Biochemical Rickets: What Does Low Vitamin D Mean in Infants? Imaging of Child Abuse Conference 2/4/2012
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1 Biochemical Rickets: What Does Low Vitamin D Mean in Infants? Imaging of Child Abuse Conference 2/4/2012 Ingrid A. Holm, MD, MPH Divisions of Genetics and Endocrinology Children s Hospital Boston Harvard Medical School
2 Overview Bone and mineral metabolism Skeletal mineralization in the fetus and neonate Rickets Congenital rickets
3 Bone Mineralized osseous tissue Bone marrow Endosteum Periosteum Nerves Blood vessels Cartilage 3
4 Bone is primarily Bone Matrix Inorganic portion Laid down as unmineralized osteoid Mineralization osteoblasts vesicles containing alkaline phosphatase Calcium and phosphate deposition as hydroxyapatite crystals Organic portion mainly Type I collagen various growth factors
5 Bone remodeling
6
7 Vitamin D Metabolism Inactive precursor Reflects vitamin D status Marker of vitamin D deficiency Active form Normal range pg/ml Concentrations 1000 fold < 25 D Higher in infants & adolescents No variation with seasons
8 1,25D responsible for active intestinal calcium transport Active, transcellular intestinal calcium transport duodenum when calcium intake is low Facilitated by the carrier protein calbindin Passive, paracellular intestinal calcium transport jejunum and ileum when dietary calcium levels are moderate or high, this pathway responsible for the bulk of calcium absorption
9 Categories of Vitamin D deficiency Categories Sufficient Insufficient Deficient Mild Moderate Severe 25D levels > 30 ng/ml ng/ml <20 ng/ml ng/ml 5-10 ng/ml < 5 ng/ml Institutes of Medicine (IOM): >20 ng/ml is adequate for bone health
10 Parathyroid Hormone (PTH)
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13 Fetal accretion of calcium with age Fetus accrues 30g of calcium, 99% in the bones
14 14 Maternal-Fetal Calcium Gradient Large amounts of calcium and phosphorus are transferred against a concentration gradient from the mother to the fetus Calcium and phosphorus levels in the fetus are higher than maternal levels Calcium levels maintained despite maternal hypocalcemia
15 Placental Parathyroid Related Protein (PTHrP) Up regulates active placental calcium transfer Chondrocyte differentiation & skeletal development Kovac 2011
16 Sources of fetal calcium PTHrP primary source Fetal PTH Controls fetal bone mineralization Responds to maternal hypocalcemia Absence of PTH or PTHRP hypocalcema Intestines Passive absorption of calcium Trivial source since is only amniotic fluid Vitamin D and VDR not important Kidney: Calcium excreted into amniotic fluid PTHrP PTH PTH
17 Vitamin D is not required for fetal skeletal development or mineralization 25D Crosses the placenta Reflects maternal vitamin D status 1,25D (calcitriol) Levels are low Does not cross the placenta Is produced in the placenta and fetal kidneys Not important for fetal calcium and bone homeostasis
18 The Neonate CUT THE CORD Loose PTHrP and calcium from placenta At birth: calcium higher than mother hrs: Calcium decreases Switch to dependence on PTH and 1,25D intestinal calcium absorption skeletal calcium stores renal calcium reabsorption Early ionized calcium PTH to adult ranges by hours calcium 1,25(OH)2D phosphate 3 7 days: Calcium increases to childhood level
19 Neonate is dependent on intestinal absorption of calcium Initial intestinal absorption of calcium is passive Not dependent on vitamin D Lactose in milk increases calcium diffusion As neonate matures Passive absorption of calcium declines Up regulate vitamin D receptor (VDR) and calcium transporting genes and proteins Transition to active transport by weaning Explains why preterm babies do not respond to calcitriol (1,25D)
20
21 Animal Studies Kovacs et al. Am J Physiol Endocrinol Metab :E133-E144 Vdr No Vdr Vdr No Vdr Vitamin D deficient rats, mice and pigs: offspring have normal fetal blood calcium, phosphorus, PTH, normal weight, skeletal mineral and calcium content Fetuses with no Vitamin D receptor (Vdr) : normal calcium homeostasis and bone mineralization. No difference in morphology, growth plates, and periosteal thickness
22 Children with genetic disorders of vitamin D do not have rickets at birth 25(OH)D 1 hydroxylase deficiency Unable to convert 25D to 1,25D Low 1,25D levels Hereditary 1,25D resistant rickets Vitamin D receptor defect End organ resistance to 1,25D Very high 1,25D levels Normal at birth Hypocalcemia, hypophosphatemia, and rickets develop late in the 1st year of life or 2nd year of life
23 Vitamin D deficiency in the mother does not appear to affect the neonate No difference in total calcium content in newborns who died of obstetrical accident was the same in neonates born of normal mothers compared to mothers who had extreme vitamin D deficiency. Bone mineral content does not differ at any site in babies within 15 days of life in vitamin D sufficient vs. deficient mothers. (Weiler HA 2008) Randomized trials of vitamin D supplementation during pregnancy find no effect on cord blood calcium or phosphorus, anthropometric measurement, or radiologic evidence of rickets.
24 Randomized controlled trial of 1000 IU D vs. no supplement in 126 Asian mothers (Brooke, et. al, Brit Med J 1980) Cord blood 25D 10 nmol/l (4 ng/ml) in control group 138 nmol/l (55 ng/ml) in treated group No difference in serum calcium between treated and control group Craniotabes in 6 infants in control group and 2 in treated group No rickets in the 5 infants in control group with hypocalcemia
25 Trial of vitamin D supplementation during pregnancy (400, 2000 or 4000 IU per day) in 350 women (Hollis, et. al., JBMR 2011) Neonatal 25(OH)D was significantly correlated with maternal 25(OH)D and was significantly different by treatment group: 18.2 ng/ml, control 22.8 ng/ml, 2000 IU group 26.5 ng/ml, 4000 IU group; p< No difference in clinical status of the newborns
26
27 History of Rickets First described in 1650 Industrial Revolution 19th century Lack of sunlight, poor diet & poor working conditions of children & mothers Cod liver oil described but not used Vitamin D identified in 1920s Lead to treatment & prevention of nutritional rickets Vitamin D refractory or vitamin D resistant rickets A heterogenous group of disorders of various pathogenesis Sir Edward Mellanby, 1939 Rickets in Vienna in the 1920s
28 Diagnosis of Rickets Usually presents during first 2 years of life & in puberty Presenting complaints Decreased growth rate Skeletal deformities genu varum or valgum Delayed standing or walking Symptoms of hypocalcemia: Muscle weakness, lethary, recurrent respiratory infections, stridor, irritability, tetany, seizures
29 Physical Findings in Rickets Swelling around growth plates wrists, ankle, costrochondral junction (rachitic rosary) Skeletal deformities mechanical stresses on undermineralized bone Chest deformities: Harrison s grooves Spine: scoliosis, kyphosis, lordosis Long bones once children walk Genu varum, genu valgum, Waddling gait Craniotabes & frontal bossing Harrison s grooves Rachitic rosary Craniotabes
30 Vitamin D Deficiency Rickets (Nutritional Rickets) Peak incidence 6 18 months Even in regions where severe vitamin D deficiency during pregnancy is endemic The maturation of intestinal calcium absorption to a vitamin D dependent process likely explains why vitamin D deficient rickets does not usually develop until later Typical scenario Unsupplemented breast fed infants > 6 months of age Breast milk is low in vitamin D (50 IU/L) Darkly pigmented children Limited exposure to the sun
31 Effect of vitamin D deficiency Vachharajani A J et al. Neoreviews 2009;10:e402-e411 e411
32 Vitamin D Deficient Rickets Stage 1 Decreased 25(OH) D decreased 1,25D hypocalcemia Stage 2 secondary hyperparathyroidism > normocalcemia Increased conversion of 25(OH) D to 1,25(OH)2 D Hypophosphatemia Radiographic & clinical manifestations of rickets Stage 3 Further increase in PTH without effect hypocalcemia Severe manifestations of rickets Stage 1 Stage 2 Stage 3 Calcium Low Normal Low Phosphorus Normal Low Low PTH Normal High high Alkaline phosphatase High Higher Highest 1,25D Normal-low High Normal-low
33 Treatment of Nutritional Rickets Vitamin D 200, ,000 IU vitamin D in 1 oral dose Lasts about 3 months 5000 IU vitamin D daily for 1 2 months Calcium mg/d Ca To avoid hungry bone syndrome Prevention IU vitamin D Recommendations Vitamin D supplements for all breast fed children over 6 months
34
35 Congenital rickets Very rare Study of million in India ( ): 3 newborns were identified with congenital rickets (Teotia and Teotia, Indian J Med Res. 2008) Usually in developing countries when women are covered and vitamin D intake is low Results when maternal vitamin D and calcium are low and mothers have osteomalcia
36 Normal ranges: Calcium mmol/l Phosphorus mmol/l alkaline phosphatase IU for baby, IU for mother PTH micromol/l 25 hydroxyvitamin D micromol/l Orbak, et. al., West Indian Medical Journal 2007
37 Normal ranges: Calcium mmol/l Phosphorus mmol/l alkaline phosphatase IU for baby, IU for mother PTH micromol/l 25-hydroxyvitamin D micromol/l Orbak, et. al., West Indian Medical Journal 2007
38 Pathophysiology of congenital rickets Severe maternal calcium depletion Fetal hypocalcemia Maternal hypocalcemia PTH Calcium released Fetal parathyroids Fetal bone
39 Summary Fetal calcium and bone development is dependent on placental PTHrP dependent calcium transfer and fetal PTH Vitamin D does not play a direct role in fetal calcium and bone development Maternal vitamin D supplementation does not effect fetal bone development Children with genetic defects of vitamin D metabolism who make no 1,25D or are resistant to 1,25D are normal at birth. Intestinal calcium absorption becomes critical after birth and is initially passive but soon becomes vitamin D dependent Congenital rickets is very rare and can reliably be excluded as a cause of fractures in young infants in the face of normal calcium, phosphorus, 25D, and alkaline phosphatase
40 The End!
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