cholecalciferol and Growth-Disorders

Vitamin D deficiency is widespread in both the pediatric and adult chronic kidney disease (CKD) population. CKD is characterized by dysregulation of vitamin D and mineral metabolism. Secondary hyperparathyroidism and its management puts patients with CKD at increased cardiovascular risk. Emergence of experimental and some clinical data suggesting beneficial effects of vitamin D on proteinuria, blood pressure, inflammation and cardiovascular outcomes has pushed it to the center stage of CKD research. Pediatric data on vitamin D dysregulation and its consequences are still in its infancy. Ongoing prospective studies such as Chronic Kidney disease in Children (CKiD) and the Cardiovascular Comorbidity in Children with CKD (4 C) should help to delineate the evolution of disturbances in mineral metabolism and its adverse effects on growth, CKD progression and cardiovascular outcomes.

Topics: Child; Cholecalciferol; Dietary Supplements; Ergocalciferols; Growth Disorders; Humans; Hyperparathyroidism, Secondary; Kidney; Renal Insufficiency, Chronic; Vitamin D; Vitamin D Deficiency; Vitamins

Observational studies suggest that vitamin D deficiency among people living with HIV is associated with a greater risk of disease progression and death. Low levels of vitamin D in pregnancy are also associated with poor fetal and infant growth. Therefore, vitamin D supplementation may improve clinical outcomes for pregnant women living with HIV and improve fetal and postnatal growth for their infants.. We conducted a randomized, triple-blind, placebo-controlled trial of vitamin D3 supplementation among pregnant and lactating women living with HIV in Dar es Salaam, Tanzania (ClinicalTrials.gov NCT02305927). Participants were randomized with 1:1 allocation stratified by study clinic to receive either daily 3,000 IU vitamin D3 supplements or matching placebo supplements from the second trimester of pregnancy (12-27 weeks) until 1 year postpartum. The primary outcomes were (i) maternal HIV progression or death, (ii) small-for-gestational-age (SGA) live births (<10th percentile), and (iii) infant stunting at 1 year of age (length-for-age z-score < -2). We also examined the effect of vitamin D3 supplementation on secondary maternal and infant health outcomes, maternal and infant serum 25-hydroxyvitamin D (25[OH]D) concentrations, and maternal hypercalcemia. An intent-to-treat analysis was used as the primary analytic approach. We enrolled 2,300 pregnant women between June 15, 2015, and April 17, 2018, and follow-up of mothers and infants was completed on October 20, 2019. There were 1,148 pregnant women randomly assigned to the vitamin D3 group, and 1,152 to the placebo group. The proportion of mothers lost to follow-up at 1 year postpartum was 6.6% in the vitamin D3 group (83 of 1,148) and 6.6% in the placebo group (76 of 1,152). The proportion of children lost to follow-up at 1 year of age was 5.5% in the vitamin D3 group (59 of 1,074 live births) and 5.2% in the placebo group (57 of 1,093 live births). There was no difference in the risk of maternal HIV progression or death, with 166 events during 1,461 person-years of follow-up in the vitamin D3 group and 141 events during 1,469 person-years of follow-up in the placebo group (hazard ratio 1.21, 95% CI 0.97 to 1.52, p = 0.09). There was no difference in the risk of SGA birth between the vitamin D3 (229 SGA births among 1,070 live births) and placebo groups (236 SGA births among 1,091 live births) (relative risk 1.03, 95% CI 0.87 to 1.22, p = 0.70). There was also no difference in the risk of infant stunting at 1 year of age between the vitamin D3 (407 events among 867 infants) and placebo groups (413 events among 873 infants) (relative risk 1.00, 95% CI 0.92 to 1.10, p = 0.95). In terms of adverse events, no cases of maternal hypercalcemia were identified. One hypersensitivity reaction to the trial supplements occurred for a pregnant woman in the placebo group. A limitation of our study is that our finding. The trial findings do not support routine vitamin D supplementation for pregnant and lactating women living with HIV in Tanzania.. ClinicalTrials.gov Identifier: NCT02305927.

Topics: Child; Cholecalciferol; Dietary Supplements; Double-Blind Method; Female; Growth Disorders; HIV Infections; Humans; Hypercalcemia; Infant; Lactation; Pregnancy; Tanzania; Vitamin D; Vitamin D Deficiency

Vitamin D regulates bone mineral metabolism and skeletal development. Some observational studies have suggested that prenatal vitamin D deficiency increases the risk of adverse pregnancy and/or birth outcomes; however, there is scant evidence from controlled trials, leading the World Health Organization to advise against routine vitamin D supplementation in pregnancy. Importantly, little is known about the effect of maternal vitamin D status on infant linear growth in communities in South Asia where stunting is highly prevalent and maternal-infant vitamin D status is commonly suboptimal.. The Maternal Vitamin D for Infant Growth study is a randomized, placebo-controlled, dose-ranging trial of maternal vitamin D supplementation during pregnancy and lactation in Dhaka, Bangladesh. The primary aims are to estimate (1) the effect of maternal prenatal oral vitamin D3 supplementation (4200 IU/wk, 16,800 IU/wk, or 28,000 IU/wk, administered as weekly doses) versus placebo on infant length at 1 year of age and (2) the effect of maternal postpartum oral vitamin D3 supplementation (28,000 IU/wk) versus placebo on length at 1 year of age among infants born to women who received vitamin D 28,000 IU/wk during pregnancy. Generally healthy pregnant women (n = 1300) in the second trimester (17-24 weeks of gestation) are randomized to one of five parallel arms: placebo 4200 IU/wk, 16,800 IU/wk, or 28,000 IU/wk in the prenatal period and placebo in the postpartum period or 28,000 IU/wk in the prenatal period and 28,000 IU/wk in the postpartum period. Household- and clinic-based follow-up of mother-infant pairs is conducted weekly by trained personnel until 26 weeks postpartum and every 3 months thereafter. The primary trial outcome measure is length for age z-score at 1 year of age. Anthropometric measurements, clinical information, and biological specimens collected at scheduled intervals will enable the assessment of a range of maternal, perinatal, and infant outcomes.. The role of vitamin D in maternal and infant health remains unresolved. This trial is expected to contribute unique insights into the effects of improving maternal-infant vitamin D status in a low-income setting where stunting and adverse perinatal outcomes represent significant public health burdens.. ClinicalTrials.gov identifier: NCT01924013. Registered on 13 August 2013.

Topics: Administration, Oral; Age Factors; Bangladesh; Body Height; Child Development; Child, Preschool; Cholecalciferol; Clinical Protocols; Developing Countries; Dietary Supplements; Double-Blind Method; Drug Administration Schedule; Female; Growth Disorders; Humans; Infant; Infant Nutritional Physiological Phenomena; Infant, Newborn; Lactation; Male; Maternal Nutritional Physiological Phenomena; Nutritional Status; Pregnancy; Prevalence; Research Design; Time Factors; Treatment Outcome

X-linked hypophosphatemic rickets (XLHR) is frequently associated with growth retardation and short adult stature, even with an appropriate conventional treatment associating phosphate and calcitriol or 1 alpha-hydroxyvitamin D. Its pathogenesis is unclear; growth hormone (GH) secretion is usually normal. Six children with XLHR and growth retardation were treated with GH during 6 years. In addition, they received the conventional treatment. At the beginning of the treatment mean age was 7.8 +/- 1.8 years, and height mean Z score was -3.4 +/- 0.5. A control group was composed of six children with XLHR (age: 7.9 +/- 2.5 years) receiving the conventional treatment only. Under GH treatment statural growth was improved, with significant increase in Z score and predicted adult height; the height gain was significantly higher in the GH treated group as compared with the group receiving the conventional treatment only. In addition, radial bone mineral density increased significantly under GH treatment. GH treatment thus appears to be a useful treatment to improve statural growth in children with XLHR.

Topics: Adult; Body Height; Bone Density; Calcitriol; Child; Cholecalciferol; Drug Therapy, Combination; Female; Follow-Up Studies; Growth Disorders; Growth Hormone; Humans; Hypophosphatemia, Familial; Male; Phosphates; Treatment Outcome

PIBIDS syndrome (photosensitivity, ichthyosis, brittle hair, intellectual impairment, decreased fertility and short stature) is a variant of trichothiodystrophy. It is a rare form of autosomal recessive congenital ichthyosis. Short stature is a vital component of PIBIDS syndrome. We present the cases of two siblings in whom we diagnosed PIBIDS syndrome. On evaluation for short stature, they were found to have severe vitamin D deficiency, which on correction led to the patients having considerable gain in stature. With this case, we would also like to propose that vitamin D deficiency could be one of the treatable causes of short stature in PIBIDS syndrome.

Topics: Adolescent; Child; Cholecalciferol; Consanguinity; Emollients; Growth Disorders; Hair Diseases; Humans; Ichthyosis; Male; Photosensitivity Disorders; Siblings; Sunscreening Agents; Trichothiodystrophy Syndromes; Vitamin D Deficiency; Vitamins

Topics: Cerebral Palsy; Cholecalciferol; Female; Growth Disorders; Humans; Hypercalcemia; Infant; Male; Muscle Hypotonia; Pregnancy; Prenatal Exposure Delayed Effects

Holstein suckling calves on a farm manifested severe emaciation, generalized alopecia, dome-like cranial deformation, and high mortality (Case 1). Metaphyseal growth plates of the femur were achondroplastic; segmented, partially resorped, and replaced with immature bony trabeculae containing degenerated chondrocytes. The skull was thin and partially replaced with connective tissue. Diffuse and severe fatty degeneration was observed in the hepatic stellate (Ito') cells. After 6 mo, surviving calves manifested unthrifty with short and irregular hindquarters (Case 2). The metaphyseal growth plates were poorly formed, irregular, partially disappeared centrally, and often sealed with thin bony trabeculae. The cartilage matrix was not homogeneous but was finely fibrous, and chondrocytes were flat and degenerated. The bone lesion was diagnosed as chondrodysplasia due to premature physeal closure. These calves had been administered excessive amounts of vitamins A, D3 and E, and blood chemistry of acute case showed hypervitaminosis A and E. Case I demonstrated acute disease, while Case 2 demonstrated chronic sequelae. Hypervitaminosis A was the suspected cause.

Topics: Animals; Animals, Newborn; Cattle; Cattle Diseases; Cholecalciferol; Drug Overdose; Emaciation; Femur; Growth Disorders; Growth Plate; Skull; Vitamin A; Vitamin E

The changes in bone metabolism and morphology of chondrocytes in bovine Hyena disease caused by administration of vitamin AD3E premix (V-AD3E) or vitamin A (V-A) were examined. At the each age, 5 calves were used. Among them, Hyena disease was recognized in 3 calves; a calf administered a high dose of V-AD3E premix (V-A 3,000,000, V-D3 300,000, and V-E 1,200 I.U./day), a calf administered a half dose of the V-AD3E premix, and a calf administered only V-A 3,000,000 I.U./day. The remaining calves without Hyena disease were a calf administered only V-D3 300,000 I.U./day and a control calf. Each agent was administered orally for 10 days from 1 week after birth. In the 3 calves with Hyena disease, the bone metabolism in bone histomorphometry of ilium was in the state of low turnover at the age of 50 days. The bone volume was small at the age of 12 months. The epiphysial growth plates of the distal femurs and the proximal tibias partially disappeared and the chondrocyte lacunas in them were flattened. The matrix fibers of epiphysial growth plates were thinner in diameter and higher in density than those of the control calf. In the calf administered only V-D3, the values of bone volume decreased with aging. In conclusion, Hyena disease may be caused by excessive administration of V-A, because hypervitaminosis A suppressed the activity of differentiation and proliferation in chondrocytes and osteoblasts, and excessive administration of V-D3 may promote these actions.

Topics: Animals; Bone and Bones; Bone Development; Cattle; Cattle Diseases; Cholecalciferol; Growth Disorders; Growth Plate; Microscopy, Electron, Scanning; Reference Values; Vitamin A; Vitamin E; Vitamins

Topics: Animals; Child; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Growth; Growth Disorders; Humans; Kidney Failure, Chronic; Rats

Vitamin D-deficient rat pups were produced by feeding normal impregnated rats a diet deficient in vitamin D after mating. The rat pups appeared normal at birth but stopped growing at 1 week of age. Despite this growth failure, these pups were normocalcemic. Analyses of calvaria from a similar group of dams given vitamin D3 showed that these dams mobilized skeletal calcium to meet the calcium requirements of their growing pups.

Topics: Animals; Calcium; Cholecalciferol; Female; Growth Disorders; Lactation; Maternal-Fetal Exchange; Pregnancy; Rats; Vitamin D Deficiency

Topics: Child; Child, Preschool; Cholecalciferol; Female; Follow-Up Studies; Growth; Growth Disorders; Humans; Kidney Failure, Chronic; Renal Dialysis

Topics: Animals; Appetite Regulation; Cholecalciferol; Chronic Kidney Disease-Mineral and Bone Disorder; Financing, Government; Graft Rejection; Growth Disorders; Humans; Kidney Transplantation; Kidneys, Artificial; Rats; Research; Transplantation, Homologous; Uremia

Topics: Adolescent; Affective Symptoms; Age Factors; Cardiovascular Diseases; Child; Child, Preschool; Cholecalciferol; Depression; Erythropoiesis; Family; Female; Glomerulonephritis; Growth Disorders; Humans; Infant; Kidney Transplantation; Male; Renal Dialysis; Seizures; Terminal Care; Transplantation, Homologous; Uremia

Topics: Cholecalciferol; Follow-Up Studies; Growth; Growth Disorders; Humans; Long-Term Care; Osteomalacia; Phosphates; Rickets; Vitamin D