Search PubMed⌕ Search

Biomedical subjects

W W Koo

Publications and source records attributed to W W Koo.

At least 55 records · Page 3Linked to original sources
PubMed1989

Serum alkaline phosphatase and serum zinc concentrations in preterm infants with rickets and fractures.

This study aimed to determine the longitudinal changes in serum zinc concentrations and the relationship between serum alkaline phosphatase (AP) activity and serum zinc concentrations in small preterm infants. The total serum AP and serum zinc concentrations were determined serially at 3, 6, 9, and 12 months in 72 infants with mean (+/- SEM) birth weights of 1000 +/- 29 g and gestational ages of 28.6 +/- 0.3 weeks. Twenty-four of 72 infants had radiographic evidence of rickets and/or fractures (R/F). In infants with R/F, group mean (+/- SEM) serum AP (371 +/- 42 U/L) and serum zinc (12.5 +/- 1.0 mumol/L) concentrations were significantly higher at 3 months compared with infants in the non-R/F group (193 +/- 12 U/L and 9.6 +/- 0.3 mumol/L, respectively). During the study, the serum AP concentrations decreased, and the serum zinc concentrations increased; both stabilized after 6 months. The serum AP concentrations were not related to the serum zinc concentrations. We speculate that in preterm infants, an increased bone turnover and a release of tissue (bone) zinc may contribute to the higher group mean serum AP and serum zinc concentrations at the time of diagnoses in infants with R/F compared with those infants without R/F.

Alkaline Phosphatase↗
PubMed1989

Serum vitamin D metabolites in very low birth weight infants with and without rickets and fractures.

Seventy-one very low birth weight (less than or equal to 1500 gm) infants were studied to determine the sequential changes in serum vitamin D metabolite concentrations between infants with and without radiographically documented rickets, fractures, or both (R/F). Usual intake of vitamin D included 20 IU/kg/day from parenteral nutrition or 400 IU/day supplementation with enteral feeding. Radiographs of both forearms and serum samples were obtained at 3, 6, 9, and 12 months. Twenty-two infants had R/F. At 3 months, significantly lower mean (+/- SEM) serum phosphorus levels (4.5 +/- 0.4 vs 6.1 +/- 0.2 mg/dl), higher 1,25-dihydroxyvitamin D (1,25-[OH]2D) concentrations (96 +/- 5 vs 77 +/- 4 pg/ml), and higher free 1,25-(OH)2D index (1,25-[OH]2D:vitamin D binding protein ratio; 5.2 +/- 0.3 x 10(5) vs 4.0 +/- 0.2 x 10(5] were found in the R/F group. These values returned to normal and were similar between groups on subsequent measurements. Serum calcium, magnesium, and 25-hydroxyvitamin D (25-OHD) concentrations were normal and similar between groups. In both groups, serum vitamin D binding concentrations increased initially but remained stable and normal beyond 6 months. We conclude that in very low birth weight infants with R/F, the vitamin D status (as indicated by serum 25-OHD concentrations) is normal, and that lowered serum phosphorus levels, higher serum 1,25-(OH)2D levels, and a higher free 1,25-(OH)2D index support the thesis that mineral deficiency (especially of phosphorus) may be important in the pathogenesis of R/F in small preterm infants.

Calcifediol↗
PubMed1989

Minimal vitamin D and high calcium and phosphorus needs of preterm infants receiving parenteral nutrition.

Preterm infants (birth weight, 1,089 +/- 91 g; gestational age, 28.9 +/- 0.7 weeks; mean +/- SEM) with mixed medical and surgical indications for parenteral nutrition (PN) were observed to determine the adequacy of infusates with fixed, low-dose vitamin D (25 IU/dl) and two combinations of calcium and phosphorus. The duration of low-dose vitamin D PN ranged from 5 to 52 days, with a median of 27 days. Twelve infants were randomly assigned to low (standard) Ca and P doses (5 mM each; 20 mg/dl of Ca and 15.5 mg/dl of P) and 13 high Ca and P doses (15 mM each; 60 mg/dl of Ca and 46.5 mg/dl of P). The maximum daily vitamin D intake was similar for both groups (31 +/- 1.3 versus 33 +/- 1.2 IU/kg). Vitamin D status in either group, as indicated by serum 25-hydroxyvitamin D (25-OHD) concentrations, was normal. There was no significant difference in observed changes of serial measurements of serum calcium, magnesium, phosphorus, alkaline phosphatase, creatinine (Cr), 25-OHD, and vitamin D-binding protein concentrations or urinary Ca:Cr and Mg:Cr ratios. In the low-dose Ca and P group, the serum P level was consistently less than 4 mg/dl in five infants, serum 1,25-dihydroxyvitamin D concentrations were higher, and tubular reabsorption of phosphorus was consistently greater than 95% and significantly higher than in the high-dose Ca and P groups. Severe bone demineralization apparent on X-ray occurred in two infants, with a fractured distal left ulna in one of the two infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium, Dietary↗
PubMed1988

Sequential bone mineral content in small preterm infants with and without fractures and rickets.

Seventy-four infants with birth weights 1009 +/- 28 grams and gestational age 28.6 +/- 0.3 weeks (M +/- SEM) were studied prospectively to test the hypotheses that bone mineral content (BMC) measured by photon absorptiometry, would be: (1) lower in very low birth weight (VLBW) infants with radiographic evidence of fractures and/or rickets (F/R), and (2) will continue to be lower over the first year when compared to VLBW infants without F/R. BMC and bone width (BW) of the distal one-third of left radius and ulna were measured at 5 weeks (n = 8), 14 weeks (n = 61), 26 weeks (n = 58), 40 weeks (n = 59), and 1 year (n = 52). Standardized radiographs of both forearms, and weight, length, and head circumference were also determined at each study age. Investigators and technicians involved in the photon absorptiometry measurements were unaware of the radiographic findings and vice versa. Twenty-three of 74 infants were found to have F/R. BMC of studied infants remained markedly below our previously determined range of "intrauterine bone mineralization," even at 26 weeks after birth. There was no significant difference in BMC or BW between infants with and without F/R, either at the time of confirmation of F/R or during early follow-up; however, BMC was lower at greater than or equal to 6 months and BW was lower at greater than or equal to 9 months in infants with F/R. We suggest that the extremely low BMC measurements in early infancy predispose all VLBW infants to fractures and rickets.

Birth Weight↗
PubMed1988

Aluminum and bone disorders: with specific reference to aluminum contamination of infant nutrients.

Aluminum (Al) impairment of bone matrix formation and mineralization may be mediated by its direct effect on bone cells or indirectly by its effect on parathyroid hormone and calcium metabolism. Its toxic effects are proportional to tissue Al load. Al contamination of nutrients depends on the amount of Al present naturally in chemicals or from the manufacturing process. Intravenous calcium, phosphorus, and albumin solutions have high Al (greater than 500 micrograms/L), whereas crystalline amino acid, sterile water, and dextrose water have low Al (less than 50 micrograms/L) content. Enteral nutrients including human and whole cow milk have low Al, whereas highly processed infant formulas with multiple additives, such as soy formula, preterm infant formula, and formulas for specific disorders are heavily contaminated with Al. Healthy adults are in zero balance for Al. The gastrointestinal tract excludes greater than 95% of dietary Al, and kidney is the dominant organ for Al excretion. However, even with normal renal function, only 30-60% of an Al load from parenteral nutrition is excreted in the urine, resulting in tissue accumulation of Al. The risk for Al toxicity is greatest in infants with chronic renal insufficiency, recipients of long term parenteral nutrition, i.e., no gut barrier to Al loading, and preterm infants with low Al binding capacity. The rapid growth of the infant would theoretically potentiate Al toxicity in all infants, although the critical level of Al loading causing bone disorders is not known. To minimize tissue burden, Al content of infant nutrients should be similar to "background" levels, i.e., similar to whole milk (less than 50 micrograms/L).

Aluminum↗
PubMed1988

Urinary sodium excretion in young infants: role of gestational and postnatal ages.

Fractional urinary sodium excretion (FENa) and urinary sodium excretion (UNaE) were determined 88 times in 42 healthy, appropriate weight-for-gestational age infants. Gestational ages (GA) were 28-41 weeks; birthweights were 930-4135 g. Nineteen preterm infants were studied serially a total of 59 times between 1 and 55 days after birth. During the first 4 days after birth, multiple hierarchical regression analyses showed that FENa and UNaE were inversely related to GA (P less than 0.001). Postnatal age (PN) was not significantly related to FENa or UNaE. However the effect of GA on FENa and UNaE was not significantly greater than the effect due to postnatal age (PA) (P = 0.31 and P = 0.80, respectively). UNaE (1.6 +/- 0.2 mmol/kg per day) was significantly greater than sodium intake (1.1 +/- 0.2 mmol/kg per day) at 2.6 +/- 0.2 days (P less than 0.05). Longitudinal studies extending beyond 4 days indicated that GA and PA had interactive effects on FENa and UNaE; hence the contribution for a given GA was dependent on PA (and vice versa). Sodium intake remained stable (average 1.8 mmol/kg per day) beyond 7 days after birth and was consistently greater than UNAE (P less than 0.01). It is suggested that in healthy preterm infants beyond 2 weeks PA, a sodium intake of 2-3 mol/kg per day may be adequate to meet the renal sodium losses.

Aging↗
PubMed1988

Parenteral vitamins A, D, and E for premature infants.

Dosage recommendations for parenteral multivitamin preparations in infants are approximations of what is believed to be necessary and are usually based on oral allowances. These recommendations for extremely immature infants are further complicated by the narrow margin of safety of some vitamins. This article is a review of the current recommendations for parenteral administration of vitamins A, D, and E in premature infants.

Body Weight↗
PubMed1988

Calcium, phosphorus, and vitamin D requirements of infants receiving parenteral nutrition.

Calcium and phosphorus form the major inorganic constituents of bone and serve a vital role in cell function and cell metabolism. Metabolism of calcium, phosphorus, and vitamin D are intimately related and the requirement of these nutrients should take into account this relationship. For high-risk infants, the use of parenteral nutrition may be associated with disturbances in calcium, phosphorus, and vitamin D metabolism. Acute alterations in calcium and phosphorus metabolism, as reflected by excessively elevated or decreased concentrations of circulating calcium and phosphorus concentrations, are frequently iatrogenic in origin and may be minimized by attention to details of fluid, electrolyte, glucose, and other non-calcium, non-phosphorus nutrients. Calcium and phosphorus content up to 15 mM each (60 mg calcium and 46.5 mg phosphorus/dl) with a calcium:phosphorus ratio of 1.3 to 1 by weight or 1 to 1 by molar ratio, at average fluid intakes (approximately 120 ml/kg/day), are suitable to maintain calcium and phosphorus homeostasis. This stable metabolic milieu is reflected by normal and stable serum concentrations of 1.25 dihydroxyvitamin D, and normal and stable renal tubular reabsorption of phosphorus. A low content of vitamin D, 25 IU/dl, in the presence of calcium and phosphorus appears to be sufficient to maintain normal vitamin D status as reflected by the maintenance of normal serum 25 hydroxyvitamin D concentrations.

Calcium, Dietary↗
PubMed1986

Elevated serum calcium and osteocalcin levels from calcitriol in preterm infants. A prospective randomized study.

The hypothesis of this study was that pharmacologic doses of calcitriol (1,25-dihydroxyvitamin D3) would result in elevated levels of serum osteocalcin, the major noncollagenous bone protein, and calcium in infants of very low birth weight (less than 1500 g). Twenty-four infants of very low birth weight but of the appropriate weight for gestational age were matched in 250-g weight ranges and randomized into calcitriol treatment and control groups on the first day after birth. Treated infants received 4 micrograms/kg of calcitriol intravenously on entry and on the second and third study days. Controls did not receive calcitriol. Four infants from each group were hypocalcemic (serum calcium level, less than 7.0 mg/dL [less than 1.75 mmol/L]) on entry (five to 20 hours after birth) to the study. Seven infants received calcium replacement; data analyses with and without these infants were similar. Of the remaining 17 infants, eight were in the treatment group and nine were in the control group. Calcitriol significantly increased serum calcium and osteocalcin concentrations on days 2, 3, and 4 after birth compared with the control group. None of eight treated infants manifested hypocalcemia after calcitriol vs eight of nine controls. There were no acute changes in heart rate, respiratory rate, systolic blood pressure, or urinary calcium loss nor were there changes at the infusion site, but the diastolic blood pressure increased with treatment. Although high doses of calcitriol may elevate serum calcium concentrations in infants of very low birth weight, we suggest that the long-term or subtle biologic effects of high doses of calcitriol remain to be studied and that its routine use not be recommended at present.

Calcitriol↗
PubMed1986

Response to aluminum in parenteral nutrition during infancy.

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.

Aluminum↗
PubMed1986

Growth failure and decreased bone mineral of newborn rats with chronic furosemide therapy.

To test the hypothesis that chronic furosemide treatment in otherwise healthy newborn animals may lead to lowered bone mineral [calcium (Ca) and magnesium (Mg)] content, healthy littermates within each litter of Sprague-Dawley rat pups were randomly assigned to three groups: control, low dose furosemide (5 mg/kg/day), and high dose furosemide (15 mg/kg/day). The pups were treated between days 4 and 28 postnatally. The wet and dry weights of kidneys and tibiae significantly correlated with body weights at sacrifice. Furosemide-treated pups demonstrated a dose-dependent growth delay, decreased total bone (tibiae) Ca and Mg, increased urine Ca and Mg concentration, and a significant inverse correlation between bone Ca and urine Ca concentration. There was no significant difference among the groups when bone Ca and Mg were normalized to per gram of bone dry weight. There were no significant differences among the groups with respect to bone phosphorus or urinary phosphorus concentration; kidney and serum Ca and Mg; or serum sodium, potassium, alkaline phosphatase and immunoreactive parathyroid hormone concentration. We conclude that chronic furosemide therapy leads to growth failure and to increased urinary losses of Ca and Mg. Total bone Ca and Mg in the furosemide-treated pups were diminished in proportion to growth retardation but the bone mineral content per unit of dry weight remained similar to control pups.

Animals↗
PubMed1984

Continuous nasogastric phosphorus infusion in hypophosphatemic rickets of prematurity.

Radiologic and biochemical abnormalities associated with nutritional hypophosphatemic rickets were discovered in a 945-g preterm infant despite daily supplementation with 800 to 1,600 IU of ergocalciferol (vitamin D2) and an elevated serum 25-hydroxyvitamin D concentration. Vitamin D supplementation was stopped, and the rickets was corrected by phosphorus supplement alone with the use of a unique technique of long-term, continuous nasogastric phosphorus infusion. Normophosphatemia was rapidly achieved and effectively maintained. Hypocalcemia did not occur at rates of infusion of 100 mg of elemental phosphorus per day. The data are consistent with specific phosphorus deficiency as the cause of rickets in this infant, rather than insufficient vitamin D intake or disturbed vitamin D metabolism. We speculated that continuous phosphorus infusion prevents the intermittent hyperphosphatemia of bolus phosphorus supplement and that continuous phosphorus infusion may be useful in the treatment of other hypophosphatemic states of infancy.

Female↗
PubMed1984

Bone mineralization in infants.

The major physiologic control of bone mineralization in infancy involves calcium and phosphorus. Ca and P metabolism in turn is affected by endogenous stores at birth and the ability to deliver and absorb exogenous sources of these minerals. Calciotropic hormones (parathyroid hormone, calcitonin and 1,25 dihydroxyvitamin D) modulate the response of major end organs - intestine, kidney and bone - to balance the need to maintain a relatively stable extracellular biochemical environment with the need for adequate mineralization of the bone. Many other factors such as glucocorticoids under pathological circumstances may disturb bone mineralization; however, the mechanisms by which they control bone mineralization in infancy under physiologic circumstances is ill understood. Clinical bone demineralization occurs primarily in infants born with extreme prematurity. In the presence of conventional vitamin D supplementation, deficiency of calcium and phosphorus appears to play a major role in its causation.

24,25-Dihydroxyvitamin D 3↗