In 1988 and in 1991, i.e. two and five years after the introduction of a general iod salt supply (32 mg KJO2/kg salt) in our region, we investigated the frequency of goiters and the level of iodine excretion in urine in 504 and 336 school children of 11 to 16 years of age. In 1988 the assessment of goiter size was made by inspection and palpation according to the recommendation of WHO. 36% of the school children were found to have goiters of type I b or II. The average urine excretion of iodine amounted to 46.2 +/- 37.2 micrograms Iod/g creatinine (n = 353). In 1991 we selected school children with goiters by the same criteria and found frequency (34%) to be nearly unchanged compared to 1988. Furthermore we investigated these goiters with ultrasound and confirmed the diagnosis in 100 from 107 children. The average daily urine excretion of iodine was significantly higher in 1991 (57.7 +/- 24.8 micrograms/Iod/g creatinine, n = 328) than in 1988. However this value is below the level recommended by the WHO (minimum 75 micrograms Iod/g creatinine). Despite the increase of the iodine intake over the last years, the frequency of goiters in pubertal school children in the Jena region is endemic. This fact supports the demand for a general and sufficient iodine supply.

Adolescent↗

PubMedDate not supplied

Nephrocalcinosis, hypercalciuria and elevated serum levels of 1,25-dihydroxyvitamin D in children. Possible link to vitamin D toxicity.

Ten children age 1 1/2 to 14 years, had bilateral nephrocalcinosis and hypercalciuria, but normal serum calcium (Ca) and phosphate (P) concentrations. Patients with hypercalciuria were divided into absorptive (n = 4) and renal (n = 6) subgroups, and in the latter four patients had a primary Ca-leak and two had a P-leak. All the children had received intermittent high dose vitamin D prophylaxis during infancy. At the time of investigation all had normal serum levels of 25-hydroxyvitamin D, yet all but one had elevated values of 1,25-(OH)2D. Although the hypercalciuria was indistinguishable from the various known forms of idiopathic hypercalciuria, the previous clinical course and the pattern of bone mineral homeostasis suggest that both clinical features, namely nephrocalcinosis and hypercalciuria were related to vitamin D toxicity through various pathogenetic pathways.

Adolescent↗