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Rickets of Vitamin D Deficiency The Second Affiliated Hospital of Shantou University Medical College

Rickets of Vitamin D Deficiency The Second Affiliated Hospital of Shantou University Medical College Ma Lian. Review. Rickets ： signifying a failure in inernalization of growing bone or osteoid tissue.

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Rickets of Vitamin D Deficiency The Second Affiliated Hospital of Shantou University Medical College

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  1. Rickets of Vitamin D DeficiencyThe Second Affiliated Hospital of Shantou University Medical College Ma Lian

  2. Review Rickets：signifying a failure in inernalization of growing bone or osteoid tissue. Failure of mature bone to mineralize is called osteomalacia.

  3. Etiology • Inadequate direct exposure to ultraviolet rays in sunlight • Inadequate intake of vitD (diet may contain little vitD) • Growth • drug • Disease:hepatic and renal lesions、celiac disease、steatorrhea or cystic fibrosis Or both

  4. About Vitamin-D • Two forms : vitD2 /vitD3 • vitD2 :most as irradiated ergosterol,largely replaced the fish liver oils as source • vitD3 :available in human skin as 7-dehydrocholesterol. • both are hydroxylated in the liver to 25－ (OH)2D • in the renal to 1. 25－(OH)2D: facilitate calcium and phosphorus absorpted

  5. Pathology • the epiphyseal plate of metaphysis is well demonstrated. • The cartilage cell is orderly • The calcified matrix forms the epiphyseal plate is regular

  6. The degenerating cartilage, islands of capillaries, osteoblasts, and unmineralized osteoid compose of broad , irregular, rachitic imtermediate zone

  7. Chemical pathology can be conceptualized to be the body’s attempt to maintain normal serum calcium levels. When calcium is lessparathormone is secretedincrease the calcium and phosphorus concentration

  8. Alkaline phosphatase (ALP). (normal level ≦200IU/dL) can be 500UI/dL. But may be normal in infants who have rickets and who are protein or zinc depleted.

  9. aminoaciduria, a decrease of citrate ,and its increased urinary excretion, decreased ability of the kidneys to make an acid urine, phosphaturia, and occasionally ,mellituria. • The parathyroid glands hypertrophy

  10. Clinical manifestations • Early signs: Increased sweating, particularly around the head ,which result in the occipital bone bare

  11. Clinical manifestations • Advanced rickets: • Head: • early signs is craniotabes, • Like a derby hat or ping pong ball .

  12. Thorax: rachitic rosary Harrison’s groove Pigen breast deformity children are late in standing and walking

  13. The deformities of the long bones :knobbing and prominence of the epiphyses

  14. Other manifestations: Teeth-erupting may be delayed,the enamel and extensive aries are defected. Muscle tone is poor

  15. Roentgenographic findings

  16. Diagnosis • The diagnosis is based on: • a history of inadeuate intake of vitamin D and on clinical observation; • then confirmed chemically ; • by roentgenographic examination .

  17. Differential diagnosis • Scurvy: a ledgelike depression with the chondral or sternal portion is displaced below the osseous ribs. • Chondrodystrophy :irregular、concave outlines of the distal ends of the bones ,no roentgenographic evidence of fraying

  18. Other epiphyseal lesions: congenital epiphyseal dysplasia,cytomegalic inclusion isease ,syphilis ,rubella ,and copper deficiency. • Bowlegs :maybe a familial characteristic. • Vitamin D-resistant rickets and other metabolic disturbances with osseous lesions resembling rickets

  19. Complications • Respiratory infections :bronchitis and bronchopneumonia • pulmonary atelectasis • Anemia due to iron deficiency or accompanying infections

  20. Treatment • Natural and artificial light • oral administration of vitD(preferred) daily administration:vitD3:50-150 µg or 1.25(OH)-D: 0.5-2 µg (except vitD refractory rickets

  21. Administering 15000 µg of vitamin D in a single dose without further therapy for several months may be advantageous. More rapid healing follows, possibly with earlier differential diagnosis from genetic vitamin D-resistant rickets .

  22. Roentgn-ray appearance showing healing • A: active rickets • B: healing after 27 day: new line of calcification • C: after 34 day calcification line dense;periosteal calcification increase • D: complete healing after 3 months

  23. Prognosis • If therapy is given in time , healing begins within a few days and progresses slowly until the normal bony structure is restored • It is not a fatal disease,but complications are more likely to cause death of rachitic children than normal children

  24. Prevention • Can be prevented by exposure to ultraviolet light • Administered vitD :daily requirement of vitamin D is 10µg or 400IU • Vitamin D should also be administered to pregnant and lactating mothers

  25. thank you

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