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Vitamin D: The Sunshine vitamin
- 1. Swati Chaudhary M-5429 Division VeterinaryPathology IVRI
- 2. History In 1922,Edward Mellan and Elmer McCollum discovered Vitamin D. Fourth vitamin to be discovered. Fortification of food with vitamin D was patented. Complete eradication of rickets in US.
- 3. fat solublevitamin More than 50 genes are known to be transcribed by it
- 4. Vitamin D fitsthe definition of hormone It is produced by body Has specific tissue targets Does not have to be supplied by the diet.
- 5. Two Major Formsof Vitamin D Vitamin D3, cholecalciferol Vitamin D2, ergo-calciferol
- 6. Other Forms ofVitamin D Vitamin D1: molecular compound of ergocalciferol with lumisterol, 1:1 Vitamin D4: 22-dihydroergocalciferol Vitamin D5: sitocalciferol (made from 7-dehydrosisterol)
- 7. Synthesis Vitamin Dis produced in the two innermost layers of epidermis, the stratum basale and stratum spinosum. The precursor of vitamin D3 is 7- dehydrocholesterol 10,000 to 20,000 IU of vitamin D are produced in 30 minutes of whole- body exposure 7-Dehydrocholesterol reacts with UVB light with peak synthesis occurring between 295 and 297 nm.
- 9. Groff & Gropper,2000 Vitamin D Affects Absorption of Dietary Ca and P 1,25-(OH)2 D binds to vitamin D receptor (VDR) in nucleus The epithelial calcium channel, transient receptor potential vanilloid6 (TRPV6), transports calcium into the cell where it binds to calbindin and is transported across the cell A Ca2+ATPase and Na+/Ca2+ exchanger then discharges calcium into the bloodstream. K.E.Dittmer and K.G.Thompson
- 10. Bone remodeling.In the skeleton, 1,25(OH)2D3, in association with PTH, promotes mobilization of calcium from bone RANKL, a surface ligand on osteoblasts, bind to osteoclasts via RANK (receptor activator for NF-kB) When RANKL binds to RANK, it induces differentiation and maturation of osteoclast progenitor cells to osteoclasts. RANKL is stimulated by 1,25(OH)2D3 via VDREs on the RANKL promoter, thereby inducing osteoclastogenesis, resorption of bone, and mobilization of calcium. K.E.Dittmer and K.G.Thompson
- 11. Parathyroid glands Active vitamin D up regulate calcium-sensing receptor expression by binding to VDREs on the calcium-sensing receptor gene promoter, leading to increased sensitivity of the parathyroid gland to plasma calcium Deficiency of vitamin D results in hypocalcemia, which leads to parathyroid hyperplasia and secondary hyperparathyroidism Kidney. The main role of 1,25(OH)2D3 in the kidney is to control its own production by inhibition of renal 1a-hydroxylase and stimulation of CYP24 (24-hydroxylase) K.E.Dittmer and K.G.Thompson
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- 13. The renalsynthesis of calcitriol is tightly regulated by two counter-acting hormones, with up-regulation via parathyroid hormone and down-regulation via fibroblast-like growth factor-23
- 14. VDRs areexpressed in several white blood cells, including monocytes and activated T and B cells Activated macrophages and lymphoma cells also make 1,25(OH)2 Vitamin D Excessive unregulated production of 1,25(OH)2 Vitamin D by activated macrophages and lymphoma cells is responsible for the hypercalciuria associated with chronic granulomatous disorders and hypercalcemia seen in lymphoma (Adams, 1989; Davies et al., 1994).
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- 16. Nutritional vitaminD 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
- 17. NUTRITIONAL VITAMIN D DEFICIENCY Most common cause globely Etiology • Poor intake - Neonate • Inadequate cutaneous synthesis
- 18. 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 intrauterine growth retardation decreased bone ossification, classic rachitic changes
- 19. SECONDARY VITAMIN DDEFICIENCY. Inadequate absorption - cholestatic liver disease, -defects in bile acid metabolism, - other causes of pancreatic dysfunction, celiac disease, and Crohn disease -intestinal lymphangiectasia -after intestinal resection Decreased hydroxylation in the liver,-insufficient enzyme activity Increased degradation - medications, by inducing the P450 system, Anticonvulsants, such as phenobarbital or phenytoin Antituberculosis medications- isoniazid and rifampin
- 20. 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. They have normal levels of 25-D, but low levels of 1,25-D
- 21. VITAMIN D–DEPENDENT RICKETS, TYPE2. Mutations in the gene encoding the vitamin D receptor Autosomal recessive disorder Levels of 1,25-D are extremely elevated
- 22. GROUPS AT RISK Infants Elderly Dark skinned Covered women Kidney failure patients Patients with chronic liver diseases Fat malabsorption disorders Genetic types of rickets Patients on anticonvulsant drugs
- 23. RICKETS :Defective mineralization of growing bone before epiphyseal fusion OSTEOMALACIA : Defective mineralization of bone after epiphyseal fusion Vitamin D deficiency diseases
- 24. Rickets Pathogenesis Defective mineralizationof osteoid and cartilaginous matrix of developing bone Persistence and continued growth of hypertrophic epiphyseal cartilage Poorly calcified spicules of diaphysis of bone resulting in bowing of legs Broadening of epiphysis with apparent enlargement of joints
- 25. Grossly Enlargement ofends of long bone and costo-chondral articulations Long bones become distorted and deviated Enlarged costo-chondral articulations appear as a string Of beads Flattening of ends of long bones Bones are soft ,easily cut and fractured
- 26. Microscopically Increased proliferatingundegeraded cartilage adjacent to the metaphysis Disarrangement chondrocytes of proliferating cartilage Defective calcification of cartilage and excess un-calcified osteoid tissue in the metaphysis Fibrosis of bone marrow with reduction of myloid cells
- 27. Abnormal growth platedue to increased depth of the hypertrophic cartilage zone and failure of orderly endochondral ossification. Normal ossification
- 28. Irregularity of thegrowth plate and increased depth of the hypertrophic cartilage zone occur
- 29. , Goldner's stain.Bone forming surface with wide osteoid seam. Mineralized bone stains green, unmineralized bone matrix (osteoid) stains red. IN METAPHYSIS
- 30. Clinical signs Bonepain Stiff gait Swelling in the area of the metaphysis Difficulty in rising Bowed limbs Enlargement of costo-chondral junction Lameness Arching of back And pathologic fractures
- 31. Diagnosis Radiographic examination Theradiopacity of rachitic bones is characteristically less than that of normal bone. Growth plates appear widened and irregular. Clinical pathology Elevation of plasma alkaline phosphate Concentrations of serum phosphorus and vitamin D may be altered depending on the cause of rickets.
- 32. Osteomalacia Seen inmature bones and associated with disruption of normal bone remodeling. Osteomalacia is characterized by an accumulation of excessive un- mineralized osteoid on trabecular surfaces.
- 33. Pathogenesis Similar torickets ,no physeal lesion in adult skeleton Gross lesion Thickening of bones which appear soft , easily cut and deformed. Marrow cavity enlarged and cortex is thin and spongy
- 34. Microscopic lesion Activebone resorption /increased activity of osteoclasts Presence of uncalcified osteoid at the margin of cortices, haversian canals and bone trabeculae Expension of haversian canals
- 39. Clinical findings Unthrifty May exhibit pica. Nonspecific shifting lamenesses are common. Fractures can be seen especially in the ribs, pelvis, and long bones. Spinal deformation such as lordosis or kyphosis
- 40. Vitamin D -Sources Synthesized in body Plants (ergosterol) Sun-cured forage Oily fish Egg yolk Butter Liver Cow’s milk 0.3-4IU/100ml Egg yolk 25IU/average yolk Herring 1500IU/100g
- 41. Industrial production VitaminD3 (cholecalciferol) is produced industrially by exposing 7- dehydrocholesterol to UVB light, followed by purification. The 7-dehydrocholesterol is a natural substance in fish organs, especially the liver, or in wool grease (lanolin) from sheep. Vitamin D2(ergocalciferol) is produced in a similar way using ergosterol from yeast or mushrooms
- 42. Vitamin toxicity HypervitaminosisD is a state of vitamin D toxicity. The normal range for blood concentration is 30.0 to 74.0 nanograms per milliliter (ng/mL). Causes hypercalcemia which manifest as: Nausea & vomiting Excessive thirst & polyuria Severe itching Joint & muscle pains Disorientation & coma.
- 43. Vitamin D Toxicity Calcificationof soft tissue Lungs, heart, blood vessels Hardening of arteries (calcification ) Excess blood calcium leads to stone formation in kidney.
- 44. Plants containing 1,25-dihydroxycholecalciferol (calcitriol)glycoside Cestrum diurnum (wild jasmine) Trisetum flavescens (golden oats or yellow oat grass) Nierembergia veitchii Solanum esuriale S. torvum and S malacoxylon
- 45. Treatment No practicaltreatment for vitaminD3 toxicity is currently available.
- 46. references K. E.Dittmer and K. G. Thompson ,Vitamin D Metabolism and Rickets in Domestic Animals A Review Veterinary Pathology48(2) 389-407. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride Ross AC, Taylor CL, Yaktine AL, et al. Dietary Reference Intakes for Calcium and Vitamin D (2011). Vegad JL , A Textbook of Veterinary General Pathology
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