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Single-photon absorptiometry (SPA), developed in 1963 and adapted for infants by Steichen et al. in 1976, is an important tool to quantitate bone mineralization in infants. Studies of infants in which SPA was used include studies of fetal bone mineralization and postnatal bone mineralization in very low birth weight infants. The SPA technique has also been used as a research tool to investigate longitudinal bone mineralization and to study the effect of nutrition and disease processes such as rickets or osteopenia of prematurity. At present, it has little direct clinical application for diagnosing bone disease in single patients. The bones most often used to measure bone mineral content (BMC) are the radius, the ulna, and, less often, the humerus. The radius appears to be preferred as a suitable bone to measure BMC in infants. It is easily accessible; anatomic reference points are easily palpated and have a constant relationship to the radial mid-shaft site; soft tissue does not affect either palpation of anatomic reference points or BMC quantitation in vivo. The peripheral location of the radius minimizes body radiation exposure. Trabecular and cortical bone can be measured separately. Extensive background studies exist on radial BMC in small infants. Most important, the radius has a relatively long zone of constant BMC. Finally, SPA for BMC in the radius has a high degree of precision and accuracy.

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The purpose of this study was to evaluate the adequacy of a soy protein-based formula versus a cow milk protein-based formula for body growth and skeletal mineralization in the first year of life. Thirty-six healthy, term, appropriate for gestational age infants were assigned randomly and prospectively to one of two feeding groups and observed longitudinally over the first year of life. Group 1 infants (n = 18) were fed soy protein isolate-based formula (Isomil with Iron); group 2 infants (n = 17) were fed a cow milk protein-based formula (Similac with Iron). All infants were given the formula within the first 24 hours of life, and were fed the study formula through the first year of life. Weight, length, and head circumference were recorded; bone mineral content (BMC) and bone width (BW) were measured at one-third distal length (midshaft) of the left radius and ulna during the first 18 days of life, and again at 6 weeks, and 3, 6, 9, and 12 months postnatally. Baby food was provided to all infants, and except for type of formula, food intake was similar for all infants. Weight, length, and head circumference were normal in all infants and not different between groups. BMC and BMC/BW were similar for both groups at entry into the study. Group 1 infants had significantly lower BMC and BMC/BW at 3, 6, 9, and 12 months of age (P less than 0.05 to P less than 0.0001) compared with group 2 infants, but their values were similar to those in previously studied infants receiving human milk with vitamin D supplementation. The long-term implication of differences in bone mineralization in early infancy for long-term skeletal mineralization remains to be determined.

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The response to aluminum loading from parenteral nutrition (PN) solutions was determined in 20 infants with gestational ages 29 to 41 weeks and birth weights 880 to 3630 gm. Mean duration of PN was 43 days (range 5 to 175 days). Ten infants received a high Al load (from an experimental high calcium- and phosphorus-containing PN solution, with a measured Al content of 306 +/- 26 micrograms/L (mean +/- SE), n = 11), for up to 6 weeks. Ten infants received a lower Al load (from standard Ca-P solutions, measured Al content 144 +/- 16 micrograms/L, n = 11). Five infants received PN with a low Al load for longer than 6 weeks. The mean urine Al/creatinine (Cr) ratio (micrograms/mg) increased threefold, from 0.3 +/- 0.09 to 0.97 +/- 0.17 during PN in the entire group (P less than 0.001), and was significantly higher in infants who received greater Al loading (P less than 0.001). There was no significant difference between preterm and term infants in the rate of change in urine Al/Cr during the study. Urine Al was calculated to account for less than 50% of Al load. During the study, serum Al concentrations ranged from 6 to 318 micrograms/L (median 37 micrograms/L, compared with the median 18 micrograms/L for normal infants and children). Serum Al concentrations were not significantly changed during the study, or between infants in high or lower Al loading groups. Vertebrae from autopsy of two infants who received the lower Al containing PN for 71 and 152 days, respectively, stained positive for Al at the bone mineralization front. Thus, currently used PN solutions are contaminated with Al, urine Al concentration is higher with higher Al loading, and is not different in term and preterm infants. We suggest that renal elimination of Al in infants is incomplete, as assessed by lower urine Al excretion versus load, elevated serum Al concentration, and bone deposition of Al.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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The effect of rapid or slow infusion of hypertonic sodium bicarbonate on acid-base balance and serum osmolality was studied in 36 acidotic newborn dogs. Respiratory acidosis and hypoxia were produced by mechanically fixed hypoventilation. One group of animals breathed 100% O2 to prevent hypoxemia. Rapid infusion of HCO3- in acidotic and hypoxic animals resulted in only a transient (1 minute) and small (0.05 pH units) elevation of arterial pH followed by a continuous fall, resulting in a lower pH and a worsened metabolic condition than in the nontreated controls. In nonhypoxic acidotic animals, rapid infusion of HCO3- had little effect on arterial pH. PaCO2 increased suddenly by 17 Torr in hypoxic and, by 13 Torr, in nonhypoxic animals. There was a concomitant fall in PaO2 (15 Torr). Serum osmolality rose rapidly after rapid infusion of HCO3-. Rapid infusion of hypertonic bicarbonate into an animal or infant whose ventilation is fixed thus results in a less than predicted elevation of arterial pH. PaCO2 rises, PaO2 falls, and serum osmolality rises. The net result may be a worsening rather than an improvement in the animals' metabolic state.

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