الفهرس 
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Abstract
Rickets develops when growing bones fail to mineralize. In most cases, the diagnosis is established with a thorough history and physical examination and confirmed by laboratory evaluation.Nutritional Rickets has recently re-emerged as a problem in many countries where it was thought to have been eradicated. Recent analysis shows that hospitalization rates for rickets in England are now the highest in five decades. Nutritional rickets can be caused by inadequate intake of nutrients (vitamin -D in particular); however, it is very common in dark-skinned children who have limitedsun exposure and in infants who are breastfed exclusively. Vitamin D deficiency represents one of causes of delayed motor development especially delayed walking in infants.
Vitamin D–dependent rickets, type I results from abnormalities in the gene coding for 25(OH)D3-1-a-hydroxylase, and type II results from defective vitamin D receptors. The vitamin D–resistant types are familial hypophosphatemic rickets and hereditary hypophosphatemic rickets with hypercalciuria.Other causes of rickets include renal disease, medications, and malabsorption syndromes. Nutritional rickets is treated by replacing the deficient nutrient. Mothers who breastfeed exclusively need to be informed of the recommendation to give their infants vitamin D supplements beginning after the first two months of life to prevent nutritional rickets. Vitamin D–dependent rickets, type I is treated with vitamin D; management of type II is more challenging.Familial hypophosphatemic rickets is treated with phosphorus and vitamin D, whereas hereditary hypophosphatemic rickets with hypercalciuria is treated with phosphorus alone. Families with inherited rickets may seek genetic counseling.
The aim of early diagnosis and treatment is to resolve biochemical derangements and prevent complications such as severe deformities that may require surgical intervention. In the current work we have studied 100 patients, with a mean age of 2.42 years, who presented with Rickets in Rickets outpatient clinic of the National Institute of Neuromotor System.
This study aimed to clincally evaluates different types of Rickets in children age from 4 months to 10 years presented to outpatient clinic of the National institute of Neuromotor System.
Rickets is a preventable disease and prevention should start in pregnancy. The simplest measure for prevention is adequate sunlight exposure; however, in populations where this is impracticable or implausible, vitamin D supplementation should be instituted.Vitamin D 400 IU per day is sufficient to maintain vitamin D status in the range in which adverse skeletal consequences are very unlikely, suggesting that a daily supplement ensures that irrespective of skin colour,latitude, sunlight exposure, pollution, and societal orcultural pressures to cover up, the growing skeleton will get what it needs.
The most physiological method to prevent vitamin D insufficiency/deficiency is to educate society, and thus, to ensure that mothers and infants are sufficiently exposed to sunlight and eat a balanced diet rich in Ca and vitamin D. Then again, detection of the maternal factors causing vitamin D insufficiency and taking measures to target these factors is essential in preventing cases of early rickets.
For infants, it was initially recommended in the USA to give 100 IU vitamin D per day for the prevention of rickets. In1963, the American Academy of Pediatrics (AAP) introduced the protocol of 400 IU/day of vitamin D starting from the2nd month of life for rickets prophylaxis.