No abstract

Febrile children are often given antibiotics empirically and unnecessarily. MxA is a protein induced in peripheral lymphoid cells by type 1 interferons during active viral infection. The ability of a whole blood ELISA assay for MxA to identify children with viral illness was studied in 122 children who presented with acute onset fever and 52 age-matched healthy controls. The febrile children were divided into three groups according to their final diagnoses: etiologically diagnosed viral infection, clinically diagnosed viral infection, and bacterial infection. MxA levels in the bacterial infection group and controls were similar and low (90.9 Ϯ 69.7 and 76.9 Ϯ 63.2 ng/mL, respectively). In contrast, mean MxA levels in the two viral infection groups were higher than in both the bacterial and control groups (719.2 Ϯ 386.4 and 827.0 Ϯ 651.1, respectively). A receiver operating characteristic analysis showed that the area under the curve of the MxA level was greater than under the curves of both the white blood cell count and the C-reactive protein concentration. Whole blood assay of MxA is a clinically useful tool for diagnosing viral illness in febrile children and should help reduce use of unnecessary antibiotics. (Pediatr Res 60: 770-774, 2006)

No abstract

We have developed a new ELISA for measuring MxA protein in human whole blood using mAbs specific for the GTP-binding domain of MxA. This ELISA has analytical performance enough for routine clinical assay and can be used in detecting the possibility of viral infection.

A patient with a new variant of multiple sulphatase deficiency (MSDv) is reported. Unlike the usual type, onset was late and progress was slow. The phenotypic changes were those usually seen in multiple sulphatase deficiency but much milder. Cytoplasmic accumulations were found in skin fibroblasts, and urinary mucopolysaccharides and sulphatides were high. Arylsulphatases A, B and C (ASA, B and C), heparan N-sulphatase sulphoiduronate sulphatase, and N-acetylgalactosamine 6-sulphatase all had low activity in lymphocytes and cultured skin fibroblasts. Complementation for ASA activity was found in hybrids between MSDv and metachromatic leukodystrophy (MLD) as well as between multiple sulphatase deficiency (MSD) and MLD. Complementation for ASC activity was also seen in hybrids between MSDv and X-linked ichthyosis (XLI), and between MSD and XLI. However, neither ASA nor ASC activity increased in hybrid cells of MSDv and MSD. These results suggested that the mutations of MSDv and of MSD were allelic, although of different phenotypes.