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Biomedical subjects

R C Tsang

Publications and source records attributed to R C Tsang.

At least 19 recordsLinked to original sources
PubMed1992

Prospective study of vitamin D supplementation and rickets in China.

To determine whether amounts of vitamin D lower than recommended doses are effective in preventing rickets, 256 term infants from two northern and two southern cities in China were studied in a randomized trial of vitamin D supplementation (100, 200, or 400 IU/day) during the first 6 months of life. Cord blood and 6-month blood samples were collected and radiographs were obtained at 3 to 5 days and at 6 months of age. Cord serum 25-hydroxyvitamin D concentrations were lower in the north than in the south (5 vs 14 ng/ml (12.5 vs 35.0 nmol/L); p less than 0.01). Wrist ossification centers were less likely to be present at birth in the northern children than in the southern children (p = 0.009) and were more likely to be present in infants born in the fall who had higher cord serum concentrations of 25-hydroxyvitamin D (p = 0.04). Serum 25-hydroxyvitamin D concentrations were lower in northern children 6 months of age than in southern children (p = 0.005) and were higher with an increasing supplemental dosage of vitamin D (p less than 0.001), particularly in infants in the north. None of the infants had rickets at 6 months of age. Because of the low serum 25-hydroxyvitamin D concentrations, especially among infants in the north, it may be prudent to supplement the diet with vitamin D at a dose of 400 IU/day.

China↗
PubMed1992

Effect of chronic maternal dietary magnesium deficiency on placental calcium transport.

Metabolisms of calcium (Ca) and magnesium (Mg) are closely interrelated in the intestine, bone, and kidney. Interaction of Ca and Mg at the placental level, however, is not well defined. The occurrence of decreased bone mineral content and hypocalcemia in infants of hypomagnesemic mothers led us to test the hypothesis that chronic dietary maternal Mg deficiency decreases placental Ca transport. On day 10 of gestation, 20 Sprague-Dawley rats were randomized to a Mg-deficient diet (3.3 mg/day, n = 10) or to a control diet (70 mg/day, n = 10). On day 20 of gestation (term = 22 days), intact placentas were perfused in situ through the umbilical artery and perfusate was collected through the umbilical vein. Calcium 45 (45Ca) and chromium 51-EDTA (51Cr-EDTA) (a diffusional marker for placental membrane integrity) were injected to the dam and steady state maternofetal clearance (Kmf45Ca, microliter/min/g placenta) of both isotopes were calculated. There was no difference in the clearance of 45Ca and 51Cr in both groups (55 +/- 10 vs 57 +/- 16 and 3.2 +/- 0.4 vs 3.6 +/- 0.4, respectively, mean +/- SEM). We conclude that, in the rat, placental Ca transfer is unaffected by chronic maternal dietary Mg deficiency. We speculate that Ca and Mg cross the placenta by independent mechanisms.

Animals↗
PubMed1992

Low bone mineral content in summer-born compared with winter-born infants.

Possible seasonal differences in newborn bone mineral content (BMC) have not been studied. Adult studies show seasonal variations with lower BMC in winter versus summer. Assuming that BMC variations may relate in part to vitamin D status, we hypothesized that newborn BMC would be lower in winter than summer. BMC of one third distal radius was measured in 55 healthy term newborns using a single beam photon absorptiometer [coefficient of variation (CV) for phantom standard 2.1%]. Infants were enrolled during summer (July-September, 1988) and winter (January-March, 1989) for a longitudinal nutrition study. Contrary to our hypothesis, there was a 12% lower BMC in summer versus winter (mean +/- SD 75.94 +/- 17.42 vs. 86.55 +/- 17.54 mg/cm, respectively; p = 0.035). The difference remained significant after controlling for possible race and gender effects (p = 0.02). We conclude that BMC is lower in summer- compared with winter-born infants. Since any seasonal effects on fetal bone are presumably related to effects through the mother, we speculate that if maternal vitamin D status influences fetal bone mineralization, the effect (possible sunshine deprivation in winter) may operate especially in early pregnancy, thus resulting in lower BMC, evident at birth in summer.

Black People↗
PubMed1992

d-Alpha-tocopheryl polyethylene glycol-1000 succinate enhances the absorption of vitamin D in chronic cholestatic liver disease of infancy and childhood.

Rickets and osteopenia, common problems in chronic childhood cholestasis, have been attributed to vitamin D malabsorption leading to reduced serum levels of 25(OH)-vitamin D. d-alpha-Tocopheryl polyethylene glycol-1000 succinate (TPGS), a water-soluble form of vitamin E, forms micelles at low concentration. We evaluated the potential role of TPGS in enhancing vitamin D absorption in eight children (aged 5 mo to 19 y) with severe chronic cholestasis (three extrahepatic biliary atresia, three nonsyndromic intrahepatic cholestasis, and two Alagille syndrome). To evaluate vitamin D absorption, the subjects received vitamin D3 1000 IU/kg (maximum dose of 50,000 IU); they then received the same dose of vitamin D3 mixed with TPGS (25 IU/kg). Serial serum vitamin D3 levels and areas under the curve were measured. All patients had enhanced absorption of vitamin D when it was administered in a mixture with TPGS. Mean area under the curve for serum vitamin D3 was 403.0 +/- 83.1 nmol x h/L (155.6 +/- 32.1 ng x h/mL), with a mean rise above baseline of 13.5 +/- 1.8 nmol/L (5.2 +/- 0.7 ng/mL) with vitamin D/TPGS compared with no rise when vitamin D was given alone (both p less than 0.001). Seven patients have been followed for at least 3 mo while receiving the vitamin D/TPGS combination. Those with initially low serum 25(OH)-vitamin D levels (less than 37.5 nmol/L or 15 ng/mL) had normalization (range 37.5-146 nmol/L) within 1 mo, whereas those with initially normal levels remained normal. While the patients were receiving vitamin D/TPGS, serum vitamin E to total lipid ratio either normalized or remained normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Low serum calcium and high parathyroid hormone levels in neonates fed 'humanized' cow's milk-based formula.

We previously suggested that "late" neonatal hypocalcemia is related to a low calcium-phosphorus ratio of current cow's milk-based formula compared with human milk. However, there are no longitudinal studies of ionized calcium and parathyroid hormone concentrations in neonates receiving formulas with varying Ca/P ratios. Sixty-nine term neonates were studied through 2 weeks of age, and formula-fed neonates were randomized at birth to receive formula with molar ratios of 0.9, 1.2, or 1.4. Serum phosphate concentrations on days 2 and 6 of age were higher, and ionized calcium levels lower on days 6 and 14, in formula-fed vs human milk-fed neonates. Serum intact parathyroid hormone level increased between days 2 and 6 in formula-fed neonates compared with a decrease in human milk-fed neonates. Serum parathyroid hormone level on day 6 correlated with phosphorus intake among formula-fed neonates. No differences were noted in serum mineral or hormone levels among formula-fed groups. We speculate that the lowering of serum ionized calcium concentrations in neonates fed a modern "humanized" cow's milk formula may be a factor in late neonatal hypocalcemia.

Analysis of Variance↗
PubMed1991

Severe rickets in Lowe syndrome: treatment with continuous nasogastric infusion.

A boy with Lowe syndrome who manifested renal Fanconi syndrome by severe hypophosphatemic rickets, failure to thrive, and metabolic acidosis failed to improve with conventional bolus therapy of phosphate and bicarbonate. He was then placed on home continuous nasogastric infusion of phosphate and bicarbonate in addition to caloric supplementation. Rapid reversal of metabolic acidosis and hypophosphatemia was achieved. There was significant improvement in clinical and radiological signs of rickets and in bone mineral content. After 9 months therapy, his ponderal age improved dramatically from 7.5 to 29.5 months and his statural age from 16 to 26 months. We conclude that continuous nasogastric infusion of phosphorus and bicarbonate is a useful alternative mode of therapy in patients with renal Fanconi syndrome who are resistant to conventional bolus therapy.

Acidosis↗
PubMed1991

A role for magnesium in neonatal parathyroid gland function?

Little is known of the factors regulating parathyroid function in the neonatal period. Twenty-seven term infants born after uncomplicated pregnancies, labors, and deliveries were studied to test the hypothesis that in normal newborns the amplitude of parathyroid hormone (PTH) response to decreasing serum ionized calcium (iCa) correlates with serum magnesium (Mg) concentrations. Serum iCa (ion selective electrode, Radiometer ICA 1), PTH (1-84 intact molecules, radioimmunoassay) and Mg (atomic absorption) were measured at birth (cord blood) and 24 hours of age. Repeated measures analysis of covariance showed decreasing serum iCa (p less than 0.01) and increasing serum Mg (p less than 0.01) and PTH (p less than 0.01) over time. The change in PTH over the first 24 hours was directly correlated with cord blood (r = 0.38, p less than 0.05) and 24-hr Mg concentrations (r = 0.53, p less than 0.01). We conclude that the ability of the parathyroid gland to respond to decreasing serum iCa after birth is directly related to Mg status. We speculate that neonatal hypomagnesemia may lead to a blunted PTH secretory response, thus contributing to early neonatal hypocalcemia.

Analysis of Variance↗
PubMed1991

A case-control study of hypocalcemia in high-risk neonates: racial, but no seasonal differences.

A role for vitamin D in the defense against falling serum calcium (Ca) concentrations following cord clamping has been suggested. Since race and season are known to affect vitamin D status, we theorized that black race and birth in winter are additional risk factors for neonatal hypocalcemia (NHC). We retrospectively studied 13,462 infants born at University Hospital (Cincinnati, OH) between January 1, 1984 and December 31, 1987. Serum Ca was measured at 24 hours of age routinely in infants with low birth weight (less than 2500 g), preterm delivery (less than 2500 g), preterm delivery (less than 37 weeks), neonatal asphyxia, and diabetic mothers. After exclusion of infants of diabetic mothers (to remove maternal diabetes as a major confounder) and infants with major congenital anomalies, 714 infants remained. In multiple regression analysis, low serum Ca values were significantly associated with low gestational age (p less than 0.01), low Apgar score (p less than 0.01), and white race (p less than 0.01) (R2 = 0.457). Season or month of birth was not significant. In pair-matched analysis controlling for factors other than season, season of birth did not affect serum Ca. In pair-matched analysis controlling for factors other than race, white race was once again a risk factor for hypocalcemia. Thus, low gestational age, low Apgar score, and white race, but not black race and delivery in winter, are risk factors for NHC. We speculate that in our climate and with the prevailing diet in pregnancy, vitamin D deficiency does not appear to play a role in NHC.(ABSTRACT TRUNCATED AT 250 WORDS)

Black or African American↗
PubMed1991

Mineral requirements of low-birth-weight infants.

The minerals calcium (Ca), magnesium (Mg), and phosphorus (P) are essential for tissue structure and function. Recent studies have resulted in a more rational approach to the management of mineral intake in preterm infants receiving parenteral nutrition (PN) and enteral nutrition (EN). For preterm infants requiring PN, the use of PN solutions with a Ca content of 1.25-1.5 mmol/dl (50-60 mg/dl), a P content of 1.29-1.45 mmol/dl (40-45 mg/dl), and an Mg content of 0.2-0.3 mmol/dl (5-7 mg/dl) is supported by studies of mineral homeostasis with serial chemical and calciotropic hormone measurements, standard balance studies, and improved radiographic indices of bone mineralization. For infants requiring EN, an intake of approximately 4 mmol (200 mg) of Ca, 3.2 mmol (100 mg) of P, and 0.33 mmol (8 mg) of Mg/kg/day based on an average retention rate of 64% for Ca, 71% for P, and 50% for Mg should be sufficient to meet the requirements of preterm infants in early infancy. This level of intake is supported by data from balance studies using standard and stable isotope techniques, changes in bone mineral content (BMC) measurements, and calciotropic hormone data. Based on the timing of development of fractures and rickets, changes in BMC, and skeletal growth data, the increased Ca and P intake should continue for at least 3 months after birth or until reaching a body weight of about 3.5 kg. In addition, nonnutritional factors may have the potential to increase mineral loss and disturb mineral homeostasis; chronic diuretic therapy increases mineral loss, and aluminum contamination of nutrients theoretically may compound any skeletal disorder. Thus, attention to the level of mineral intake and factors important in mineral loss and mineral metabolism should optimize mineral retention in small preterm infants.

Calcium↗
PubMed1991

Perinatal magnesium metabolism: personal data and challenges for the 1990s.

This review addresses recent developments in the field of perinatal magnesium (Mg) metabolism. After a brief review of perinatal Mg physiology, it critically addresses the issue of possible teratogenicity of Mg deficiency; maternal hypermagnesaemia and its effects on pregnancy, the fetus, and the newborn; the role of Mg in neonatal calcium homeostasis; and the possible relationship between Mg deficiency, apnoea of prematurity, and sudden infant death syndrome.

Calcium↗
PubMed1991

Serum vitamin D metabolites and bone mineralization in young children with chronic low to moderate lead exposure.

One hundred five children (49 male, 99 black) with known lead exposure indices from birth and adequate nutrient intake of calcium, phosphorus, and vitamin D were studied at 1 of 3 ages (21, 27, or 33 months) to determine the effects of chronic low to moderate lead exposure on circulating concentrations of vitamin D metabolites and bone mineral content as determined by photon absorptiometry. Univariate multiple regression analyses showed no direct relationship of blood lead levels to vitamin D metabolites or bone mineral content. Structural equation analyses which took into account potential covariates of age, season, race, and sex showed estimated declines in serum concentrations of total calcium (from 9.72 to 9.61 mg/dL), phosphorus (from 5.4 to 4.67 mg/dL), and 25-hydroxyvitamin D (from 27.24 to 25.8 ng/mL) and estimated increases in concentrations of parathyroid hormones (from 73.03 to 83.14 microL Eq/mL), 1,25-dihydroxyvitamin D (from 62.39 to 62.69 pg/mL), and bone mineral content (from 222.66 to 234.91 mg/cm) over the observed range of average lifetime blood lead concentrations (4.76 to 23.61 micrograms/dL, geometric mean 9.74 micrograms/dL). However, the only statistically significant effect of average lifetime blood lead concentration was that for phosphorus, and the multivariate test of the combined effects of lead on these six outcomes was not statistically significant (P = .2). It is concluded that significant alterations in vitamin D metabolism, calcium and phosphorus homeostasis, and bone mineral content are not present in children whose nutritional status is adequate and who experience low to moderate lead exposure.

Bone Density↗
PubMed1991

Changes in calcium homeostasis over the first year postpartum: effect of lactation and weaning.

There is little information on the effect of lactation on maternal mineral and calcitropic hormone status. Therefore, we prospectively compared 26 lactating women with 32 nonlactating postpartum controls over the first year postpartum. Nineteen of the 26 women breast-fed their infants for fewer than 12 months and seven breast-fed for at least 12 months. During the first 6 months postpartum, serum phosphorus and parathyroid hormone (PTH) concentrations decreased with increasing time (P = .04 and P = .003, respectively) and were higher in lactating compared with nonlactating women (P less than .001 and P = .06, respectively). Mean serum phosphorus concentrations at 1, 3, and 6 months postpartum were 4.45, 4.75, and 4.34 mg/dL, respectively, in lactating women, versus 4.01, 3.64, and 3.44 mg/dL in controls. Mean PTH concentrations were 1.58, 1.48, and 1.36 ng/mL in lactating women, compared with 1.45, 1.20, and 1.16 ng/mL, respectively, in controls. At 12 months, women who were weaning had significantly higher mean serum calcium (10.11 mg/dL) and magnesium (2.36 mg/dL) concentrations than those who had weaned (8.79 and 2.03 mg/dL, respectively) or who had never lactated (8.90 and 1.95 mg/dL, respectively). Serum phosphorus, PTH, and 1,25-dihydroxyvitamin D were similar among women who were weaning (4.02 mg/dL, 1.46 ng/mL, and 54 pg/mL, respectively) and those who had weaned (3.94 mg/dL, 1.68 ng/mL, and 55 pg/mL), and were significantly higher than concentrations in women who had never lactated (3.25 mg/dL, 0.92 ng/mL, and 39 pg/mL). Our findings during lactation and the persistent differences observed during and after weaning are consistent with bone mobilization during lactation and a recovery of bone mass during and after weaning.

Calcium↗
PubMed1990

Early neonatal predictors of neonatal hypocalcemia in infants of diabetic mothers: an epidemiologic study.

Prematurity, neonatal asphyxia, hypomagnesemia, and advanced maternal diabetes are traditional risk factors for hypocalcemia in infants of diabetic mothers (IDMs). The aim of this study was to determine the relative contribution of these factors separately and combined in a cohort of diabetic pregnancies managed prospectively in the recent 9 years and to find accurate predictors of neonatal hypocalcemia in infants of diabetic mothers. We hypothesized that these factors plus low cord blood calcium (Ca) concentration allow prediction of IDMs who develop neonatal hypocalcemia. We studied 186 IDMs (White class B-RT); gestational age (GA, weeks) was by last menstrual period, confirmed +/- 2 weeks by Ballard score. The goals of glycemic control were: preprandial blood glucose less than 100 mg/dl and 90-minute postprandial blood glucose less than 140 mg/dl. Apgar scores, and cord, 24-, 48- and 72-hour serum calcium (Ca) (mg/dl) and magnesium (Mg; mg/dl) were determined. In univariate analysis, lowest serum Ca correlated with cord blood Ca (r = 0.48, p less than 0.001), GA (r = 0.37, p less than 0.001), and 1-minute Apgar score (r = 0.18, p = 0.09), but did not correlate with cord Mg or with advanced White class. In multiple regression, cord Ca and GA were dominant effects and other variables became insignificant. Lowest Ca (mg/dl) was predicted as follows: lowest Ca = 34.05 - 3.22 (Ca cord) - 0.84 (GA) + 0.10 (GA) (Ca cord). This equation predicts neonatal hypocalcemia (lowest Ca less than 8 mg/dl) with a sensitivity of 72% and a specificity of 75%. Thus, GA and cord Ca allow determination of IDMs at risk for neonatal hypocalcemia.

Asphyxia Neonatorum↗
PubMed1990

Spectrum and natural history of congenital hyperparathyroidism secondary to maternal hypocalcemia.

Fourteen cases of congenital hyperparathyroidism secondary to maternal hypocalcemia have been reported. We report two additional cases that highlight the wide spectrum of the disease. We extensively studied the parathyroid function of these infants to test the hypothesis that the biochemical hyperparathyroidism found in these infants would be transient in nature, since the presumed etiology (maternal and subsequent fetal hypocalcemia) should disappear soon after birth with establishment of enteral feedings. Infant 1 was born to a mother with idiopathic hypoparathyroidism with poor compliance to therapy and documented hypocalcemia in pregnancy. Severe congenital demineralization and intrauterine fractures with clinical and radiologic bowing of the long bones were obvious. Bone mineral content and bone mineral content/bone width ratio, measured by photon absorptiometry, were both markedly below normal. Infant 2 was born to a mother with postsurgical hypoparathyroidism with excellent compliance. The mother was normocalcemic. The infant was clinically and radiologically asymptomatic. The bone mineral content was just at the lower limit of normal, but bone mineral content/bone width ratio was below the normal limits. Biochemical features include elevation of cord serum parathyroid hormone (1-84, radioimmunoassay) in both cases, coexisting with serum calcium, phosphorus concentrations within normal limits. Serum parathyroid hormone fell to within normal ranges by 9 days of age in both infants. With no treatment, bone mineral content at 1 month of age was normal in both infants.

Adult↗
PubMed1990

Postnatal changes in serum osteocalcin and parathyroid hormone concentrations.

Cord clamping at birth leads to interruption of calcium (Ca) supply to the fetus. After birth, neonatal parathyroid hormone (PTH) secretion appears stimulated by hypocalcemia, with serum PTH increasing after birth and peaking at 24 hours of age. This rise in PTH presumably leads to bone resorption and Ca release. We theorize that bone formation may also be affected and that a serum marker of bone formation, serum osteocalcin (OC) concentrations, will decrease postnatally. OC is synthesized by osteoblasts and its serum concentrations are believed to reflect bone formation. We measured serum ionized Ca (iCa), PTH, and OC in cord blood and at 2 and 24 hours in 26 neonates born after uncomplicated pregnancies, labors, and deliveries. Serum iCa (mg/dl) decreased from 5.79 +/- 0.06 (cord, means +/- SEM) to 5.31 +/- 0.05 (2 hr), then to 4.89 +/- 0.05 (24 hr) (p less than 0.05). Serum PTH (microliter Eq/ml) increased from 35.9 +/- 4.3 (cord) to 41.7 +/- 4.0 (2 hr) (p = 0.1), and to 50.3 +/- 4.6 (24 hr) (p less than 0.01). Serum OC (ng/ml) decreased from 55.1 +/- 10.6 (cord), to 12.4 +/- 4.3 (2 hr) (p less than 0.01), then remained stable at 12.7 +/- 1.9 (24 hr). The change (cord minus 24 hr) in OC correlated inversely with the change in PTH over the first 24 hours of age (r = -0.42. p = 0.03). Therefore, there is a sudden decrease in an index of bone formation (i.e., serum OC) in the first 24 hours of life in which rising serum PTH may have had an impact.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Development↗
PubMed1990

Bone disease in chronic childhood cholestasis. II. Better absorption of 25-OH vitamin D than vitamin D in extrahepatic biliary atresia.

Infants with extrahepatic biliary atresia (EHBA) commonly develop rickets in infancy, whereas long-term survivors with EHBA commonly develop osteopenia with increasing age. We evaluated baseline vitamin D (D2 and D3), 25-OH vitamin D2 and D3, 1,25(OH)2 vitamin D, bone mineral content, and vitamin D2 and 25-OH vitamin D3 absorption in six infants and children (age 4-22 mo) with EHBA whose portoenterostomy failed to produce bile flow (group 1) and five infants and children (age 10/12 to 8-4/12 y) with EHBA whose portoenterostomy repair led to good postoperative bile flow (group 2). Baseline serum vitamin D2 and D3 were undetectable in all subjects in group 1 despite supplements of 2500-5000 IU/day, whereas all group 2 subjects given supplements (doses 400-5000 IU/d) had measurable levels. Baseline serum 25-OH vitamin D was less than 15 ng/mL in five of six (three with rickets) in group 1, whereas only one in group 2 had concentrations less than 15 ng/mL. A significantly blunted rise of vitamin D2 above baseline and reduced area under the absorption curve after 1000 IU/kg vitamin D2 were found in group 1 patients compared to group 2 (both p less than 0.01), and five pediatric controls (both p less than 0.01). The peak change and area under the absorption curve for serum 25-OH vitamin D3 from baseline after 10 micrograms/kg 25-OH vitamin D3 were significantly reduced for group 1 (both at least p less than 0.05) and group 2 compared to controls (both p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Biliary Atresia↗