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Vitamin D Deficiency Rickets
Fan Yang Associated Professor Pediatric Department
Vitamin D comprises a group of sterols Vitamin D2 = ergocalciferol
Completely synthetic form produced by the irradiation of the plant steroid ergosterol
Vitamin D3 = cholecalciferol
Produced photochemically by the action of sunlight or ultraviolet light from the precursor sterol 7-dehydrocholesterol
Vitamin D = calciferol
Humans & animal utilize only vitamin D3 & they can produce it inside their bodies from cholesterol.
Cholesterol is converted to 7-dehydrocholesterol (7DC), which is a precursor of vitamin D3.
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.
Vitamin D: The Sunshine Vitamin Not always essential Body can make it if exposed to enough sunlight Made from cholesterol in the skin .
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 .Formation of Vitamin D 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.
•Cell differentiation: particularly of collagen & skin epithelium •Immunity: important for Cell Mediated Immunity & coordination of the immune response. .FUNCTIONS •Calcium metabolism: vitamin D enhances ca absorption in the gut & renal tubules.
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 .Vitamin D .
Vitamin D Functions .
25-(OH)2 D binds to vitamin D receptor (VDR) in nucleus Increase in calbindin (Ca-binding protein) Groff & Gropper. 2000 .Vitamin D Affects Absorption of Dietary Ca 1.
25-(OH)2 D3 increases activity of alkaline phosphatase Hydrolyses phosphate ester bonds Releases phosphorus Increase in phosphate carriers .Vitamin D Affects Absorption of Dietary Phosphorus 1.
Vitamin D deficiency .
dust vapour and smoke . Lack of sunshine due to: 1) Lack of outdoor activities 2) Lack of ultraviolet light in fall and winter 3) Too much cloud.Etiology 1.
3-4IU/100ml Egg yolk 25IU/average yolk Herring 1500IU/100g 2) Improper Ca and P ratio . Improper feeding: 1) Inadequate intake of Vitamin D Breast milk 0-10IU/100ml Cow’s milk 0.Etiology 2.
increased requirement Relative deficiency 4. Fast growth. Diseases and drug: Liver diseases. renal diseases Gastrointestinal diseases Antiepileptic Glucocorticosteroid .Etiology 3.
GROUPS AT RISK •Infants •Elderly •Dark skinned •Covered women •Kidney failure patients •Patients with chronic liver disease •Fat malabsorption disorders •Genetic types of rickets •Patients on anticonvulsant drugs .
Vitamin D deficiency •Deficiency of vitamin D leads to: Rickets in small children. Osteomalacia Osteoporosis .
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 PTH required for resorption of Ca from bone Activates a calcium pump on the osteocytic membrane Activates osteoclasts 25-OH D 1.25-(OH)2 D .
P Serum Ca Function of Parathyroid .Pathogenesis Vitamin D deficiency Absorption of Ca.
P product Rickets .Pathogenesis PTH High secretion P in urine P in blood Decalcification of old bone Ca in blood normal or low slightly Ca.
Pathogenesis Low secretion of PTH Failure of decalcification of bone Low serum Ca level Rachitic tetany .
muscular system and other system are also involved. .Clinical manifestation Rickets is a systematic disease with skeletons involved most. but the nervous system.
Clinical manifestation Early stage Usually begin at 3 months old Symptoms: mental psychiatric symptoms Irritability. hidrosis Signs: occipital bald Laboratory findings: Serum Ca. AKP normal or elevated slightly. P normal or decreased slightly.25(OH)D3 decreased Roentgenographic changes: normal or change slightly . sleepless.
Clinical manifestation Advanced stage On the base of early rickets. pigeon chest. Harrison’s groove. with abnormal order. osseous changes become marked and motor development becomes delayed. Osseous changes: 1) Head: craniotables. flaring of ribs . 1. funnel-shaped chest. defects 3) Chest: rachitic rosary. boxlike appearance of skull. frontal bossing. delayed closure of anterior fontanelle 2) Teeth: delayed eruption.
Muscular system: potbelly. late in standing and walking 3. Other nervous and mental symptoms . and lordosis 5) Extremities: bowlegs.or knock knee. greenstick fracture 6) Rachitic dwarfism 2. Motor development: delayed 4.Clinical manifestation 4) Spinal column: scoliosis.kyphosis.
Clinical manifestation Laboratory findings: Serum Ca and P decreased Ca and P product decreased AKP elevated Roentgenographic changes: Wrist is the best site for watching the changes. Late appearance of ossification center Widening of the epiphyseal cartilage Blurring of the preparatory calcification line metaphyses like a cup rarefaction of the bone thinned cortex of the shaft of long bone .
. The blood chemistries become normal. but osseous deformities may be left. except AKP may be slightly elevated. Blood Chemistries and X-ray changes are recovered. Usually seen in Children after 3 years old. Sequelae stage: All the clinical symptoms and signs disappear.Clinical manifestation Healing stage: Symptoms and signs of Rickets alleviate or disappear by use of appropriate treatment.
or P . normal chick Rickets due to deficiency of vitamin D. Ca.Rachitic vs.
Rickets .Vitamin D Deficiency .
ragged.Rickets in wrist . 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 .uncalcified lower ends of bones are porous.
Physical examination 3. History 2.Diagnosis Assessed according to the followings: 1. Roentgenographic changes . Laboratory findings 4.
Differential diagnosis 1. Chondrodystrophy . Hypophosphatemic Vitamin D resistant rickets 2. Cretinism 5. Rickets of Vitamin D dependency 3. Distal renal tubular acidosis 4.
. A single large dose: For severe case. Food and nursing care 2. B. im. Vitamin D3 200000-300000IU. General method Vitamin D 2000-4000IU/day for 2-4 weeks. then change to preventive dosage (400IU). preventive dosage will be used after 2-3 months. or those who can’t bear oral therapy. Prevention of complications 3. Special therapy 1) Vitamin D therapy A. or Rickets with complication.Treatment 1.
or infants under 3 months of age. 3) Plastic therapy: In children with bone deformities after 4 years old plastic surgery may be useful. .Treatment 2) Calcium supplementation: only used for special cases. and those who have already developed tetany. Dosage:1-3 g/day. such as baby fed mainly with cereal.
Advocate sunbathing 3.Advocate breast feeding. give supplementary food on time . 2. Pay much attention to the health care of pregnant and lactating women. instruct them to take adequate amount of vitamin D.Prevention 1.
For those babies who can’t maintain a daily supplementation. inject muscularly Vitamin D3 10000-200000 IU. .Prevention 4. give Vitamin D 800IU per day. twins and weak babies. For term babies and infants the demand of Vitamin D is 400IU per day. Vitamin D supplementation: In prematures.
Calcium supplementation: 0. weak babies and babies fed mainly with cereal .Prevention 5.5-1gm/day. for premature.
Sources of Vitamin D Sunlight is the most important source Fish liver oil Fish & sea food (herring & salmon) Eggs Plants do not contain vitamin D3 .
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 .
TOXICITY •Hypervitaminosis D causes hypercalcemia. which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Disorientation & coma. .
heart.Vitamin D Toxicity Calcification of soft tissue Lungs. 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 Infants: .
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