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Rickets

Background
Rickets
is a disease of growing bone that is
unique to children and adolescents.

It is caused by a failure of osteoid to


calcify in a growing person.

Failure of osteoid to
calcify in adults is called
Osteomalacia.
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Vitamin D deficiency rickets occurs when
the metabolites of vitamin D are
deficient.
Less commonly, a dietary deficiency of
calcium or phosphorus may also
produce rickets

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Vitamin D-3 (cholecalciferol)
is formed in the skin from a derivative of
cholesterol under the stimulus of
ultraviolet- B light.

Natural nutritional sources of


vitamin D are limited
primarily to fatty, ocean-going
fish.

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Source of vitamin D
1. Ultraviolet light
2. Cod liver oil
3. Ergosterol (vitamin D-2)

Dairy milk is fortified with vitamin D


(400 IU/L)

Human milk contains little


vitamin D(less than 20-40
IU/L)
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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.
n
Cholecalciferol (i.e., vitamin D-3) is formed in
the skin from 5-dihydrotachysterol.

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This steroid undergoes hydroxylation in
2 steps .

The first hydroxylation


Occurs at position 25 in the liver, producing
calcidiol (25-hydroxycholecalciferol)

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The second hydroxylation
Occurs in the kidney at the 1
position, where it undergoes
hydroxylation to the active metabolite
calcitriol
(1,25-dihydroxycholecalciferol )

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Calcitriol
Acts at 3 known sites to tightly
regulate calcium metabolism:
(1) it promotes absorption of calcium and
phosphorus from the intestine
(2) it increases reabsorption of phosphate in the kidney

(3) it acts on bone to release


calcium and phosphate.

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Epidemiology

1.Children to use sunscreen while outdoors


2.Children spend more time
indoors watching television or
playing electronic games,
instead of playing outdoors

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Clinical Presentation

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Knock knee deformity (genu
valgum)

Bowleg deformity
(genu varum)

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Wrist
enlargement

Rib beading
(rachitic rosary)

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Frontal
bossing

Tibial
bowing

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Scoliosis

Harrison's sulcus
and pot belly

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Differential Diagnoses
1. Hypophosphatasia
2. Jansen syndrome
3. Hypophosphatemic vitamin D–
resistant rickets.
4. Severe calcium deficiency
5. Severe phosphorus deficiency

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Khorfakkan Hospital
Serum Chemistry

Calcium is low

Calcidiol (25-hydroxy vitamin D) is low

Parathyroid hormone is elevated

Phosphorus level is low

Alkaline phosphatase levels


are uniformly elevated .

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Radiography

1. Cupping of the metaphysis


2. Fraying of the edge
3. Widening of the osteoid tissue
4. Hypominiralization of bones

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Anteroposterior and lateral radiographs of the wrist of
an 8-year-old boy with rickets demonstrates cupping and
fraying of the metaphyseal region.

3/8/2012 Rickets Prof. Dr.Saad S Al ani 24


Khorfakkan Hospital
Radiograph in a 4-year-old girl with rickets depicts bowing of
the legs caused by loading.

3/8/2012 Rickets Prof. Dr.Saad S Al ani 25


Khorfakkan Hospital
Treatment & Management

Treatment for rickets may be


administered gradually over several
months or in a single-day dose of
15,000 mcg (600,000 U) of vitamin D

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If the gradual method is chosen, 125-250
mcg (5000-10,000 U) is given daily for 2-3
months until:
1. Healing is well established
2. Alkaline phosphatase
concentration is approaching normal
range

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If the vitamin D dose is administered in
a single day, it is usually divided into 4
or 6 oral doses. An intramuscular
injection is also available
In nutritional rickets:
1.Phosphorus level rises in 96 hrs
2.Radiographic healing is visible in
6-7 days

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Rickets Medications

Vitamin D is a fat-soluble vitamin used to


prevent or treat vitamin D deficiency

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Cholecalciferol
(Vitamin D3)
1.single-day dose of 15,000 mcg (600,000U),
which is usually divided into 4 or 6 oral
doses
An intramuscular injection is also available.
2.An alternative regimen is to give 125-
250 mcg (5000-10,000 U) daily for 2-3
months

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3/8/2012 Rickets Prof. Dr.Saad S Al ani 33
Khorfakkan Hospital

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