Enamel defects were commoner in preterm children, and post-natal dietary intervention had no effect on their frequency. This is the first study in which enamel defects in both primary and permanent teeth have been studied in the same group of preterm children. At age 1 and 2 yrs, 32 preterm children were examined, and the same group was examined again at 9-11 yrs. As controls, 106 healthy children were examined at 1 and 2 yrs, and 64 of them were randomly selected for comparison. When the preterm children were aged 9-11 yrs, 64 of another group of 150 10-13 yr-olds were randomly chosen as controls. All were examined by the main author. At 2 yrs, 66% of preterm children had enamel hypoplasia, and 2% of controls (P < 0.001); enamel opacity affected respectively 13% and 19% (NS). However, the proportions of teeth thus affected were respectively 16% and 0.1%, and 13% and 4%. In the permanent dentition around 10 yrs later, 38% of preterm children had hypoplasia, and 11% of controls (P < 0.01), and opacity affected respectively 47% and 25% (P < 0.05). All preterm infants had primary dentition enamel defects, and 72% also had permanent dentition defects. The preterm infants had been randomly assigned to 2 levels of vitamin D supplementa-tion up to age 6 months, and to breast milk with or without a supplement of calcium and phosphorus until reaching a weight of 2kg. These supplements had no apparent effect on enamel defects.

Although idiopathic cardiomyopathies are prognostically important and are a common indication for cardiac transplantation in all age groups, the incidence and age distribution of idiopathic cardiomyopathies in a well-defined pediatric population have been poorly characterized. A retrospective study was carried out in Finland in 1980-1991 to obtain information on the epidemiology of childhood cardiomyopathies. The medical records of all patients aged birth to 20 years with cardiomyopathy from the five university hospitals and 16 central hospitals covering the entire country were reviewed. Moreover, data on causes of death from the Finnish National Census Bureau were examined. Of the 808 potential cases screened, 118 infants, children, and adolescents, representing an average age-specific population of 1.4 million, were definitely identified as having idiopathic cardiomyopathy. The average annual occurrence of new cases was 0.65 per 100,000 population (95% confidence interval (CI) 0.53-0.79). If the 15 cases diagnosed only after death during the 12-year study period were included, the occurrence increased to 0.74 per 100,000 population per year. Fifty-six new cases of dilated cardiomyopathy and 40 new cases of hypertrophic cardiomyopathy were diagnosed during the study period, giving average annual occurrences of 0.34/100,000/year (95% CI 0.26-0.44) and 0.24/100,000/year (95% CI 0.17-0.33) for new cases of dilated and hypertrophic cardiomyopathies, respectively. At the end of 1991, the prevalence of dilated cardiomyopathy was 2.6/100,000 (95% CI 1.8-3.6) and that for hypertrophic cardiomyopathy was 2.9/100,000 (95% CI 2.0-4.0). The number of new cases of dilated cardiomyopathy per year increased over the study period, whereas the annual occurrence of hypertrophic cardiomyopathy remained relatively constant. Marked variability was seen in occurrence among the different age groups of children with dilated cardiomyopathy, suggesting that different pathophysiologic mechanisms, and possibly etiologies, may exist in different age groups.

Factors contributing to the duration of a single convulsive seizure > 5 minutes were analyzed in 157 children. The medically treated episodes were compared with seizure episodes resolving without treatment (n = 27). Major differences were in age (p = 0.016) and etiology (p = 0.003), and the association between treatment delay and response became significant after 30 minutes when this was analyzed as a single variable (p = 0.003) in Cox regression analysis.

Metabolic bone disease is recognized with increasing frequency in very-low-birth-weight infants. Radiological changes characteristic of rickets have been found in 55% of infants with a birth weight of less than 1000 g and in 23% of infants weighing less than 1500 g at birth. Twenty-four per cent of infants with a birth weight of less than 1500 g have fractures. The main aetiological factor is insufficient phosphorus supplementation. The aetiology is, however, multifactorial and also includes calcium deficiency, vitamin D deficiency, certain drugs, aluminium loading and immobilisation. The method of choice in detecting subclinical mineral bone disease of prematurity is measurement of bone mineral density, but there is as yet no single good diagnostic method available for premature infants. The optimal mineral and vitamin D requirement of the premature infant must be established so that proper recommendations can be given. The current recommended vitamin D dose in Europe (ESPGAN 800-1000 IU/day) is probably too high when extra minerals are supplied. Moreover, the duration of mineral supplementation may need to be continued until the infant has reached a body weight of 3.5 kg. This article deals with the aetiology, pathogenesis, diagnosis and future prospects of metabolic bone disease of prematurity.

A combination of the criteria "serum total alkaline phosphatase activity above 900 IU/l" and "serum inorganic phosphate concentrations below 1.8 mmol/l" yielded a sensitivity of 100% at a specificity of 70%. This was the best available screening method for low bone mineral density in preterms.