistant Diamond-Blackfan anaemia.

Two siblings with Diamond-Blackfan anaemia (DBA) and several congenital malformations were first treated with corticosteroids and blood transfusions. High steroid doses were needed, but in spite of this haemoglobin values periodically fell below acceptable levels. Cyclosporine was then given in addition to prednisolone. A slow increase in haemoglobin levels was observed over 2-3 months, and the prednisolone doses could be reduced gradually. Two short communications in the literature report similar experiences. Cyclosporine could be tried in DBA when reasonable corticosteroid doses do not give a satisfactory response. Since the main effect of cyclosporine is a specific inhibition of T-lymphocytes, the observed therapeutic effect in DBA indicates that T-lymphocytes may play an important role in the pathogenesis of this disease.