Vitamin D concentrations from neonatal dried blood spots and the risk of early-onset type 2 diabetes in the Danish D-tect case-cohort study.

AIMS/HYPOTHESIS: The aim of this study was to examine the influence of neonatal vitamin D concentration on the development of early-onset type 2 diabetes in a large population sample. METHODS: We conducted a case-cohort study utilising data from the Danish biobank and registers. Neonatal vitamin D was assessed measuring 25-hydroxyvitamin D3 [25(OH)D3] concentrations on the dried blood spot samples from the Biological Specimen Bank for Neonatal Screening. Cases of type 2 diabetes (n = 731) were retrieved from the Danish National Patient Register for all individuals born in Denmark between 1 May 1981 and 31 December 1992. The sub-cohort (n = 1765) was randomly selected from all children born in the same period. We used a weighted Cox proportional hazard model assessing the hazard of first type 2 diabetes diagnoses by quintiles of 25(OH)D3 and restricted cubic spline. RESULTS: The median 25(OH)D3 concentration (IQR) among cases was 21.3 nmol/l (13.3-34.1) and 23.9 nmol/l (13.7-35.7) in the sub-cohort. There was no indication of a potential lower risk of early-onset type 2 diabetes among individuals in the higher quintile of vitamin D concentration compared with the lowest (HRcrude 0.97 [95% CI 0.71, 1.33] p = 0.85; HRadjusted 1.29 [95% CI 0.92, 1.83] p = 0.14). CONCLUSIONS/INTERPRETATION: The results of this study do not support the hypothesis that higher neonatal vitamin D concentrations are associated with a lower risk of early-onset type 2 diabetes in adulthood.

Umbilical cord N-terminal procollagen of type l collagen (P1NP) and beta C-terminal telopeptide (ßCTX) levels in term pregnancies with vitamin D deficiency.

AIMS: The aim of the present study was to evaluate umbilical cord N-terminal procollagen of type l collagen (P1NP) and beta C-terminal telopeptide (ßCTX) levels in term pregnancies with vitamin D deficiency. MATERIALS AND METHODS: Ninety-two pregnant women between 19 and 35-years-old who delivered at term gestational age were included in the study and divided into deficient (n = 32), insufficient (n = 30), and normal (control) vitamin D levels (n = 30). RESULTS: Maternal demographic characteristics and biochemical parameters were similar among groups. The mean umbilical cord P1NP level was 221.4 (211.7-231.0, 95%CI) pg/mL in the vitamin D deficiency group, 282.5 (271.2-293.8, 95%CI) pg/mL in the vitamin D insufficiency group, and 280.9 (270.9-290.8, 95%CI) pg/mL in the control group and significantly lower in vitamin D deficiency group than others (p < .001). Umbilical cord P1NP level was similar in the vitamin D insufficiency group and control group (p = .971). The mean umbilical cord ßCTX level was 5530, 9 (5511.5-5550.3, 95%CI) pg/mL in the vitamin D deficiency group, 5516.3 (5498.4-5534.2, 95%CI) pg/mL in the vitamin D insufficiency group, and 5510 (5491.4-5528.5, 95%CI) pg/mL in the control group, which was statistically similar among the groups (p = .251). CONCLUSION: Our results indicated that vitamin D deficiency during pregnancy affects fetal bone osteoblast activity.

Vitamin D Deficiency, Prevalence and Treatment in Neonatal Period.

OBJECTIVE: Maternal vitamin D deficiency is an important risk factor that causes infantile rickets in the neonatal and infantile period. The aim of this study was to review the prevalence, clinical characteristics, and treatment of vitamin D deficiency and the follow-ups with infants and their mothers by the neonatal intensive care unit of Afiyet Hospital in Turkey. METHODS: Calcium (Ca), phosphorus (P) and 25 (OH) vitamin D were studied and prospectively recorded in infants and their mothers detected to have hypocalcemia during routine biochemistry tests performed on the third postnatal day of the patients follow up and treated with different diagnoses. RESULTS: A total of 2,460 infants were admitted into the neonatal intensive care unit between August 2014 and January 2018. Of the infants included in the study, 324 (66.1%) were male and 166 (33.8%) were female, and 366 (74.6%) of them had been delivered by cesarean section (C/S), 124 (25.3%) of them had been delivered by Normal Spontaneous Delivery (NSD). Hypocalcemia was detected in 490 (19.9%) of the infants. In a total of 190 (38.7%) infants and 86 mothers (17.5%), the levels of 25 (OH) vitamin D were found to be below the laboratory detection limit of <3 ng/ml. When vitamin D deficiency + insufficiency is assessed by season, 151 of them were found to be in summer (30.99%), 118 in spring (24.18%), 117 in the winter season(23.87%), and 93 in autumn(18.97%), respectively. There was a statistically significant positive correlation of 78.7% between the vitamins D values of the mothers and the infants (p: 0.000, p<0.05). CONCLUSION: This study conducted that a positive correlation of between the vitamin D values of the mothers and the infants. In order to prevent maternal vitamin D deficiency, the appropriate dose of prophylaxis providing optimal levels of vitamin D and should be given by according to the levels of 25 (OH) D vitamin during pregnancy.

Fetal and Maternal Genetic Variants Influencing Neonatal Vitamin D Status.

Objective: Several genetic polymorphisms determine vitamin D status. We aimed to estimate the strength of association of established 25-hydroyxvitamin D (25OHD)-associated variants in the mother and in the fetus, with 25OHD concentration in newborn umbilical cord plasma. Methods: We randomly selected 578 mother and child dyads from the prospective Norwegian Mother and Child Cohort study. 25OHD was assayed in maternal samples taken shortly after delivery and in cord samples. We genotyped the mother and child for single nucleotide polymorphisms in or near GC, DHCR7, CYP2R1, and CYP24A1, previously confirmed to be associated with 25OHD, and computed genetic risk score (GRS). The genetic associations were replicated in an independent sample of 594 subjects. Results: Although both fetal and maternal GRS were associated with cord 25OHD, only fetal GRS remained significantly associated with cord 25OHD in a regression model with maternal and fetal GRS simultaneously (1.6 nmol/L per fetal 25OHD-increasing allele; 95% confidence interval, 0.6 to 2.5, P = 0.0001). Two fetal single nucleotide polymorphisms in the GC gene (rs2282679 and rs222040) were the strongest genetic predictors of cord 25OHD [4.0 (2.1 to 5.9) and 3.0 (1.3 to 4.8) nmol/L per fetal allele, P < 0.001], followed by rs12785878 in DHCR7 [2.0 (0.1 to 3.8) nmol/L, P = 0.037]. The independent replication sample gave similar results. With fetal genotype included in a regression model with environmental factors, R2 for cord 25OHD was 0.28. Conclusions: We show that fetal 25OHD-modifying genotype was a stronger predictor of cord 25OHD than corresponding maternal genotype. This raises interesting questions about fetal acquisition and placental transfer of 25OHD.

Maternal vitamin D3 supplementation at 50 µg/d protects against low serum 25-hydroxyvitamin D in infants at 8 wk of age: a randomized controlled trial of 3 doses of vitamin D beginning in gestation and continued in lactation.

BACKGROUND: Vitamin D supplementation is recommended for breastfed infants. Maternal supplementation beginning in gestation is a potential alternative, but its efficacy in maintaining infant 25-hydroxyvitamin D [25(OH)D] concentration after birth is unknown. OBJECTIVES: We determined the effect of 3 doses of maternal vitamin D supplementation beginning in gestation and continued in lactation on infant serum 25(OH)D and compared the prevalence of infant serum 25(OH)D cutoffs (>30, >40, >50, and >75 nmol/L) by dose at 8 wk of age. DESIGN: Pregnant women (n = 226) were randomly allocated to receive 10, 25, or 50 µg vitamin D3/d from 13 to 24 wk of gestation until 8 wk postpartum, with no infant supplementation. Mother and infant blood was collected at 8 wk postpartum. RESULTS: At 8 wk postpartum, mean [nmol/L (95% CI)] infant 25(OH)D at 8 wk was higher in the 50-µg/d [75 (67, 83)] than in the 25-µg/d [52 (45, 58)] or 10-µg/d [45 (38, 52)] vitamin D groups (P < 0.05). Fewer infants born to mothers in the 50-µg/d group had a 25(OH)D concentration <30 nmol/L (indicative of deficiency) than infants in the 25- and 10-µg/d groups, respectively (2% compared with 16% and 43%; P < 0.05). Fewer than 15% of infants in the 10- or 25-µg/d groups achieved a 25(OH)D concentration >75 nmol/L compared with 44% in the 50-µg/d group (P < 0.05). Almost all infants (∼98%, n = 44) born to mothers in the 50-µg/d group achieved a 25(OH)D concentration >30 nmol/L. At 8 wk postpartum, mean maternal 25(OH)D concentration was higher in the 50-µg/d [88 (84, 91)] than in the 25-µg/d [78 (74, 81)] or 10-µg/d [69 (66, 73)] groups (P < 0.05). CONCLUSIONS: Maternal supplementation beginning in gestation with 50 µg vitamin D3/d protects 98% of unsupplemented breastfed infants against 25(OH)D deficiency (<30 nmol/L) to at least 8 wk, whereas 10 or 25 µg vitamin D/d protects only 57% and 84% of infants, respectively.

Diagnostic value of anti-microbial peptide, cathelicidin in congenital pneumonia.

OBJECTIVE: To evaluate the diagnostic value of anti-microbial peptide (cathelicidin), LL-37, in congenital pneumonia and its relation to 25 hydroxycholecalciferol [(25 OH)D] status. METHODS: The study included 30 neonates with congenital pneumonia and culture proven sepsis admitted to neonatal intensive care unit of Ain Shams University and 30 healthy neonates as control group. All neonates were subjected to history taking, clinical examination and measurement of serum 25(OH)D and cathelicidin. RESULTS: Neonates with congenital pneumonia had significantly higher serum cathelicidin and lower serum 25(OH)D compared to controls. Serum cathelicidin was negatively correlated with Apgar score at 1 and 5 min and positively correlated with length of stay among patient group. CONCLUSION: Cut-off value of cathelicidin to diagnose congenital pneumonia was 17 pg/mmol with 93% sensitivity and 86% specificity. Neonates with congenital pneumonia had significantly high cathelicidin and low 25(OH)D suggesting a possible role of fetal 25(OH)D deficiency as predisposing factor for congenital pneumonia.

Season of birth, neonatal vitamin D status, and cardiovascular disease risk at 35 y of age: a cohort study from Sweden.

BACKGROUND: Lower vitamin D status during gestation may be associated with cardiovascular disease risk later in life. No studies have assessed this hypothesis with a follow-up time reaching beyond childhood. OBJECTIVE: The objective was to assess the link between season of birth, neonatal 25-hydroxyvitamin D3 [25(OH)D3] status, and adult cardiovascular disease risk. DESIGN: Markers of cardiovascular and metabolic disease risk were measured in 284 subjects aged 35 y, born either at the end of the winter or at the end of the summer of 1975. In 275 of these 284 subjects, concentrations of neonatal 25(OH)D3 were measured in dried blood samples by using a highly sensitive liquid chromatography-tandem mass spectroscopy method. RESULTS: Subjects born after the winter had lower neonatal 25(OH)D3 concentrations than did those born after the summer (31.5 compared with 48.5 nmol/L; P < 0.001). In regression analyses adjusted for sex, season of birth, postnatal age at neonatal sample collection, preterm birth, maternal age, education, smoking, fish consumption per week, exercise per week, and current 25-hydroxyvitamin D, higher neonatal 25(OH)D3 (per 50 nmol/L) was associated with 25.8% (95% CI: 1.0%, 58.4%) higher fasting insulin in adult life, 29.6% (5.1%, 58.4%) higher triglycerides, and 4.64 (95% CI: 1.93, 7.36) mmol/L higher serum cholesterol in women. Neonatal 25(OH)D3 (per 1 nmol/L) was directly associated with risk of adult overweight (OR: 1.03; 95% CI: 1.01, 1.05) and with adult obesity in women (OR: 1.09; 95% CI: 1.02, 1.17). Neonatal 25(OH)D3 was not associated with adult aortic pulse wave velocity, blood pressure, fasting glucose, HDL, LDL, or C-reactive protein. Season of birth was not associated with any of the adult outcomes. CONCLUSIONS: Higher neonatal 25(OH)D3 was associated with higher fasting insulin, triglyceride, and cholesterol (in women) concentrations and with a higher risk of overweight at 35 y of age but not with other adult cardiovascular disease risk factors.

Maternal obesity and vitamin D sufficiency are associated with cord blood vitamin D insufficiency.

CONTEXT: An inverse relationship between total serum 25-hydroxyvitamin D (25-OH D) and increased adiposity has been established in children, adolescents, and adults. However, the relationship between neonatal adiposity and vitamin D status has not been reported. Both maternal obesity and vitamin D deficiency in pregnancy are common and are associated with adverse pregnancy outcomes. OBJECTIVE: The aim of the study was to determine the relationship between vitamin D levels in mothers and newborns, as influenced by maternal obesity, and evaluate these associations with neonatal adiposity. DESIGN, SETTING, AND PATIENTS: Sixty-one maternal-neonatal pairs participated in this cross-sectional study at an academic medical center. Mothers had a prepregnancy body mass index that was normal or obese. OUTCOME MEASURES: Maternal and cord blood sera were assayed for 25-OH D, and neonatal body composition was measured by air displacement plethysmography. RESULTS: Mothers had similar and sufficient levels of 25-OH D when measured at 36-38 wk gestation, irrespective of body mass index category (normal weight, 46.05, vs. obese, 49.84 ng/ml; P = not significant). However, cord blood 25-OH D was higher in neonates of normal-weight mothers compared to neonates of obese mothers (27.45 vs. 20.81 ng/ml; P = 0.02). The variance in cord blood 25-OH D was explained by four factors: maternal 25-OH D level, the presence of maternal obesity, maternal age, and neonatal adiposity (r(2) = 0.66). CONCLUSION: Obese women transfer less 25-OH D to offspring than normal-weight women, despite similar serum levels. Cord blood 25-OH D levels directly correlate to neonatal percentage body fat. These novel findings underscore the evolving relationships between maternal obesity, vitamin D nutritional status, and adiposity in the neonatal period that may influence subsequent childhood and adulthood vitamin D-dependent processes.

Maternal vitamin D predominates over genetic factors in determining neonatal circulating vitamin D concentrations.

BACKGROUND: There are multiple potential regulators of neonatal vitamin D status of environmental, genetic, and epigenetic origins. The relation between these factors and circulating neonatal vitamin D has yet to be fully characterized. OBJECTIVE: The aim of this study was to examine the relative contribution of genetic factors, maternal circulating 25-hydroxyvitamin D [25(OH)D] concentrations, and the placental methylation level of the gene that encodes the primary catabolic enzyme of active vitamin D [25(OH)D-24-hydroxylase encoded by CYP24A1] to neonatal 25(OH)D concentrations. DESIGN: We used the classical twin study design to determine the genetic contribution to neonatal 25(OH)D. A total of 86 twin pairs (32 monozygotic and 54 dizygotic twin pairs) were included in this study. Serum 25(OH)D was measured by using a 25(OH)D kit. CYP24A1 promoter DNA methylation was measured by means of matrix-assisted laser desorption time-of-flight mass spectrometry. RESULTS: Maternal and neonatal 25(OH)D showed a strong association (R² = 0.19). Monozygotic and dizygotic within-pair serum 25(OH)D correlations were similar (R² = 0.71 and 0.67, respectively), which suggested no genetic effect. Placental CYP24A1 methylation did not show an association with maternal or neonatal 25(OH)D concentrations. CONCLUSIONS: Our results suggest that maternal circulating 25(OH)D is the most significant regulator of neonatal circulating 25(OH)D concentrations, with underlying genetic factors playing a limited role. The placental methylation of the CYP24A1 promoter appears subject to a genetic influence, although no evidence of a relation between the methylation level of this gene and circulating maternal or neonatal 25(OH)D was apparent.

The role of vitamin D in pregnancy and lactation: insights from animal models and clinical studies.

Maternal adaptations during pregnancy and lactation appear to provide calcium to fetus and neonate without relying on vitamin D or calcitriol. Consequently, the blood calcium, calciotropic hormones, and skeleton appear normal at birth in the offspring of mothers who are severely vitamin D deficient or who lack calcitriol or its receptor. It remains unclear whether skeletal or extraskeletal problems will develop postnatally from exposure to vitamin D deficiency in utero. During the neonatal period, calcitriol-stimulated intestinal calcium absorption becomes the dominant mechanism of calcium delivery. The vitamin D-deficient neonate is at risk to develop hypocalcemia, rickets, and possibly extraskeletal disorders (e.g., type 1 diabetes). Breastfed babies are at higher risk of vitamin D deficiency because normally little vitamin D or 25-hydroxyvitamin D passes into breast milk. Dosing recommendations during pregnancy and lactation should ensure that the baby is born vitamin D sufficient and maintained that way during infancy and beyond.

Congenital vitamin D deficiency: a rare etiology of an acute life threatening event in early infancy.

Infants born to mothers with deficiency of vitamin D and/or calcium due to cultural modifications in their diets, life style and clothing habits, are at risk of developing early and fatal sequelae of hypocalcemic vitamin D deficiency. We present a 44-day-old infant with hypocalcemia secondary to congenital vitamin D deficiency, who presented as a recurrent Acute Life Threatening Event (ALTE) resulting in an unexpectedly prolonged intensive care course. This report suggests that evaluation of vitamin D status should be included as part of the workup of ALTE and we describe evidence-based preventive measures for both mothers and infants who are at risk for vitamin D deficiency.

Severity of experimental autoimmune encephalomyelitis is unexpectedly reduced in mice born to vitamin D-deficient mothers.

Accumulating data indicate that vitamin D, a sun-induced hormone, plays a key role in multiple sclerosis (MS) etiology. Notably, it has been shown that there is a remarkable season of birth effect in MS. We surmised that gestational vitamin D deficiency is a risk factor for MS. To test this hypothesis, a vitamin D deficiency was induced in C57BL/6 female mice 6 weeks prior to conception and prolonged until offspring birth. Contrary to our prediction, we show here that adult offspring exposed to developmental vitamin D deficiency (DVD) developed a striking milder and delayed experimental autoimmune encephalomyelitis (EAE), when compared to control offspring. Using reverse transcription and quantitative real-time PCR, we measured the expression level of 22 candidate transcripts in the spleen, the cerebrum and the spinal cord, at Day0 and Day30 post-immunization. We report here that, at Day30 post-immunization, TNF, osteopontin, H2-Eb were over-expressed and IFN was under-expressed in the spinal cord of control mice and not in DVD mice. Another discrepancy between nervous and immune systems was observed: expression of IL4 was dysregulated exclusively in the spleen. Reduced symptom severity in DVD mice can partially be explained by a nervous system-restricted over-expression of vitamin D receptor (VDR), two heat shock proteins (HSP90, HSPa8) and FK506 binding protein 1a (FKBP1a), at Day0. Our clinical test and molecular findings converge to indicate that maternal hypovitaminosis D imprints the foetus and alters the susceptibility of the offspring to EAE. We propose a new hypothesis to explain our unexpected observations.

Vitamin D and the adaptive immune system with special emphasis to allergic reactions and allograft rejection.

Tolerance induction is a fascinating option to prevent allergic diseases or allograft rejection. Calcitriol is the hormonal form of vitamin D and is produced by two hydroxylation steps: a hepatic 25-hydroxylation of vitamin D and a subsequent renal 1alpha-hydroxylation. Calcitriol has important immunomodulatory properties. Calcitriol can prevent those inflammatory processes which are responsible for allograft rejection, whereas its effects on immunological responses related to allergic reactions are more complex and not fully elucidated. This article summarizes present knowledge on vitamin D and the adaptive immune system. Experimental and clinical studies support the assumption that calcitriol can decrease the risk of allograft rejection. Prospective randomized clinical trials are however needed to clarify whether administration of calcitriol, some of its analogues, or simple vitamin D supplementation is able to prevent rejection in solid organ transplanted patients. With respect to allergic reactions, human data are inconsistent at present. Some argue that vitamin D deficiency may cause allergic reactions whereas others argue that vitamin D excess leads to an increased allergy risk. In this context, current strategy of vitamin D supplementation in infants and the possibility of a bimodal effect on allergic reactions of both, vitamin D deficiency and excess are discussed.

Incidental finding of vitamin-D deficient rickets in an otherwise healthy infant--a reappraisal of current vitamin-D supplementation guidelines.

In an effort to prevent rickets and vitamin-D deficiency in healthy infants, the American Academy of Pediatrics recommends a supplement of 200 IU per day of vitamin D to all breastfed and nonbreastfed infants unless they consume at least 500 ml per day of vitamin-D-fortified formula or milk. Case reports of infantile vitamin-D-deficient rickets secondary to maternal vitamin-D deficiency have been reported but focused on mothers who had predictable risk factors for such a deficiency. We report on an infant with vitamin-D-deficient rickets who did not have nutritional risk factors and whose mother did not have nutritional or medical risk factors for such a deficiency. We conclude that the current vitamin-D supplementation guidelines be extended to all infants, regardless of feeding volume or source, or at least to all infants born to dark-skinned mothers.

Long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: variable expressivity of maternal illness during pregnancy and unusual presentation with infantile cholestasis and hypocalcaemia.

Patients with long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency present with a Reye-like syndrome, cardiomyopathy, or sudden unexpected death. We describe an unusual presentation in a patient with unsuspected LCHAD deficiency. The proband presented at 2 months of age with an acute infantile hypocalcaemia and vitamin D deficiency associated with occult, unexplained cholestatic liver disease. Sudden, unexpected death occurred at 8 months. Molecular analysis revealed homozygosity for the prevalent LCHAD (1528G > C, E474Q) mutation. The mother had pre-eclampsia during the third trimester of her pregnancy. In a subsequent pregnancy, she developed severe acute fatty liver of pregnancy (AFLP) and intrauterine fetal death at 33 weeks of gestation. In conclusion, infantile hypocalcaemia is an unusual phenotype associated with LCHAD deficiency. The maternal pregnancy history documents that fetal LCHAD deficiency is associated with a spectrum of maternal illnesses ranging from pre-eclampsia to life-threatening AFLP.

Early detection of infants with hypophosphatemic vitamin D resistant rickets (HDRR).

The onset of physical signs in infants with hypophosphatemic vitamin D resistant rickets (HDRR) has generally been considered to be at the age of 12 months, but the time of appearance of hypophosphatemia and rachitic signs on radiographs remains unclear. We report a prospective study in three neonates whose mothers were HDRR. At birth, despite a low maternal serum inorganic phosphorus (Pi) level, the serum Pi level was normal together with a negligible renal Pi leak in one neonate. At age 3 months, their serum Pi levels, percentages of tubular reabsorption of Pi, and renal tubular maximal rates of Pi reabsorption in relation to the glomerular filtration rate were low except for one infant. Radiographically, their rickets were not apparent at birth but at age 3 months in all. A premature born infant, born at 28 weeks' gestation weighing 1240 g, was diagnosed as HDRR based on hypophosphatemia due to low renal tubular maximal rate of phosphorus reabsorption in relation to the glomerular filtration rate (TmP/GFR) and normal urine Ca excretion at age 5 months. They were initially treated with 1 alpha-hydroxyvitamin D3 (1 alpha OHD3) and later with 1 alpha OHD3 in combination with Pi, which results in healing of the rickets and a normal increase in height. Thus, early detection and treatment of patients born from mothers with HDRR before physical signs of bow-leg and short stature is possible, but the outcome of early treatment requires further study.

[Neonatal cardiac failure secondary to hypocalcemia caused by maternal vitamin D deficiency]. / Insuffisance cardiaque néonatale secondaire à une hypocalcémie par carence maternelle en vitamine D.

BACKGROUND: Heart failure is a rare manifestation of neonatal hypocalcemia. This paper describes such a case resulting from maternal vitamin D deficiency. CASE REPORT: A full-term boy, born in December after a normal pregnancy, was admitted at the age of 6 weeks because of dyspnea that appeared during suckling. Examination showed heart failure. Electrocardiogram showed that the corrected QT-interval was lengthened (0.54 s, normal < 0.45 s). Echocardiogram showed dilated, hypokinetic myocardiopathy. His serum calcium concentration was low (1.40 mmol/l) and phosphate was high (2.8 mmol/l); his alkaline phosphatase was 513 Ul/l. His blood PTH concentration was high (120 pg/ml) and his 25 (OH) D was low (5 ng/ml). The patient was given calcium (1 g/m2/day) and 1.25 (OH)2 D (2 micrograms/day orally). His serum calcium returned to normal within 4 days, and his cardiac abnormality was resolved within 3 months. His mother's blood 25 (OH) D concentration was very low (3 ng/ml), 6 weeks after birth. CONCLUSION: Neonatal hypocalcemia appears to have been compounded in this case by a maternal vitamin D deficiency. Hence, all pregnant women at risk of deficiency should be given vitamin D.

[The effect of unilateral nephrectomy on vitamin D metabolism in pregnant rats]. / Vliianie odnostoronnei nefréktomii na obmen vitamina D u beremennykh krys.

Unilateral nephrectomy causes a decrease in provision of vitamin D dihydro derivatives in pregnant rats, which correlated with the development of hypocalcemia and hypophosphatemia as well as with an increased content of parathyroid hormone. Fetuses of these females contained less amount of mineral components and active metabolites of vitamin D. Neonates, being born by these females with the nephrectomy, had vitamin D deficiency, which was manifested as a decrease in content of active vitamin D metabolites and minerals as well as an increase in activity of alkaline phosphatase and in the content of parathyroid hormone.