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Background: The bone mineral content of premature infants at term is lower than in mature infants at the same postconceptional age. Serum alkaline phosphatase and serum phosphate are often used [...]

The incidence, sex, seasonal and geographical patterns of juvenile-onset insulin-dependent diabetes mellitus (j.i.d.m.) were studied retrospectively on one third of the Danish population 1970–1974. The j.i.d.m. incidence remained fairly constant during the study period, the average being 13.2 per 100000 per year. The total number of boys exceeded the number of girls by 27 per cent. A marked peak of incidence was found at 12–14 years, earlier for females than for males. A seasonal variation in onset (diagnosis) of j.i.d.m. was observed with the lowest number of new cases in May–July. The j.i.d.m. incidence seemed to show socioeconomic differences, being highest in those parts of the survey area with lower status.

The local cerebral vascular response to hyperventilation vas investigated in five distressed, intubated infants by means of a T2* sensitive gradient-echo MRI technique at 1.5 T. In one preterm infant, the MR signal change during hyperventilation was sparse. In four term infants, the mean MR signal of the brain slice investigated decreased by 1.2–2.6% per kPa change inPCO2 as a reflection of decreased cerebral blood flow during hyperventilation. Pixel-wise analysis revealed absence of vascular response in the basal ganglia, the thalamus or in the occipital region. In two adult controls, who hyperventilated voluntarily, the vascular reactivity was homogeneously distributed predominantly over the grey matter. The experiments demonstrate that local impairment of vascular CO2 reactivity in the distressed infant brain can be detected by T2* sensitive gradient-echo MRI, which is also known as functional MRI.

In attempt to improve bone-mineralization and prevent the occurenoe of fractures, 2 infants with congenital osteogenesis imperfecta were treated, within the same period of time, with Salmon-Calcitonin 12–15µU/kg/wk. Treatment was given in two 6 months periods with a period of 6 months in between without treatment. Furthermore at the end of the last period HGH was added to the course (2mg HGH daily/10 days). The daily retention of calcium and phosphate was measured while the patients were on a fixed diet. Furthermore the excretion of hydroxyproline in urine was determined. In the first period of treatment there was a marked increase in calcium and phosphate retention, mostly in the first. A significant decrease in hydroxyproline excretion took place within the first month. In the period without treatment the calcium and phosphate retention decreased initially to pre-treatment values while at the end of this period an increase in retention was observed, which reached the same levels as seen under treatment. In the second period of treatment no further change in calcium or phosphate retention was seen. When HGH was added a marked decrease in retention was noted. The hydroxyproline excretion did not change significantly in the last two periods Conclusion: Treatment with calcitonin results in an increased phosphate and calcium retention and affects collagen turnover as demonstrated in the first period. The observations in the last period-may be explained by formation of calcitonin antibodies, compensatory mechanisms in mineral-metabolism or changes in absorption. No change in the occurence of fractures has hitherto been noticed.

18 boys and 12 girls with diabetes (average duration of diabetes: 4.4 years, average age: 11.1 years with age at diagnosis: 5.9 years) were studied over a 3 year period. SM was measured on 3 or 4 occasions with chick-bioassay. GH was measured with a previously reported RIA method. All children were within normal range for height although the majority was below the 50% percentile. The average retardation in bone age was about 1 year. Average SM activity was for the group as a whole 0.87 ± 0.21 U/ml (normal range 1.0 ± 0.19 U/ml). This was not related to duration of diabetes, regulation or age at diagnosis. Children with long-standing diabetes or with diagnosis at time of puberty had SM values of 1.06 ± 0.28 U/ml and 1.15 ± 0.16 U/ml respectively, most likely related to pubertal growth. Low values were found in a newly diagnosed patient (0.30 U/ml) and in 3 patients with the most pronounced growth retardation (0.48 ± 0.10 U/ml). GH in urine was slightly increased in the group with long standing diabetes due to change in glomerulo-tubular function or increased secretion. If increased levels of GH persist this does not result in increased SM levels reflecting a central role of insulin in SM generation.

In 27 IRDS infants and 52 healthy babies blood was collected 1-2 times weekly until 30 days of life. During the first 2 days of life se-TSH was lower in IRDS than in healthy babies. Se-T4 and -T3 were low in IRDS and decreased to minimal levels by day 3-5. Se-T3 increased to normal levels by day 6-10, and se-T4 by day 21-30. Se-TBG was low in IRDS reaching normal levels during recovery. Se-TBPA and se-Alb levels were normal, but se-TBPA increased and exceeded significantly TBPA-levels of healthy babies by day 11-20. The T4/TBG ratio was low during recovery from IRDS.The low se-T4 and se-T3 values in IRDS are associated with a reduced TSH stimulation and a low se-TBG in the acute stage. During recovery, a decreased saturation of se-TBG and, possibly, an increased T4 to T3 coversion occur.

AIM: To determine the diagnostic potential of magnetic resonance imaging (MRI) in neonatal seizures; to elucidate the aetiology, timing, and prognosis of the cerebral lesions detected. METHODS: Thirty one term neonates with clinical seizures underwent ultrasonography between days 1-7 (mean 2.5 days) and a high field spin-echo MRI scan on days 1-30 (mean 8.1 days), both of which were repeated at 3 months of age. Routine investigation excluded, as far as possible, infection, haematological, and metabolic-toxic causes as causes of the neonatal seizures. RESULTS: Brain abnormality was demonstrated by MRI in 68% of infants and ultrasonographically in 10%. Diffuse brain lesions (present in 29%) were associated with high mortality (58%) and morbidity (42%), whatever the aetiology. In contrast to a better short term prognosis for neonates with focal lesions where no infants died, 33% had a handicap, and the rest were normal at a mean follow up age of 2 1/2 years. Cerebral lesions were presumed to have antepartum origin in 43% of cases. Seizure aetiology was considered to be hypoxic-ischaemic in 35%, haemorrhagic in 26%, metabolic disturbances and cerebral dysgenesis in 16% and unknown in 23%. CONCLUSIONS: MRI detected a remarkably high incidence of brain lesions in neonatal seizures. Almost half of these were of prenatal origin and pathogenesis may essentially be attributed to hypoxic and/or haemodynamic causes.

A total number of 103 fullterm (FT), 47 small-for-gestational age (SGA) and 35 preterm (PT) babies were studied from day 1–8 after birth. In FT a surge of TSH was invariably seen, followed by a decrease until normal adult levels were reached on day 2–4 after birth. Serum T4and -T3, concentrations were higher than in adults, significantly correlated and decreased by 30 and 40% respectively from day 2 to 8 after delivery. In SGA the postnatal TSH hypersecretion was more variable. Serum T4and -T3, concentrations were significantly correlated and lower than in FT. Serum T4decreased insignificantly and serum T3seemed to increase during the first week of life. In PT the postnatal TSH increase was highly variably. Serum T4and -T3were lower than in FT and did not change significantly during tne study period; serum T3tended to increase. Birth weight as well as gestational age were correlated with the thyroid hormone concentrations. In babies with gestational age of more than 34–36 weeks normal serum T4and T3concentrations were often observed.It is concluded that the postnatal pituitary-thyroid hyperfunction may be subnormal in SGA and PT babies. If serum TSH concentration is not measured in screening for congenital hypothyroidism these babies may appear as false positives.

The pathogenesis of McCune-Albright Syndrome involving bone, skin, and endocrine organs remains unknown. The syndrome might be associated with dysfunctions of the hematopoietic system. A girl with severe polyostotic fibrous dysplasia and vaginal bleedings from 3 months of age is presented. The concentration of serum T3was increased from the age of 13 months but se-T4was normal. A T3-thyreotoxicosis was diagnosed at the age of 3½ years (no TSH response to TRH). Aged 3½ years she developed severe anemia, thrombocytopenia and splenomegalia. Bone marrow biopsy showed myelofibrosis. Following splenectomi the hemoglobin concentration increased and the platelet count was normalized. The patient was treated with medroxyprogesterone-acetat (MPA) during the first 3 years of life and with propylthiouracil (PTU) from the age of 3½ years. The myelofibrosis developed before unset of PTU, excluding any causal relationship. Nor the myelofibrosis seems to be associated with MPA since no such side effect of MPA is known, and the only patient previously reported with McCune-Albright syndrome and myelofibrosis was not treated this way.