Urinary iodine concentrations in mothers and their term newborns in country with sufficient iodine supply.

OBJECTIVE: The main aim of the study was to evaluate maternal and newborn urinary iodine concentrations according to the usage of iodine supplementation during pregnancy. METHODS: Thirty-seven women with singleton uncomplicated pregnancies and their newborns were included in this study. Maternal urine samples were obtained at the time of delivery and on the third day after delivery. Newborn urine samples were obtained on the third day after delivery. Urinary iodine concentrations were determined by the alkaline ashing of urine specimens followed by the Sandell-Kolthoff reaction using brucine as a colorimetric marker. RESULT: The overall rate of the usage of iodine supplementation during pregnancy was 54% (20/37). Women who used the iodine supplementation during the pregnancy did not have different urinary iodine concentrations neither at the time of delivery (p = 0.23), nor on the third day after delivery (p = 0.65) in comparison to women without extra iodine supplementation. Newborns from pregnancies with regular iodine supplementation had higher urine iodine concentrations on the third day after delivery (p = 0.02). When women were split into several subgroups based on the daily dosage of iodine supplementation (200, 150, and 50 µg daily and without iodine supplementation), no differences were found in maternal urine iodine concentrations at the time of delivery (p = 0.51) and on the third day after delivery (p = 0.63). Different levels were found in newborn urine iodine concentrations among the subgroups of newborns from pregnancies with different daily doses of iodine supplementation and from pregnancies without iodine supplementation during pregnancy (p = 0.05). CONCLUSIONS: Iodine supplementation during pregnancy affects newborn urine concentrations but not maternal urine concentrations.

Neonatal thyroid status in an area of iodine sufficiency.

BACKGROUND: Iodine deficiency constitutes a public health problem in many countries worldwide. Fetal neurodevelopment is affected by maternal iodine intake. The aim of present study was to assess urinary iodine excretion (UIE) in the 3 trimesters of pregnancy and evaluate its association with newborn thyroid function in Tehran, an area of iodine sufficiency. METHODS: Based on median urinary iodine in 3 trimesters, 138 pregnant women were divided into 2 groups with UIE<150 (group I) and UIE ≥ 150 µg/l (group II). Cord blood samples of their newborns were evaluated for serum concentrations of TSH, T3, T4, free T4 (FT4), and thyroglobolin. Quartiles of UIE were also determined. Correlations between mothers' UIE and newborns' thyroid function in both groups were investigated. RESULTS: Fifty-two pregnant women (38%) had median UIE<150 µg/l and 86 had (62%) UIE ≥ 150 µg/l. Median UIE in groups I and II in the 1st, 2nd, and 3rd trimesters were 125 and 212 µg/l, 97 and 213 µg/l, 93 and 227 µg/l, respectively. No significant difference was seen in thyroid function of newborns in the 2 groups. Mean concentrations of T4, T3, FT4, and TSH of newborn did not show significant difference in median UIE of mothers in various quartiles. CONCLUSION: This study shows that newborns, irrespective of mothers' UIE, in an area with a sustained iodine supplementation program, may not be at risk of alterations in thyroid functions.

[Neonatal vitamin D status and calcium-phosphorus homeostasis in the third week of life]. / Zasoby ustrojowe witaminy D a homeostaza wapniowo-fosforowa u noworodków donoszonych w 3 tygodniu zycia.

AIM: Assessment of vitamin D status and calcium -phosphorus homeostasis in term newborns before routine supplementation. MATERIAL AND METHOD: Calcidiol (25OHD), calcium, phosphorus and alkaline phosphatase in serum and Ca (urine)/creatinine (urine) ratio (mg/mg), P (urine)/creatinine (urine) ratio (mg/mg) and tubular phosphate reabsorption rate (TRP= [1-(P(urine) / P(serum). creatinine serum/urine)].100%) in 3rd week of life in 56 appropriate for gestational age term neonates was measured. First group contains 35 newborns (62.5%) with normal 25OHD values and second group 21 newborns (37.5%) with hypovitaminosis D (25OHD < 11 ng/ml). RESULT: Mean 25OHD concentration was 15.23 ng/ml + 8.57 ng/ml. Maternal vitamin D supplementation (10 ug/day) for more than 4 months of pregnancy was similar in both groups (55.9% vs. 52.4%) (p>0.05). There were 51.43% breastfed newborns in group one and 85.71% in group two (p=0.009). Median 25OHD concentration in breastfed newborns was 11.2 ng/ml and 18.5 ng/ml in formula fed babies (p=0.017). There were no statistical differences between groups in calcium (2.44 vs. 2.41 mmol/l), phosphorus (2.27 vs. 2.22 mmol/l) and alkaline phosphatase (261 vs. 266 U/L) blood concentration and Ca (urine)/creatinine (urine) ratio (0,34 vs. 0,25mg/mg) and TRP (86% vs. 88%) (p>0.05). The P (urine) /creatinine (urine) ratio in the first group was 2.3mg/mg and 1.42 mg/mg in the second group (p=0.048). CONCLUSIONS: Neonatal vitamin D stores in the 3rd week of life are not more dependent on maternal vitamin D supplementation during pregnancy. Breastfed infants are at greater risk of hypovitaminosis D than formula fed infants, therefore earlier vitamin D supply should be considered. The hypovitaminosis D has no influence on basic parameters of Ca-P homeostasis in the 3rd week of life.

Shift of serum osteocalcin components between cord blood and blood at day 5 of life.

Vitamin K deficiency is a relatively common condition in neonates. However, the role of vitamin K in neonatal bone metabolism remains to be determined. Osteocalcin (OC) is the most abundant noncollagenous protein in bone, and is regulated to be gamma-carboxylated by vitamin K. In this study, we measured gamma-carboxylated osteocalcin (Gla-OC) and non- or undercarboxylated osteocalcin (Glu-OC) separately, and examined the effects of vitamin K on osteocalcin metabolism. Eighteen full-term healthy neonates were enrolled in this study. In the cord and d-5 blood samples, the OC levels were determined by three different methods to examine the intact OC by immunoradiometric assay (IRMA), Gla-OC, and Glu-OC. Serum vitamin K fractions, hepaplastin test, and type 1 procollagen carboxyl extension peptide were also determined. Urine samples were also collected from the first voiding and on d 5 to determine urinary pyridinoline, deoxypyridinoline, and gamma-carboxylated glutamic acid. Serum levels of phylloquinone (PK) and menaquinone (MK)-4 increased on d 5 following vitamin K administration and increased intake in breast milk and/or formula. The OC levels determined by IRMA did not change between cord and d-5 blood samples, but the Gla-OC level increased remarkably and Glu-OC reduced to a negligible level. OC in cord blood is mainly Glu-OC, and Glu-OC is replaced with Gla-OC within 5 d of life after vitamin K supplement. The IRMA assay fails to distinguish Gla-OC from Glu-OC and caution is needed to estimate bone turnover with this method in the perinatal period.

[The iodine supply of newborns. Comparison of iodine absorption and iodine excretion of mother and child]. / Die Jodversorgung von Neugeborenen. Vergleich der Jodaufnahme und Jodausscheidung von Mutter und Kind.

BACKGROUND: Since 1989 the use of iodized salt has been allowed in Germany, additional supplementation with iodide tablets has been recommended during pregnancy and lactation. This study was undertaken to clarify whether the iodine intake of neonates and young infants improved since then. PATIENTS AND METHODS: In the first part of the study the urinary iodine excretion of 52 newborns and their mothers in 1998 was compared to data of similar studies 1983 in the area of Göttingen and 1982 in the areas of Heidelberg and Rothenburg, Germany. All these are geographically low-iodine areas. In the second part the iodine supply of infants in 1998-1999 under feeding with mother's milk or formulas in 1998 and 1999 was obtained by measuring iodide concentrations in urine and milk using a high pressure liquid chromatography (HPLC) method. RESULTS: 45% of pregnant women were without iodide supplementation in 1998. In 1998 the median urinary iodide concentration during the first week of life was 4.3 micrograms/dl, which was more than twice that found in 1983 (1.75 micrograms/dl). Infants feeding by mother's milk without maternal iodine supplementation or by semi-elementary diet had the lowest urinary iodine excretion, whereas significantly higher values were measured when feeding formulas for term or preterm infants. CONCLUSIONS: The iodine intake of newborns has markedly improved during 15 years. The WHO criterias for adequate iodine supply (TSH < 5 microU/ml and urinary iodine >/ = 10 micrograms/dl) were only partly fulfilled in Göttingen indicating that a mild iodine deficiency still exists with the risk of iodine deficiency disorders.

Hydroxyl radical generation in oxygen-treated infants.

OBJECTIVE: Because the hydroxyl radical is capable of oxidizing phenylalanine to O-tyrosine, we sought to determine whether increased levels of O-tyrosine are found in urine of infants treated with supplemental oxygen. METHODS: A total of 39 consecutively admitted neonates to an intensive care unit were included. Twenty-seven received supplemental oxygen therapy for respiratory disease, and 12 did not. Urinary O-tyrosine levels were determined on two or more occasions using high-performance liquid chromatography with results expressed as a percentage of the urinary phenylalanine concentration. Using simple and stepwise multiple linear regression analyses, urinary O-tyrosine was examined for associations with relevant clinical conditions and laboratory measurements. RESULTS: Infants supplemented with oxygen showed significantly higher mean +/- SEM urinary O-tyrosine levels (0.40% +/- 0.028) compared with those remaining in room air (0.18% +/- 0.012). Mean daily FIO2 was the clinical and laboratory variable most highly correlated with urinary O-tyrosine (r = 0.66). In the stepwise regression, significant associations were also found for renal fractional sodium excretion and Apgar score at 5 minutes. CONCLUSIONS: Hydroxylation at the O position of phenylalanine, a specific direct marker for the hydroxyl radical attack, was strongly associated with oxygen treatment in neonates. This finding increases our understanding of the pathogenesis of oxygen injury and suggests a basis for developing therapeutic approaches.

Maternal iodine status and thyroid volume during pregnancy: correlation with neonatal iodine intake.

Differences in pregnancy-associated alterations in thyroid volume and urinary iodine (UI) excretion have been attributed to geographical variations in dietary iodine intake. In this study, ultrasound-measured thyroid volume and UI excretion were assessed during the 3 trimesters of pregnancy, at delivery, and at 6 weeks postpartum. Urine specimens also were obtained from mothers and both breast- and formula-feeding infants at 3 days after delivery. Thyroid volume showed a significant increase (maximum 47.0%), compared with nonpregnant control values over the 3 trimesters of pregnancy, which occurred as early as the first trimester and was paralleled by increased UI excretion, followed in turn by a precipitous fall at delivery. UI excretion in breast-feeding neonates (100 +/- 6.8 micrograms/L) was significantly higher than in their mothers (76 +/- 5.6 micrograms/L; p < 0.01) but was significantly lower (43 +/- 3.5 micrograms/L) in formula-fed infants. The results suggest that in an area of moderate dietary iodine intake, UI loss during pregnancy may result in maternal thyroid enlargement. The ability of the breast to transport iodine compensates for this loss in breast-fed infants, but this protection may be lost in formula feeding.

Factors influencing the development of melatonin rhythmicity in humans.

The emergence of melatonin rhythmicity was studied in 163 infants between 46-55 weeks postconception by monitoring the excretion of the urinary melatonin metabolite 6-sulfatoxymelatonin (aMT.6S). From this population, we examined the effects of gender, season, multiple birth, home birth, previous sudden infant death syndrome in the family, premature labor, spontaneous rupture of membranes, preeclampsia, intrauterine growth restriction, and nursery lighting on pineal rhythmicity. As previously reported, rhythmic excretion of aMT.6S appeared between 49-55 weeks postconception (9-15 weeks of age) in singleton babies born at term in the hospital. Full-term infants who had a sibling die of sudden infant death syndrome had a pattern of melatonin rhythm development no different from that of the control full-term infants. In contrast, full-term infants born at home and full-term twins born in the hospital had significantly lower aMT.6S excretion than hospital-born singleton infants at the same ages despite similar body weights (e.g. at 52 weeks postconception; 1.8 +/- 0.4, 1.1 +/- 0.3, and 3.6 +/ -0.5 nmol/day, respectively). In full-term infants, there was no difference in the development of melatonin rhythmicity between the sexes, with season or method of delivery (vaginal vs. caesarean). The premature infants were divided into 5 groups (babies born after premature labor, premature rupture of membranes, preeclampsia, intrauterine growth restriction, and fetal distress). All premature infants had a delay in the appearance of aMT.6S rhythms in the urine in relation to chronological age. When the infants were compared on the basis of weeks since conception, those infants born after spontaneous premature labor excreted amounts of aMT.6S no different from those of full-term singleton infants during the period of study. In contrast, the premature rupture of membranes, preeclampsia, and fetal distressed infants excreted 50% less aMT.6S, and intrauterine growth restricted infants excreted 67% less at the same postconceptional ages. These differences were due to reduced nocturnal excretion of the metabolite. In an attempt to accelerate the development of melatonin rhythmicity, premature labor and premature rupture of membranes infants were randomly assigned to be totally deprived of light (using phototherapy eye shields) or partially deprived of light by moving them to a dimly lit room each night for the last 3-8 weeks of their stay in the hospital nursery. Babies born after premature labor produced normal amounts of aMT.6S between 46-52 weeks postconception, and this pattern was not affected by the nocturnal light deprivation. Infants born after premature rupture of membranes and totally deprived of light at night had aMT.6S excretion rhythms at 52 weeks postconception no different from those of full-term hospital-born infants or premature labor infants, whereas those in infants placed in dim light were similar to those in untreated premature rupture of membranes infants. These results suggest that premature birth alone is not the sole cause of altered rhythm development; other factors, such as preeclampsia, growth restriction, and nursery lighting, play an important role. The consequences of the delayed appearance of melatonin in infants are not known, but deserve further study.

Accuracy of urine output measurement with regular disposable nappies.

Evaporation of urine from four types of disposable absorbent infant nappies (A, B, C, D) was assessed under a radiant warmer or in an incubator, with or without phototherapy. Each nappy was weighed dry and then 5, 10, 15 or 30 ml of urine were added. The nappy was immediately reweighed, placed in its study environment and then weighed 5, 15, 30, 60 and 120 min later. Under all conditions, the percentage evaporation from each type of nappy increased during the 120 min and was inversely correlated with urine volume. Without phototherapy, the maximum evaporation at 120 min with a 5-ml urine sample was 15.9% +/- 6.1% for nappy B in the incubator and 20.8% +/- 4.0% for nappy A in the radiant warmer. Phototherapy was associated with slight but significant changes in evaporation in the incubator and the radiant warmer. Nappy D allowed the lowest percentage evaporation in the incubator with or without phototherapy and in the radiant warmer with phototherapy (8.8% +/- 4.4%, 2.4% +/- 1.8% and 16.0% +/- 10%, respectively for a 5-ml urine sample).

Amelioration of some pregnancy-associated variations in thyroid function by iodine supplementation.

Knowledge of the effect of differences in iodine intake levels on public health in areas with no endemic goiter is limited. Groups at risk when iodine intake is relatively low are pregnant and lactating women and their newborns. A prospective randomized study was performed to evaluate the effect of iodine supplementation in an area where the median daily iodine excretion in urine is around 50 micrograms. Fifty-four normal pregnant women were randomized to be controls or to receive 200 micrograms iodine/day from weeks 17-18 of pregnancy until 12 months after delivery. In the control group, serum TSH, serum thyroglobulin (Tg), and thyroid size showed significant increases during pregnancy. These variations were ameliorated by iodine supplementation. Iodine did not induce significant variations in serum T4, T3, or free T4. Cord blood Tg was much lower when the mother had received iodine, whereas TSH, T4, T3, and free T4 levels were unaltered. The results suggest that a relatively low iodine intake during pregnancy leads to thyroidal stress, with increases in Tg release and thyroid size. However, the thyroid gland is able to adapt and keep thyroid hormones in the mother and the child normal, at least under normal circumstances, as evaluated in the present study. It is not known whether this stress is sufficient to be of importance for late development of autonomous thyroid growth and function.

Urinary N-acetyl-beta-D-glucosaminidase activity in healthy, polycythemic and hypoxic neonates.

The authors investigated the urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in the case of 101 normal healthy and 20 polycythemic newborns and prematures, and 50 prematures suffering from hypoxia on the 1st, 2nd, 4th, 14th, and 28th day after birth. The obtained activities were referred to the creatinine concentrations of the urine samples and given as NAG index. There were no significant differences in the NAG indices either between fullterm and preterm babies or between appropriate for gestational age (AGA) and small for gestational age (SGA) neonates of the normal group. The NAG indices on the first day of life were significantly higher in the case of polycythemic newborn in comparison with the normal group (p less than 0.01). On the 14th day, after the partial plasma exchange, the NAG indices returned to the normal range. The premature babies suffering from IRDS received an average 10.1 days oxygen supplementation. Their NAG indices were significantly (p less than 0.01) higher on the 1st, 2nd, 4th days than those of the healthy prematures of the normal group and decreased considerably up to the 14th day. Finally the NAG indices reached the normal value on the 28th day. These results support the assumption that the urinary NAG index is a suitable indicator of the renal tubular damage during the newborn period.

Urinary and blood levels of adenosine 3',5'-monophosphate, phosphorus and calcium in infants.

The changes during the first year of life in urinary and nephrogenous cAMP levels were determined in 152 normal, full-term infants using spot urine samples. The use of spot tests simplifies considerably the logistics of the cAMP determination which can be used for the investigation of parathyroid function. Levels of urinary and nephrogenous cAMP (expressed both as a function of creatinine excretion as well as glomerular filtration rate) rose from birth to 1 year of age, whereas plasma cAMP levels did not change significantly. Levels of cAMP (both urinary and nephrogenous) were significantly correlated with age, length, weight, and urinary phosphorus concentrations of the infants. No significant correlation could be observed, however, between serum phosphorus or serum and urinary calcium on the one hand, and urinary or nephrogenous cAMP on the other.