[Rickets of prematurity and its prevention].
Explore the source record for details and available documents.
Humans↗
Biomedical subjects
M Ala-Houhala
Publications and source records attributed to M Ala-Houhala.
Long-term anticonvulsant therapy and vitamin D metabolism in ambulatory pubertal children.
Parameters of calcium metabolism were thoroughly examined in 28 adolescents with long-term (over 6 years) anticonvulsant therapy (phenytoin, carbamazepine or combination) and in 10 normal controls in September and in March. The adolescents did not receive any vitamin D supplementation during the study. Serum calcium, inorganic phosphorus, parathyroid hormone and alkaline phosphatase levels in the anticonvulsant group did not differ from those of the control group. Serum 25(OH)D and 24,25(OH)2D levels were in all groups consistently higher in September than in March, but no seasonal variation was found in the 1,25(OH)2D levels in any group. The serum 25(OH)D levels in the phenytoin group in March were the lowest among the three groups treated with anticonvulsants, but the levels in the anticonvulsant groups did not differ significantly from each other or from the control group in the same season. The 24,25(OH)2D and 1,25(OH)2D levels in the anticonvulsant groups did not differ significantly from those of control group in September or in March. There was no correlation between anticonvulsant serum free fraction levels and vitamin D metabolites. The bone mineral content in the distal radius was not significantly decreased in the epileptic patients. In conclusion, the long-term anticonvulsant therapy did not induce the so-called "anticonvulsant rickets" in this ambulatory adolescent material. Our data do not indicate that anticonvulsant drugs alter significantly the vitamin D metabolism. Thus, routine vitamin D supplementation does not appear to be indicated in children on anticonvulsant therapy.
Adolescent↗
Maternal compared with infant vitamin D supplementation.
Vitamin D metabolites were studied in mother-infant pairs at delivery and eight and 15 weeks after that to evaluate the possibility of vitamin D supplementation of infant through the mother. Healthy mothers (n = 49) delivering in January received daily either 2000 IU (group 1), 1000 IU (group 2), or no (group 3) vitamin D. Their infants were exclusively breast fed, and those in group 3 received 400 IU of vitamin D a day. After eight weeks of lactation the infantile vitamin D concentrations were similar in groups 1 and 3 but significantly lower in group 2. The serum 24,25-dihydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations were also lower in group 2. The mean mineral, parathyroid hormone, and alkaline phosphatase values showed no intergroup differences at any point. No infants showed any clinical or biochemical signs of rickets, and their growth was equal. In conclusion, a daily postpartum maternal supplementation with 2000 IU of vitamin D, but not with 1000 IU, seems to normalise the vitamin D metabolites of breast fed infants in winter. Maternal safety with such supplementation over prolonged periods, however, should be examined.
Breast Feeding↗
Vitamin D status of children and adolescents in Finland.
3-,9- and 15-year-old children were studied in autumn in order to evaluate their serum 25-hydroxy-vitamin D (25-OH-D) concentration and their vitamin D intake. The 25-OH-D was significantly lower in the 15-year-old than in the other children, but it was satisfactory in all groups as compared to the 25-OH-D of healthy, young adults. The mean dietary vitamin D intake as well as the mean total vitamin D intake including supplements was low in all groups of children. With a vitamin D intake as low as in this study, every house-bound child would be at risk of vitamin D deficiency.
Adolescent↗
Serum levels of vitamin D metabolites, calcium, phosphorus, magnesium and alkaline phosphatase in Finnish women throughout pregnancy and in cord serum at delivery.
Serum concentrations of 25(OH)D, 24,25(OH)2D, 1,25(OH)2D, total calcium, protein, phosphorus, magnesium and alkaline phosphatase were measured in two groups of Finnish women throughout pregnancy and in cord serum at delivery. The autumn group delivered in August-September and the spring group in February-March. There was strong seasonal variation in the 25(OH)D concentrations in both groups. Maternal values (mean +/- s.d.) at delivery were 44.3 +/- 20.8 nmol/l in autumn and 26.0 +/- 13.0 nmol/l in spring. Fetal concentrations were 28.8 +/- 14.3 and 18.3 +/- 11.3 nmol/l, respectively. In both mothers and infants low 25(OH)D values were measured in winter. In the autumn group 7 out of 21 mothers (33 per cent) and in the spring group 17 out of 36 mothers (47 per cent) had values below 17 nmol/l, which is the lowest winter reference value recorded in our laboratory. No significant seasonal variation was observed in dihydroxylated vitamin D metabolites, although 24,25(OH)2D values were a little higher in summer than in winter. Concentrations of 1,25(OH)2D tended to rise towards delivery. Corrected calcium, magnesium and phosphorus concentrations did not change during pregnancy. Fetal calcium and phosphorus concentrations were significantly (P less than 0.001) higher than maternal ones. The data indicate that many mothers and infants have poor vitamin D status in the latitude of Finland. Our results support the concept that vitamin D supplementation should be considered in Finland for pregnant women at least in winter.
24,25-Dihydroxyvitamin D 3↗
25-Hydroxyvitamin D levels during breast-feeding with or without maternal or infantile supplementation of vitamin D.
Serum 25-hydroxyvitamin D (25-OHD), calcium, phosphorus, magnesium, and alkaline phosphatase levels of breast-fed infants and their mothers were studied by following 100 healthy term mother-infant pairs with different supplementation protocols of vitamin D. A pilot study in winter revealed that six of eight breast-fed infants without vitamin D supplementation had serum 25-OHD levels below the risk limit for rickets (5 ng/ml) at the age of 8 weeks. In the main study in winter groups, it was found that the 25-OHD levels were low (5.6 +/- 3.7 ng/ml) at the age of 8 weeks in the unsupplemented breast-fed infants, whose mothers were given vitamin D supplementation of 1,000 IU/day during lactation (group I), compared with the levels of those infants receiving either 400 (18.0 +/- 8.4 ng/ml, group II) or 1,000 IU (22.8 +/- 11.2 ng/ml, group III) vitamin D (group I vs. group II or III, p less than 0.001; group II vs. group III, NS). In group I 10 of 18 infants had serum 25-OHD levels less than 5 ng/ml compared with none of the infants in groups II and III. Yet the infants with 25-OHD levels less than 5 ng/ml showed no signs of clinical or biochemical rickets at the age of 8 or 20 weeks. In summer at delivery the maternal 25-OHD levels were good, but decreased thereafter. Also in summer groups, the infantile 25-OHD concentrations decreased; however, because the levels at delivery were high, they stayed in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Serum 25-hydroxyvitamin D levels in Finnish children aged 2 to 17 years.
Serum levels of 25-hydroxyvitamin D (25-OHD) in summer and winter were studied in 564 children aged 2-17 years living in the northern, central or southern parts of Finland. The mean levels of 25-OHD were significantly lower in winter (13.3 +/- 10.8 ng/ml) than in summer (27.2 +/- 10.3 ng/ml) in all age groups (p less than 0.001). The mean 25-OHD levels in the northern part of the country did not differ significantly from the others. In both seasons the levels of 25-OHD were lower in the 11-17 year age group than in younger children. In that age group 22.4% of the children had serum levels of 25-OHD below 5 ng/ml (the limit of risk for rickets), compared to 16.8% of children 6-10 years old and 7.5% of children 2-5 years old, but none of the children showed any laboratory evidence of rickets.
Adolescent↗
A method for routine estimation of vitamin D activity in human and bovine milk.
To estimate the antirachitic activity of human and bovine milk, we developed a modern biochemical method for determining vitamin D metabolites in milk. Vitamin D metabolites were assayed from milk whey and from whole milk. Milk whey yielded poor recovery of both endogenous and added vitamin D, suggesting a marked loss of vitamin D activity to milk fat during homogenization and separation of the milk whey. A method for assaying the vitamin D metabolites in whole milk involves 1) lipid extraction, 2) cold methanol and ether precipitation, 3) alkaline backwash to reduce the amount of interfering lipids, 4) an efficient reverse-phase preparative purification, 5) an additional silica purification for vitamin D, 6) an analytical high-performance liquid chromatography, and 7) separate sensitized protein-binding assays for vitamin D and 25-hydroxyvitamin D. The method for whole milk resulted in good recovery of added vitamin D, and levels of assayed metabolites and their calculated antirachitic activity agreed well with earlier reports, that is, about 10-50 IU of vitamin D activity per liter.
Animals↗
Cholic acid, chenodeoxycholic acid, alpha-1-fetoprotein and alpha-1-antitrypsin serum concentrations in breast-fed infants with prolonged jaundice.
Thirteen breast-fed one-month-old infants with prolonged jaundice not due to known causes were included in this study. All infants were investigated at one and twelve months of age. Serum concentrations of total (TB) and conjugated bilirubin (CB), aspartate (ASAT) and alanine aminotransferase (ALAT), alkaline phosphatase (AP), alpha-1-antitrypsin (alpha-1-AT), alpha-1-fetoprotein (AFP) and the two primary bile acids; cholic (CA) and chenodeoxycholic acid (CDCA) were determined at both ages. The Pi-phenotype of alpha-1-AT was determined at the age of twelve months. The serum concentrations of TB, CB, AP and AFP were elevated at the age of one month but were normal at the age of twelve months. No changes in the serum concentrations of ASAT or ALAT were observed between one and twelve months of age, and the values were within the reference ranges. The serum concentrations of alpha-1-AT were within the reference range at both ages. Two infants were heterozygous for MZ, and they had normal serum alpha-1-AT concentrations. The serum concentrations of CA and CDCA were elevated at the age of one month and were still significantly elevated at the age of twelve months indicating that the infants had slight cholestasis at the age of one month, and that the cholestasis had largely subsided by the end of the first year of life.
Alanine Transaminase↗
Chronic lung damage caused by adenovirus type 7: a ten-year follow-up study.
Twenty-seven children aged 0.6 to 7.0 (mean 2.1) years were admitted to the hospital in 1967 and 1968 with type 7 adenoviral pneumonia. All ran a prolonged course. Type 7 adenovirus was isolated from 14 children, and in the other 13, the rise in the titer of complement-fixing antibodies to adenovirus was fourfold or greater. The outcome of the disease in these 27 children was reassessed in 1979, 9.6 to 12.1 (mean 10.7) years after the adenovirus type 7 pneumonia. Twenty-two were examined clinically and roentgenographically and all had lung function tests. Twelve had abnormal chest roentgenograms, and of these, six had bronchiectasis. Six of the ten children with normal chest x-ray films and ten of the 12 with abnormal chest roentgenograms had abnormal pulmonary function tests. Of the six patients with bronchiectasis, four showed no discernible cause of bronchiectasis other than the antecedent type 7 adenoviral infection. The other two patients had bronchial asthma, which can be a risk factor for bronchiectasis.
Acute Disease↗
Peritoneal dialysis in children under 5 years of age.
OBJECTIVE: We report our experience with maintenance peritoneal dialysis (PD) in small children. DESIGN: This is a retrospective analysis of the patient records of all children under the age of 5 years treated with continuous peritoneal dialysis (CPD) between 1986 and 1994 in Finland. SETTING: Treatment was started and the patients were seen at the outpatient clinic at the Hospital for Children and Adolescents, University of Helsinki, every 3 months. Between these visits, they had controls at their local hospital every 2-4 weeks. PATIENTS: The most common primary renal disease in these 34 patients was congenital nephrotic syndrome of the Finnish type (27 patients). Others were: congenital nephrotic syndrome (3 patients), polycystic kidney disease (1), urethral valve (1), neuroblastoma (1), and renal dysplasia (1). RESULTS: Mean age at onset was 1.6 years and median treatment time 9.3 months. Time spent in hospital decreased from 270 days/year in the 1980s to 150 days/year in the 1990s. Two children died (5.9%). The peritonitis rate on continuous cyclic peritoneal dialysis was 1:11.5 patient-months. Hernias were diagnosed in 29% of the patients. After 3 months half of the patients were on antihypertensive medication. Pulmonary edema was diagnosed once in 12 patients and twice in 2 patients. During the first 6 months on PD the mean height standard deviation score (hSDS) increased from -2.13 to -1.66 (p < 0.0001). The 6-month change in hSDS before initiation and 6 months after the start of CPD increased from -0.12 +/-0.68 to +0.59 +/- 0.64 (p = 0.0008). CONCLUSIONS: Our results indicate that peritoneal dialysis is feasible and safe in small children. Mortality was low and growth was good. The major challenges presented by CPD therapy were maintenance of optimal nutrition, avoidance of peritonitis, and control of volemia.
Age of Onset↗