Cerebrospinal fluid protein concentrations in children: age-related values in patients without disorders of the central nervous system.

BACKGROUND: The published reference values for cerebrospinal fluid (CSF) total protein concentrations in children suffer from two major drawbacks: (a) the age-related range often is too broad when applied to the steeply falling concentrations in early infancy; and (b) no values have been published for widely used dry chemistry methods. METHODS: We conducted a 2-year retrospective survey of CSF results obtained in a children's hospital with a dry chemistry-based method set up on the Vitros 700 analyzer. RESULTS: The data related to ambulatory children up to 16 years of age and term neonates with no clinical or biological signs of brain disease (n = 1074). Seven age groups with significantly different CSF protein values were identified, and their age-related percentiles (5th, 50th, and 95th) were determined. On the basis of the upper 95th percentile, from age 0 to 6 months the CSF protein concentrations fell rapidly from 1.08 to 0.40 g/L. A plateau (0.32 g/L) was reached from age 6 months to 10 years, followed by a slight increase (0.41 g/L) in the 10-16 years age range. CONCLUSIONS: These results imply that CSF total protein concentrations in the pediatric setting, particularly in infants, must always be interpreted with regard to narrow age-related reference values to avoid false-positive results.

Skeletal growth in fetal rats. Effects of glucose and amino acids.

The modified hyperglycemia-hyperinsulinism hypothesis, which characterizes intrauterine growth of diabetic pregnancy, was studied in fetal rats. From day 19 to day 21 postconception, pregnant rats were constantly infused with saline, amino acids, or glucose. In the fetus, serum somatomedin activity was determined, with the porcine bioassay and the incorporation of 3H-thymidine into rib cartilage and isolated chondrocytes in vivo in response to serum from normal maternal or fetal rats. In comparison with control fetuses, body weights were decreased in glucose-exposed fetuses (4.66 +/- 0.25 versus 3.75 +/- 0.99, N = 121; P less than 0.001), and increased (4.87 +/- 0.57, N = 105; P less than 0.05) in amino acid-exposed fetuses. Serum somatomedin activity (U/ml) was higher in glucose-treated (0.79 +/- 0.40, N = 11; P less than 0.05) and amino acid-treated animals (0.90 +/- 0.16, N = 10; P less than 0.001) than in controls (0.55 +/- 0.04, N = 13). In vivo labeling with thymidine resulted in a higher radioactivity of cartilage in small fetuses compared with large fetuses when the dams had been infused with saline (r = -0.531, N = 56; P less than 0.001) or amino acids (r = -0.292, N = 52; P less than 0.01). Opposite results were obtained in hyperglycemic animals (r = 0.542, N = 54; P less than 0.001). When isolated chondrocytes were incubated with serum from normal fetal rats, the incorporation of thymidine was about 10 times higher into cells from small fetuses than from large fetuses, irrespective of the infusion regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Interrelationship of insulin and somatomedin activity in fetal rats.

The effects of glucose and glibenclamide on fetal body weight and fetal serum somatomedin activity were studied. From day 18 to day 20 post-conception, pregnant rats were continuously infused with saline or 40% glucose, which raised the maternal blood sugar to about 200 mg/dl. On day 21 of gestation, fetal body weight was not different, while fetal serum somatomedin activity was significantly elevated in the hyperlycemic animals. Glibenclamide, 1 mg/kg body weight, was injected on day 20 of gestation to the rat mother. The sulfonylurea crossed the placenta. A daily glibenclamide injection from day 16 to day 20 post-conception did not change the fetal body weight, but it significantly augmented the fetal serum somatomedian activity. The results suggest that insulin stimulated the generation of somatomedian activity in the fetus. Both insulin and somatomedian may act as fetal growth factors.