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![RENAL LOSSES
X-linked hypophosphatemic rickets[*]
Autosomal dominant hypophosphatemic rickets[*]
Hereditary hypophosphatemic rickets with
hypercalciuria
Overproduction of phosphatonin
Tumor-induced rickets[*]
McCune-Albright syndrome[*]
Epidermal nevus syndrome[*]
Neurofibromatosis[*]
Fanconi syndrome
Dent disease
DISTAL RENAL TUBULAR ACIDOSIS](https://image.slidesharecdn.com/presentation2-120707063852-phpapp01/85/rickets-27-320.jpg)
![RENAL OSTEODYSTROPHY
Low phospharous diet [low phosphate formulas to
infants].
Phosphate binders to enhance fecal excretion –
calcium carbonate & calcium acetate, newer non-
calcium based binders – sevelamer [Aluminum based
binders should be avoided].
Vit. D therapy :
If 25 (OH) D levels are low treat with ergocalciferol.
If 25 (OH) D levels are normal but PTH is high, treat
with calcitriol or 1,25 (OH) D 0.01-0.05 mg/kg/24hr](https://image.slidesharecdn.com/presentation2-120707063852-phpapp01/85/rickets-93-320.jpg)
![FANCONI’S SYNDROME
Treating the cause
Eliminating heavy metal exposure, chelation
therapy.
Discontinuation of toxic drug.
Cystemine in cystinosis.
Avoiding tyrosine in tyrosinemia.
Bicarbonate & phosphorous supplementation [to
correct acidosis and hypophosphatemia]
Oral calcitriol.](https://image.slidesharecdn.com/presentation2-120707063852-phpapp01/85/rickets-94-320.jpg)
Uploaded byKamal Gupta
rickets
Vitamin D is essential for calcium absorption and bone health. It is produced in the skin upon exposure to sunlight and is also obtained through dietary sources. Vitamin D must undergo hydroxylation in the liver and kidneys to become its active form. Deficiency can result in rickets in children or osteomalacia in adults due to impaired bone mineralization. Risk groups include those with inadequate sun exposure or dietary intake, as well as patients with liver or kidney disease.
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- 1. Kamal kishor gupta residentof orthpaedics
- 2. VITAMIN D Humans& animal utilize only vitamin D3 & they can produce it inside their bodies from cholesterol. Cholesterol is converted to 7-dehydro- cholesterol (7DC), which is a precursor of vitamin D3.
- 3. VITAMIN D Exposure to the ultraviolet rays in the sunlight convert 7DC to cholecalciferol. Vitamin D3 is metabolically inactive until it is hydroxylated in the kidney & the liver to the active form 1,25 Dihydroxycholecalciferol. 1,25 DHC acts as a hormone rather than a vitamin, endocrine & paracrine properties.
- 4. Vitamin D: TheSunshine Vitamin Not always essential Body can make it if exposed to enough sunlight Made from cholesterol in the skin
- 6. Formation of VitaminD Skin (UV light) 7-dehydro cholesterol Vitamin D3 Ergosterol Vitamin D2 Liver OH-group added 25-Hydroxy vitamin D3 Storage form of vitamin (~3 months storage in liver) Kidney OH-group added by 1-hydroxylase 1,25-dihydroxy vitamin D3 Active form of vitamin D, a “steroid hormone” OH-group added by 24-hydroxylase 24,25-dihydroxy vitamin D3 Inactive form of vitamin D, ready for excretion
- 8. FUNCTIONS •Calcium metabolism: vitaminD enhances ca absorption in the gut & renal tubules. •Cell differentiation: particularly of collagen & skin epithelium •Immunity: important for Cell Mediated Immunity & coordination of the immune response.
- 9. Vitamin D -Functions Bone development Calcium absorption (small intestine) Calcium resorption (bone and kidney) Maintain blood calcium levels Phosphorus absorption (small intestine) Hormone Regulation of gene expression Cell growth
- 10.
- 11. Vitamin D AffectsAbsorption of Dietary Ca 1,25-(OH)2 D binds to vitamin D receptor (VDR) in nucleus Increase in calbindin (Ca-binding protein) Groff & Gropper, 2000
- 12. Vitamin D AffectsAbsorption of Dietary Phosphorus 1,25-(OH)2 D3 increases activity of alkaline phosphatase Hydrolyses phosphate ester bonds Releases phosphorus Increase in phosphate carriers
- 13.
- 14. Etiology 1. Lackof sunshine due to: 1) Lack of outdoor activities 2) Lack of ultraviolet light in fall and winter 3) Too much cloud, dust vapour and smoke
- 15. Etiology 2. Improperfeeding: 1) Inadequate intake of Vitamin D Breast milk 0-10IU/100ml Cow’s milk 0.3-4IU/100ml Egg yolk 25IU/average yolk Herring 1500IU/100g 2) Improper Ca and P ratio
- 16. Etiology 3. Fastgrowth, increased requirement Relative deficiency 4. Diseases and drug: Liver diseases, renal diseases Gastrointestinal diseases Antiepileptic Glucocorticosteroid
- 17. GROUPS AT RISK •Infants •Elderly •Darkskinned •Covered women •Kidney failure patients •Patients with chronic liver disease •Fat malabsorption disorders •Genetic types of rickets •Patients on anticonvulsant drugs
- 18. Parathyroid Hormone (PTH) Calcium-sensor protein in the thyroid gland Detects low plasma calcium concentrations Effects of parathyroid hormone Urine / kidneys Increases calcium reabsorption Increases phosphorus excretion Stimulates 1-hydroxylase activity in the kidneys 25-OH D 1,25-(OH)2 D PTH required for resorption of Ca from bone Activates a calcium pump on the osteocytic membrane Activates osteoclasts
- 19. Pathogenesis PTH High secretion P in urine Decalcification of old bone P in blood Ca in blood normal or low slightly Ca, P product Rickets
- 20. Pathogenesis Low secretion of PTH Failure of decalcification of bone Low serum Ca level Rachitic tetany
- 21. Vitamin D deficiency •Deficiencyof vitamin D leads to: Rickets in small children. Osteomalacia Osteoporosis
- 22. RICKETS : Defectivemineralization of growing bone before epiphyseal fusion RENAL OSTEODYSTROPHY : Alteration in skeletal growth & remodelling in CRF OSTEOMALACIA : Defective mineralization of bone after epiphyseal fusion OSREOPOROSIS : Proportionate loss of bone volume & minerals OSTEOPENIA OF PREMATURITY : Post natal inadequate bone mineralization in preterm babies
- 23. - Causes ofRickets VITAMIN D DISORDERS CALCIUM DEFICIENCY PHOSPHORUS DEFICIENCY RENAL LOSSES DISTAL RENAL TUBULAR ACIDOSIS
- 24. VITAMIN D DISORDERS Nutritional vitamin D deficiency Congenital vitamin D deficiency Secondary vitamin D deficiency Malabsorption Increased degradation Decreased liver 25-hydroxylase Vitamin D–dependent rickets type 1 Vitamin D–dependent rickets type 2 Chronic renal failure
- 25. CALCIUM DEFICIENCY Lowintake Diet Premature infants (rickets of prematurity) Malabsorption Primary disease Dietary inhibitors of calcium absorption
- 26. PHOSPHORUS DEFICIENCY Inadequateintake Premature infants (rickets of prematurity) Aluminum-containing antacids
- 27. RENAL LOSSES X-linkedhypophosphatemic rickets[*] Autosomal dominant hypophosphatemic rickets[*] Hereditary hypophosphatemic rickets with hypercalciuria Overproduction of phosphatonin Tumor-induced rickets[*] McCune-Albright syndrome[*] Epidermal nevus syndrome[*] Neurofibromatosis[*] Fanconi syndrome Dent disease DISTAL RENAL TUBULAR ACIDOSIS
- 28. NUTRITIONAL VITAMIN D DEFICIENCY Most common cause globely Etiology –poor intake - Neonate -Infant -on formula diet -on breast milk - inadequate cutaneous synthesis
- 29. NUTRITIONAL VITAMIN D DEFICIENCY Clinical Manifestation The clinical features are typical of rickets with a significant minority presenting with symptoms of hypocalcemia prolonged laryngospasm occasionally fatal. these children have an increased risk of pneumonia and muscle weakness, adding to a delay in motor . developments.
- 30. CONGENITAL VITAMIN D DEFICIENCY. severe maternal vitamin D deficiency during pregnancy Maternal risk factors poor dietary intake of vitamin D, lack of adequate sun exposure closely spaced pregnancies presentation symptomatic hypocalcemia, intrauterine growth retardation decreased bone ossification, classic rachitic changes
- 31. SECONDARY VITAMIN D DEFICIENCY. inadequate absorption -cholestatic liver disease, -defects in bile acid metabolism, - cystic fibrosis - other causes of pancreatic dysfunction, celiac disease, and Crohn disease -intestinal lymphangiectasia -after intestinal resection decreased hydroxylation in the liver,-insufficient enzyme activity more than 90% increased degradation - medications, by inducing the P450 system,- -anticonvulsants, such as phenobarbital or phenytoin; -antituberculosis medications isoniazid and rifampin
- 32. VITAMIN D–DEPENDENT RICKETS, TYPE1. autosomal recessive disorder, mutations in the gene encoding renal 1α- hydroxylase preventing conversion of 25-D into 1,25-D. present during the 1st 2 yr of life classic features of rickets including symptomatic hypocalcemia. They have normal levels of 25-D, but low levels of 1,25-D (see Table 48-4
- 33. VITAMIN D–DEPENDENT RICKETS, TYPE2. mutations in the gene encoding the vitamin D receptor, Levels of 1,25-D are extremely elevated autosomal recessive disorder Most patients present during infancy, although less severely affected patients may not be diagnosed until adulthood. Less severe disease is associated with a partially functional vitamin D receptor. 50–70% of children - alopecia, -more severe alopecia areata alopecia totalis. Epidermal cysts.
- 34. CHRONIC RENAL FAILURE decreased activity of 1α-hydroxylase in the kidney, hyperphosphatemia as a result of decreased renal excretio Along with inadequate calcium absorption and secondary hyperparathyroidism, the rickets may be worsened by the metabolic acidosis of chronic renal failure. In addition, failure to thrive and growth retardation may be accentuated because of the direct effect of chronic renal failure on the growth hormone axis.
- 35. PHOSPHOROUS DEFICIENCY INADEQUATEINTAKE. -rare ,severe anorexia -long-term use of aluminum- containing antacids PHOSPHATONIN. humoral mediator that decreases renal tubular reabsorption of phosphate and therefore decreases serum phosphorus. decreases the activity of renal 1α-hydroxylase, Fibroblast growth factor-23 (FGF-23) is the most well characterized phosphatonin
- 36. X-LINKED HYPOPHOSPHATEMIC RICKETS. X-linkedhypophosphatemic rickets (XLH) most common, with a prevalence of 1/20,000. The defective gene is on the X chromosome, but female carriers are affected, so it is an X-linked dominant disorder . PHosphate-regulating gene with homology to Endopeptidases on the X chromosom –PHEX gene role in inactivating a phosphatonin or phosphatonins. FGF-23 may be the target phosphatonin.
- 37. Clinical Manifestations. Thesepatients have rickets, but abnormalities of the lower extremities and poor growth are the dominant features. Delayed dentition and tooth abscesses are also common. Some patients have hypophosphatemia and short stature without clinically evident bone disease.
- 38. AUTOSOMAL DOMINANT HYPOPHOSPHATEMIC RICKETS. Less common mutation in the gene encoding FGF-23. The mutation prevents degradation of FGF-23 by proteases, leading to increased levels of this phosphatonin hypophosphatemia, and inhibition of the 1α- hydroxylase in the kidney, causing a decrease in 1,25-D synthesis.
- 39. HEREDITARY HYPOPHOSPHATEMIC RICKETS WITHHYPERCALCiuRIA. The primary problem is a renal phosphate leak that causes hypophosphatemia, which then stimulates production of 1,25-D. The high level of 1,25-D increases intestinal absorption of calcium, suppressing PTH. Hypercalciuria ensues due to the high absorption of calcium and the low level of PTH, which normally decreases renal excretion of calcium
- 40. OVERPRODUCTION OF PHOSPHATONIN Tumor-inducedosteomalacia McCune-Albright syndrome , an entity that includes the triad of polyostotic fibrous dysplasia, hyperpigmented macules, and polyendocrinopathy epidermal nevus syndrome, sporadic disorder consisting of congential epidermal nevi associated with anomalies of other organ systems, especially the skeleton and central nervous system Rickets due to phosphate wasting is an extremely rare complication in children with neurofibromatosis
- 41. FANCONI SYNDROME Fanconisyndrome is secondary to generalized dysfunction of the renal proximal tubules There are renal losses of phosphate, amino acids, bicarbonate, glucose, urate, and other molecules that are normally reabsorbed in the proximal tubule. hypophosphatemia -- phosphate losses proximal renal tubular acidosis -- bicarbonate losses. The findings of aminoaciduria, glucosuria, and a low serum uric acid level are helpful diagnostically. genetic disorder –cystinosis -wilson disease Secondary to –heavy metal exposure -drug toxicity ,(ifosfamide, valproate, aminoglycosides
- 42. DENT DISEASE X-linkeddisorder ,,,,male mutations in the gene encoding a chloride channel that is expressed in the kidney. hematuria, nephrolithiasis, nephrocalcinosis, ric kets, and chronic renal failure. Almost all patients have low molecular weight proteinuria and hypercalciuria . Rickets occurs in approximately 25% of patients, and it responds to oral phosphorus supplements.
- 43. Aetiological classification – enal causes – R Renal osteodystrophy Familial hypophosphataemic rickets Renal tubular acidosis Fanconi syndrome Primary Secondary - cystinosis, wilsons disease,lowe syndrome,tyrosinemia Vitamin D dependent type 1 rickets Vitamin D dependent type 2 rickets
- 44. Non renal causes– Nutritional Intestinal – malabsorption Hepatobiliary Metabolic – anticonvulsant therapy Oncogenic- mesenchymal tumours Rickets of prematurity
- 45. Biochemical classification – CALCIUM DEFICIENCY WITH SECONDARY HYPERPARATHYROIDISM – Vitamin D deficiency rickets Rickets with malabsorption hepatic disease anticonvulsant therapy Renal osteodystrophy Vitamin D dependent type 1 rickets
- 46. Primary phosphate deficiency(no secondaryhyperparathyroidism) Familial hypophosphatemic rickets. Fanconi syndrome Renal tubular acidosis Oncogenic hypophosphatemia Phosphate deficiency - malabsorption, low phosphate level.
- 47. End organ resistanceto 1,25 Dihydroxy Vit D3 Vitamin D dependent type 2 rickets.
- 48. Bones…. What dothey need to be strong? calcium/ PO4 Vit D PTH Ph
- 49. Pathophysiology of rickets– Low active vitamin D levels Hyperparathyroidism Metabolic Acidosis Hypophosphatemia Multiple factors in renal disease – Anorexia Diet restriction Uremic toxins
- 50. Age of presentation VITAMIN D DEFICIENCY RICKETS – 6 to 18 months. NON NUTRITIONAL RICKETS Beyond this age group.
- 51. Skeletal manifestations HEAD– Craniotaes Delayed closure of anterior fontanelle Frontal and parietal bossing Delayed eruption of primary teeth Enamel defects and caries teeth
- 53. chest Rachitic rosary Harrison groove Respiratory infections and atelectasis
- 55. back Scoliosis Kyphosis Lordosis
- 56. Vitamin D Deficiency- Rickets
- 58. Skeletal manifestations EXTREMITIES– Enlargement of long bones around wrists and ankles Bow legs, knock knees, anterior curving of legs Coxa vara and green stick fractures Deformities of spine, pelvis and leg – rachitic dwarfism Lower extremities are extensively involved in Familial hypophosphatemic rickets. Upper limb more involved than lower limbs in Hypocalcemic rickets.
- 62. chief complaint skeletaldeformities, difficulty walking due to a combination of deformity failure to thrive and symptomatic hypocalcemia (
- 63. Extra – skeletalmanifestations SEIZURES AND TETANY – Secondary to hypocalcemia in Vit D deficiency rickets and VDDR type 1 HYPOTONIA AND DELAYED MOTOR DEVELOPMENT In rickets developing during infancy. PROTUBERANT ABDOMEN, BONE PAIN, WADDLING GAIT AND FATIGUE. In older children presenting with rickets
- 64. Extra – Skeletalmanifestations. Features of primary problems Features of hepatic disease renal failure recurrent vomiting. acidotic breathing or failure to thrive. ASYMPTOMATIC Radiologists detect in X ray chest film taken for a different reason in a child.
- 66. Investigations, BASIC INVESTIGATIONSTO CONFIRM RICKETS Serum Ca, P and SAP X rays of ends of long bones at knees or wrists CLASSICAL RADIOLOGICAL CHANGES Disappearance of provisional zone of calcification Widening, fraying, cupping of the distal ends of shaft.
- 67. radiology most easilyvisualized on posteroanterior radiographs of the wrist ,knee ,chest Decreased calcification leads to thickening of the growth plate. The edge of the metaphysis loses its sharp border, which is described as fraying. In addition, the edge of the metaphysis changes from a convex or flat surface to a more concave surface. This is termed cupping,
- 68. and ismost easily seen at the distal ends of the radius, ulna, and fibula. There is widening of the distal end of the metaphysis, corresponding to the clinical observation of thickened wrists and ankles, as well as the rachitic rosary. Other radiologic features include coarse trabeculation of the diaphysis and generalized rarefaction
- 72. Second level investigations Blood urea, creatinine, electrolytes, ABG Tubular reabsorption of phosphate( Trp) Urine analysis for specific gravity, glucose, protein, aminoacids, potass ium and calcium. USG abdomen LFT, malabsorption and IEM studies
- 73. Tertiary level investigations Estimation of vitamin D metabolites to differentiate VDDR type 1 from type 2 Receptor vitamin D interaction – in vitro study to assess VDDR type 2 Bone mineral content Bone densitometry
- 74. VIT D LEVELIN SERUM - 25 (OH) D3 level ng/ml DEFICIENT < 10 INSUFFICIENT 10 - 20 OPTIMAL 20 - 60 HIGH 60 - 90 TOXIC >90
- 75. Practical approach tochild with rickets. Level 1. Is it true rickets or rickets like states ? Do preliminary investigations – Serum calcium, phosphate, SAP Have a close look at the x rays Consider the following conditions – Hypophosphatasia, Metaphyseal dysplasia
- 76. Level 1 –is it true rickets or rickets like states ? Features Radiological signs similar to rickets. But growth plate are not wide with differential involvement of bones in a joint. Eg. Femur shows changes but tibia is normal. Levels of serum Ca, P and SAP normal. Diagnosis Metaphysial dysplasia.
- 77. Features .---- Clinical signs or rickets are present but x rays show tongue like radiolucency projecting from growth plate into metaphysis whereas in rickets growth plate is uniformly wide. SAP levels are low but S. ca, P Levels are normal. Diagnosis -- Hypophasphatasia
- 78. Practical approach torickets Level 2 – is it nutritional or non nutritional ? Look for clues in the history or examination- prematurity neonatal cholestasis anticonvulsant therapy chronic renal disease
- 79. Level 1.. Isit nutritional or non nutritional? Useful clues Jaundice - hepatobiliary disease metabolic disorders Cataract - galactosemia, wilsons Positive family history - metabolic disease, RTA Mental retardation, seizures - Galactosemia, drug induced rickets in primary CNS problem Alopecia - VDDR type 2.
- 80. Level 2.. Isit nutritional or non nutritional? In the absence of clues – Presume and treat it as vit D deficiency rickets. Give vitamin D2 (inj. arachitol) 600000 units 2 doses at two to three weeks interval . Improvement occurs in nutritional rickets. Healing is indicated by the presence of provisional zone of calcification. Non healing favours a non nutritional cause.
- 81. Level 2.. Isit nutritional or non nutritional? Features of non nutritional causes Presentation before six months or after two years of age Associated failure to thrive Positive family history Obvious clues mentioned earlier Failure of vitamin D therapy
- 82. Level 3. ifit is non nutritional and lack any obvious clues it could be either due to GI or renal cause Features …. Recurrent diarrhea, oily stools. Recurrent abdominal pain and distension. Anemia, hypoproteinemia. Multiple vitamin and mineral deficiencies. Diagonosis - Malabsorption with rickets.
- 83. If it isnon nutritional and lack any obvious clues it could be either due to GI or renal cause Features … Hepatobiliary findings. Raised serum billirubin, low serum albumin and prolonged prothrombin time. Diagnosis - Hepatic rickets
- 84. Level 3.. Ifit is non nutritional and lack any obvious clues it could be either due to GI or renal cause Features… Failure to thrive, rec. vomiting, lethargy, acidotic breathing. Hypertension, anemia with or without edema. Positive findings in urine analysis. Abnormalities in electrolytes, blood urea and creatinine. Renal abnormalities in ultrasound abdomen. Diagnosis –Renal rickets.
- 85. Level 4.. Ifit is rickets due to renal causes what is the underlying renal problem that led to rickets.? Depends on the clinical features of chronic renal failure and on laboratory investigations. Do urine analysis.. blood for electrolytes, urea and creatinine. blood gas analysis. ultrasonography of abdomen.
- 86. Features… Vomiting, lethargy, growth retardation Hypertension, anemia, with or without edema. Features of obstructive uropathy. Raised blood urea, creatinine.. S. potassium may be high. Abnormalities in USG, MCU and DMSA scan. Diagnosis – Chronic renal failure - renal osteodystrophy.
- 87. Features… Recurrentvomiting, diarrhoea with acidotic breathing. Positive family history. Metabolic acidosis with normal anion gap, hypokalemia, and raised serum chloride Normal blood urea and serum creatinine. No proteinuria or glycosuria. Diagnosis - Renal tubular acidosis.
- 88. Features…. Severeform of rickets with stunting and deformity. Features mentioned in RTA. Proteinura, glycosuria present. Normal or slightly increased B.urea and S.creatinine. Features of underlying causes such as cystinosis. diagnosis. - Fanconi syndrome.
- 89. Features… Lowerlimb deformity, stunted growth. Often with family history. Frequent dental abscess and early decay. Low serum phosphate and low TRP. Diagnosis – Familial hypophosphataemic rickets(FHR).
- 90. Level 5.. Childwith rickets, no clues so far, what else? Features… Often presenting in early infancy. Hypocalcemic tetany. Improvement with vitamin D therapy and recurrence of symptoms on discontinuation. Diagnosis - vitamin D dependent rickets type1
- 91. Features… Alopeciawith or without any response to any form of vitamin D High serum levels of 1,25 dihydroxy vitamin D. Diagnosis – vitamin D dependent rickets type2 1,25(OH)2 vit D level is high in contrast to VDDR type 1 where it is low.
- 92. Types of ricketsand treatment Vit D deficiency rickets – 1 alpha vit D3 or vit D2(arachitol) 6,00,000 IU every two to three weeks IM 2 to 3 doses. (STOSS REGIMEN) VDDR 1 – 1,25 vit D 0.25 to 1.0 mcg/day orally. VDDR 2 – 1,25 vit D or 1 alpha Vit D 6 mcg/kg/day (total of 30 to 60 mcg orally) with calcium supplements.
- 93. RENAL OSTEODYSTROPHY Lowphospharous diet [low phosphate formulas to infants]. Phosphate binders to enhance fecal excretion – calcium carbonate & calcium acetate, newer non- calcium based binders – sevelamer [Aluminum based binders should be avoided]. Vit. D therapy : If 25 (OH) D levels are low treat with ergocalciferol. If 25 (OH) D levels are normal but PTH is high, treat with calcitriol or 1,25 (OH) D 0.01-0.05 mg/kg/24hr
- 94. FANCONI’S SYNDROME Treatingthe cause Eliminating heavy metal exposure, chelation therapy. Discontinuation of toxic drug. Cystemine in cystinosis. Avoiding tyrosine in tyrosinemia. Bicarbonate & phosphorous supplementation [to correct acidosis and hypophosphatemia] Oral calcitriol.
- 95. RTA 3-5 meq/kg/dayof alkali in distal RTA 5-15 meq/kg/day of alkali in proximal RTA K supplementation accoding to S.k level
- 96. RICKETS OF PREMATURITY Calcium 100 mg/kg/day Po4 50mg/kg/day Vit D according to daily requirement for 3 months
- 97. FAMILIAL HYPOPHOSPHATEMIC RICKETS Replacementof po4 every 4 to 6 hourly 1 alpha Vit D
- 98. Rickets in wrist- uncalcified lower ends of bones are porous, ragged, and saucer-shaped (A) Rickets in 3 month old infant A (B) Healing after 28 days of treatment (C) After 41 days B C of treatment
- 99. Prevention 1. Paymuch attention to the health care of pregnant and lactating women, instruct them to take adequate amount of vitamin D. 2. Advocate sunbathing 3.Advocate breast feeding, give supplementary food on time
- 100. Prevention 4. VitaminD supplementation: In prematures, twins and weak babies, give Vitamin D 800IU per day, For term babies and infants the demand of Vitamin D is 400IU per day, For those babies who can’t maintain a daily supplementation, inject muscularly Vitamin D3 10000-200000 IU.
- 101. Prevention 5. Calciumsupplementation: 0.5-1gm/day, for premature, weak babies and babies fed mainly with cereal
- 102. Sources of VitaminD Sunlight is the most important source Fish liver oil Fish & sea food (herring & salmon) Eggs Plants do not contain vitamin D3
- 103. Vitamin D -Sources Not found naturally in many foods Synthesized in body Plants (ergosterol) Sun-cured forages Fluid milk products are fortified with vitamin D Oily fish Egg yolk Butter Liver Difficult for vegetarians
- 104. TOXICITY •Hypervitaminosis D causes hypercalcemia,which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Disorientation & coma.
- 105. Vitamin D Toxicity Calcification of soft tissue Lungs, heart, blood vessels Hardening of arteries (calcification) Hypercalcemia Normal is ~ 10 mg/dl Excess blood calcium leads to stone formation in kidneys Lack of appetite Excessive thirst and urination