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Biomedical subjects

J J Steichen

Publications and source records attributed to J J Steichen.

At least 37 records · Page 2Linked to original sources
PubMed1983

Optimal timing for diagnostic cranial ultrasound in low-birth-weight infants: detection of intracranial hemorrhage and ventricular dilation.

Intracranial hemorrhage and posthemorrhagic ventricular dilation are common problems in small preterm infants. To determine the optimal timing for ultrasound diagnosis of these abnormalities, we studied 64 preterm infants (less than 1,500 gm) by sequential cranial ultrasonography from birth until one year of age or until death. The optimal timing for ultrasound diagnosis of intracranial hemorrhage is days 4 to 7 with follow-up at day 14. The most efficient time for ultrasound examination to diagnose ventricular dilation was day 14 with follow-up at 3 months. Intracranial hemorrhage was diagnosed by ultrasound in 35 of the 64 patients (55%). In 18 of the 64 infants (28%) significant ventricular dilation was diagnosed by ultrasound during the first three months.

Cerebral Hemorrhage↗
PubMed1983

Decreased bone mineral content in small-for-gestational-age infants compared with appropriate-for-gestational-age infants: normal serum 25-hydroxyvitamin D and decreasing parathyroid hormone.

Bone mineral content was determined by photon absorptiometry, adapted for use in neonates, in 23 small-for-gestational-age (SGA) infants of 31 to 42 weeks of gestational age, for 12 weeks. At birth, term SGA infants had lower bone mineral content than term appropriate-for-gestational-age (AGA) infants; postnatal increase in bone mineral content was slow and lagged significantly behind that of term AGA infants. Preterm SGA infants had bone mineral content that was similar to that of preterm AGA infants at birth; postnatal bone mineral content was similar to that of preterm AGA infants, but was decreased compared with the expected intrauterine bone mineral content. Serum 25-hydroxyvitamin D concentrations and parathyroid hormone levels were the same for SGA and AGA infants. Serum 25-hydroxyvitamin D concentrations decreased slightly with postnatal age and remained within normal limits. Serum parathyroid hormone concentrations decreased in both SGA and AGA infants and reached undetectable levels at 10 to 12 weeks of age.

25-Hydroxyvitamin D 2↗
PubMed1982

Calcium and phosphate supplements in breast milk-related rickets. Results in a very-low-birth-weight infant.

Rickets developed in a very-low-birth-weight infant fed exclusively human milk. Serum 25-hydroxyvitamin D concentration was normal, and serum 1,25-dihydroxyvitamin D level was elevated; parathyroid hormone and calcitonin levels were normal. Rickets responded to supplements of calcium and phosphate, as determined by roentgenograms and measurement of bone mineral content by direct photon absorptiometry. Human-milk feeding in very-low-birth-weight infants requires observation for hypophosphatemia and clinical and radiological signs of rickets. In such infants, it may be necessary to supplement breast-milk feeding with calcium and phosphate.

Bone and Bones↗
PubMed1982

Mineral homeostasis during lactation- relationship to serum 1,25-dihydroxyvitamin D, 25-hydroxyvitamin D, parathyroid hormone and calcitonin.

During lactation maternal losses of calcium and phosphorus through human milk average 220 to 340 and 110 to 170 mg/day, respectively. The present study reports maternal serum concentrations of vitamin D metabolites, parathyroid hormone, calcitonin, calcium, magnesium, and phosphorus during the first 6 months of lactation. Serum calcium and magnesium concentrations increased during the first 6 months of lactation. Serum 1,25-(OH)2 vitamin D was increased at 6 months of lactation compared to values in nonpregnant nonlactating controls. During this same period, serum parathyroid hormone decreased slightly and serum calcitonin remained unchanged. Our data do not support the observation that lactation represents a state of physiological hyperparathyroidism. On the contrary, our results suggest that lactating women are able to adequately compensate for the losses of calcium and phosphorus during the early months of lactation, although increased serum 1,25-(OH)2 vitamin D concentrations may be necessary to maintain calcium homeostasis with lactation beyond 6 months.

Calcifediol↗
PubMed1982

Effects of increased calcium, phosphorus, and vitamin D intake on bone mineralization in very low-birth-weight infants fed formulas with Polycose and medium-chain triglycerides.

The ideal postnatal rate of bone mineralization in preterm infants is unknown. In this study the effect of a new formula on bone mineralization in very low-birth-weight infants (28 to 32 weeks' gestation) was studied using infant-adapted direct photon absorptiometry. The 81 calories/dl experimental formula (Similac Special Care) contained 50% of the carbohydrate as Polycose, 50% of the fat as medium-chain triglycerides, and a whey:casein protein ratio of 60:40. It also contained large amounts of calcium (140 mg/dl), phosphorus (75 mg/dl), and vitamin D (120 IU/dl). Over a three- to five-week period, bone mineralization increased in two-thirds of the infants and decreased in the remainder, but all values remained in the range expected for bone mineral content in utero. Serum calcium, phosphate, magnesium, alkaline phosphatase, 25-hydroxy-vitamin D, and parathyroid hormone concentrations remained stable, whereas calcitonin concentrations fell.

Bone and Bones↗
PubMed1981

Elevated serum 1,25 dihydroxyvitamin D concentrations in rickets of very low-birth-weight infants.

Elevated 1,25 dihydroxyvitamin D concentrations were found in five VLBW infants who developed rickets at two to three months postnatal age or term postconceptual age; 25 hydroxyvitamin D concentrations were low. Bone mineralization was found to be extremely low as measured by infant-adapted direct photon absorptiometry. After treatment with a formula supplemented with additional Ca and P, there was a rapid improvement in bone mineralization with a concomitant decrease of 1,25(OH)2D to normal adult values, whereas 250HD values increased and parathyroid hormone values decreased. In the VLBW infants studied, we suggest that rickets may be caused by Ca and P deficiency rather than by a deficiency of vitamin D metabolism.

Calcitriol↗
PubMed1981

Bone mineral content and serum 25-hydroxyvitamin D concentration in breast-fed infants with and without supplemental vitamin D.

Eighteen term, healthy, appropriate for gestational age, breast-fed infants were studied in a double-blind prospective study to determine whether or not supplemental vitamin D affected bone mineralization. All patients were from a single, private pediatric practice. Nine infants were randomly assigned to a vitamin D supplement of 400 IU/day and nine infants to a placebo. By 12 weeks of age, infants receiving placebo had a significant decrease in bone mineralization and in serum 25-hydroxyvitamin D concentrations compared to the vitamin D-supplemented group. It is not known whether or not the increased BMC at 12 weeks of age in vitamin D-supplemented breast-fed infants is of ultimate value. Supplemental vitamin D may be necessary for optimal bone mineralization in term breast-fed infants. A longer follow-up study and additional analyses are required to make conclusive statements.

25-Hydroxyvitamin D 2↗
PubMed1980

Vitamin D homeostasis in the perinatal period: 1,25-dihydroxyvitamin D in maternal, cord, and neonatal blood.

To investigate vitamin D homeostasis in term pregnancy, we measured 1,25-dihydroxyvitamin D (1,25(OH)2D) in serum samples from 19 term pregnant women and in samples from the placental veins of their infants. Samples were obtained from 14 neonates at 24 hours of age. At delivery, maternal concentrations of 1,25(OH)2D were elevated above normal adult values; placental-vein concentrations in the infants were significantly lower than adult normal or maternal values and bore no relation to maternal values. By the time the infants reached 24 hours of age, their serum concentrations had reached normal adult values, concomitant with a decrease in serum concentration of ionized calcium. We speculate that low 1,25(OH)2D concentrations in utero suggest that there is no need for intestinal calcium absorption in the fetus. Postnatal increase of 1,25(OH)2D may result from its production as a prerequisite to extrauterine requirements for intestinal absorption of calcium and phosphorus.

Adult↗
PubMed1980

Neonatal hypermagnesemia: effect on parathyroid hormone and calcium homeostasis.

Twenty pre-eclamptic mothers treated with MgSO4 and their newborn infants were studied prospectively to determine the clinical and biochemical effects of hypermagnesemia. Maternal serum magnesium concentration rose to 4.4 mg/dl at delivery and was accompanied by a fall in maternal serum calcium concentration during labor. Neonatal serum Mg concentration remained elevated for the first 72 hours of life (mean at 72 hours = 3.0 mg/dl). Serum Mg concentration was higher in premature infants and in babies with birth asphyxia and/or hypotonia. Serum Ca concentration was higher and serum PTH was lower in hypermagnesemic study infants when compared to a retrospectively selected, matched froup of control infants. We speculate that elevated serum Mg values in these infants result in a shift of Ca from bone to plasma, and that elevated Mg and Ca concentrations further suppress neonatal parathyroid function.

Calcium↗
PubMed1980

Osteopenia of prematurity: the cause and possible treatment.

By photon absorptiometry, extrauterine bone mineralization in low-birth-weight infants fed a standard commercial formula lags significantly behind intrauterine bone mineralization. In the present study, infants of 28- to 32-week and 33- to 35-week gestational age were studied. The calcium content in a standard formula was increased to provide a daily calcium intake of 220 to 250 mg/kg/day. Phosphate intake was 110 to 125 mg/kg/day. Extrauterine bone mineralization by photon absorptiometry appeared to approximate the intrauterine bone mineralization rate.

Bone Diseases↗
PubMed1979

1,25-Dihydroxyvitamin D3 in childhood hepatic osteodystrophy.

Osteodystrophy frequently accompanies severe childhood hepatobiliary disease. Proposed causes include malabsorption of vitamin D and calcium, and diminished 25-hydroxylation of vitamin D. Two children, ages 23 and 35 months, with radiographic and biochemical evidence of rickets with extrahepatic biliary atresia, were treated with 1,25-dihydroxyvitamin D3. The minimal effective therapeutic dose and efficacy of 1,25-(OH)2D3 in the treatment of rickets associated with severe childhood hepatic disease were determined. Oral 1,25-(OH)2D3 was ineffective at doses of 0.10 microgram/kg/day. Parenteral doses of 0.20 microgram/kg/day effectively produced radiographic, bone mineral (photon absorptiometric), and biochemical evidence of healing. The need for four times the physiologic dose of 1,25-(OH)2D3 by the parenteral route suggested enhanced catabolism of, or end-organ resistance to, 1,25-(OH)2D3 in our patients with severe cholestatic liver disease treated with phenobarbital.

Bile Ducts↗
PubMed1979

Bone mineral content in term and preterm appropriate-for-gestational-age infants.

Photon absorptiometry adapted for use in small infants was utilized to measure bone mineral content in 42 term and 30 perterm appropriate-for-gestational-age infants. BMC at birth correlated significantly with gestational age and birth weight. Sequential measurements of BMC in premature infants during the first three months showed that the postnatal increase in BMC was significantly less than the BMC expected in utero. We speculate that decreased intake of calcium and phosphate effects postnatal bone mineralization in premature infants.

Birth Weight↗