[Evaluation of the measurement of capillary glucose concentration versus plasma glucose in the newborn]. / Fiabilité de la mesure de la glycémie capillaire par rapport à la glycémie plasmatique chez le nouveau-né.

BACKGROUND: The reliability of blood glucose monitoring in neonatology is not always confirmed. The aim of this study was to evaluate the reliability of blood glucose measurements made with three different devices in newborns. PATIENTS AND METHODS: The study was prospective, conducted in a medical and neonatal intensive care department over a period of 4 months. Capillary glucose level was measured with three different glucometers and compared with venous glucose level determined using the hexokinase method. An ANOVA and Scheffe test were used for the correlation analysis. RESULTS: Three hundred and nine infants were included, with a mean age of 55h and a mean term of 39 weeks of gestation. Mean blood glucose in the laboratory was 0.62±0.15g/L, 0.71±0.17g/L for Accu-Chek(®) Active, 0.80±0.17g/L for Accu-Chek(®) Performa, and 0.83±0.12g/L for Bionime. An ANOVA showed statistically significant differences between the measurements made by glucometers compared to the reference blood glucose levels, and the Scheffé method showed that glucometers overestimated the real plasma glucose levels. CONCLUSION: None of the devices used in this study was satisfactory. However, an estimation of blood glucose taking into consideration this numerical overestimation would allow early detection of hypoglycemia.

Sanjad-Sakati syndrome in a Tunisian child.

Sanjad-Sakati syndrome (SSS) (OMIM 241410) is a rare autosomal recessive disorder characterized by congenital hypoparathyroidism with growth and mental retardation associated with seizures and a characteristic physiognomy. SSS molecular pathology has been shown to be due to mutations in the TBCE gene on chromosome 1q42-q43. All affected patients of Arab origin are homozygous for a 12-bp (155-166del) deletion in exon 3 of this gene. We report on a Tunisian child with SSS who was homozygous for the 155-166del mutation. Our findings provide additional support of the common (155-166del) deletion founder effect in exon 3 of the TBCE gene in Arab patients. It is very likely that this mutation originated in the Middle East and was introduced in Tunisia by the Banu Hilal invaders.