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Biomedical subjects

M Raad

Publications and source records attributed to M Raad.

3 recordsLinked to original sources
PubMed1990

Inorganic sulfate metabolism in the very low birthweight infant.

The effect of vitamin D supplementation on inorganic sulfate metabolism was examined in very low birth weight (less than 1,500 g) infants at biweekly intervals after birth until 6 weeks of postnatal age. Baseline serum sulfate concentrations were significantly higher in all infants (471 +/- 24 mumol/l, n = 80) than in adults (299 +/- 25 mumol/l, n = 17). In controls, the levels did not change significantly over the ensuing 6 weeks, although serum creatinine declined. Urinary sulfate excretion rose significantly to near adult levels by 2 weeks. Both urine and serum sulfate were correlated with weight gain but not with estimated glomerular filtration rate, suggesting that factors other than renal clearance have a preponderant influence on serum sulfate in these infants. At 6 weeks, the mean serum sulfate in the high-dose group (receiving 2,170 +/- 23 U/day of vitamin D, n = 41) was significantly higher than in controls (receiving 360 +/- 22 U/day, n = 40). In all infants, there was a significant correlation (r = 0.36, p less than 0.001) between serum sulfate and 25(OH)-vitamin D concentrations, but not other analytes or clinical variables, suggesting that vitamin D may be one of the factors modulating sulfate metabolism in the newborn period.

Creatinine↗
PubMed1979

Oculodento-osseous dysplasia: heterogeneity or variable expression?

Oculodento-osseous dysplasia (ODOD) has been recognised in three South African patients from two kindreds of Dutch descent. Their ocular, nasal, dental and digital stigmata resembled those of previously reported cases, but their cranial hyperostosis and mandibular overgrowth were of much greater degree. In addition, the two survivors had serious neurological complications consequent upon spinal cord compression at the base of the skull and calcification of the basal ganglia. Two of the patients were the product of marriages between a pair of brothers and a pair of sisters, who were themselves clinically normal. This situation is best explained by autosomal recessive inheritance. As ODOD is usually transmitted as an autosomal dominant, and in view of the unusual severity of the manifestations in our patients, it is possible that the condition is heterogeneous and that they had a distinct autosomal recessive form of the disorder. The presence of minimal stigmata in the mother and two prior generations of our third patient could be equally well interpreted as representing great variation in phenotypic expression of a single dominant gene or manifestation in a heterozygote for a recessive gene.

Abnormalities, Multiple↗