儿
科
医
院
徐
秀
Vitamin D deficiency
Provitamin D3
Ultraviolet light
In the
skin,7-dehydrocholesterol
Vitamin D3
(an inactive form)
25-hydroxy vitamin D3
Hydroxylation
In the
Liver:
foods
1,25-hydroxy vitamin D3
(active form)
Hydroxylation
In the
kidneys:
Vitamin D Synthesis and Activation
Vitamin D roles
? Facilitate intestinal absorption of
calcium and phosphorus
? Promote renal reabsorption of
phosphorus
? Direct effect on bone deposition and
reabsorption of calcium and phosphorus
? Maintain calcium and phosphorus
homeostasis
Ca,P
Homeostasis
+1,25(OH)2D
+PTH
-CT
+1,25(OH)2D
-PTH
-CT
+1,25(OH)2D
Bone
Intestine
Kidneys
Parathormone
(PTH)
Calcitonin
(CT)1,25(OH)2D
Ca,P
Homeostasis
Causes of Vitamin D deficiency
?Inadequate direct exposure to sunlight
?Inadequate vitamin D intake
?Higher requirement
?Some diseases,which interfere with
vitamin D absorption or metabolic and
activation
Vitamin D-Deficient Rickets
Epidemiology:
? rare in industrialized countries
? Common in China
20% in the South of China
30-40% in the North of China
Vitamin D deficiency
Osteoid tissue
failure to
mineralize
Osteoid tissue
accumulation
Less Ca absorbed from the intestine
Urine phosphorus
increased
Parathormone secreted
Serum AKP increased
Mobilized
bone Ca,P
Vitamin D-deficient
Rickets
Serum Ca concentration decrease
Low serum
phosphorus
Pathophysiology of Vitamin D-deficient Rickets
Normal or slight decrease in
serum calcium concentration
? General manifestations,irritability,temporary
teeth eruption delayed,anterior fontanel
closure delayed
?Muscles lack of tone
?Head,craniotabes,Ping-Pong ball,caput quadratum
?Chest,beading of the ribs,
pigeon breast deformity,Harrison groove
?Limb,Thickening of the wrists and ankles
Bow-legs,knock-knees
Cliniacl manifestations
Caput
quadratum
Pigeon breast
deformity
The beaning of
ribs (Rachitic
rosary)
Harrison groove
Thicking of the wrists
boxlegsknock-knees
Thicking of the ankles
Biochemical changes
?Normal or low serum calcium
?Serum phosphorus level less than 4mg/dl
?Serum AKP level elevated
?Low serum 25-hydroxycholecalciferol
?Active rickets,Distal ends,cupping and
fraying of the radius and ulna
?Healing rickets,Zones of preparatory
calcificaiton (ZPC); rachitic metaphysis
calcification taken place
Radiographic findings
? Based on:
? a history of inadequate intake of
vitamin D,inadequate exposure to
sunlight
? Characteristic clinical signs of rickets.
? Confirmed by:
Chemical and radiographic examination
Diagnosis
Differential Diagnosis
?Cretinism
?Chondrodystrophy
?Hydrocephalus
?Vitamin D-resistant Rickets
Vitamin D-resistant Rickets
? Familial Hypophosohatemia
(X-linked Hypophosphatemia)
?Vitamin D-Dependent Rickets
(Hypocalcemic Vitamin D-Resistant Rickets)
?Rickets Associated with Renal Tubular Acidosis
?Renal Rickets
Treatment
? Both natural and artificial light of the
appropriate wavelength are effective
therapeutically
?Oral adiministration of Vitamin D is
preferred,5,000-10,000IU/d;
?300,000IU im; repeat one months later,if
needed.
Prevention
? Adequate exposure to ultraviolet light
? Oral administration of Vitamin D
400IU daily
Tetany of Vitamin D Deficiency
(infantile tetany)
? Accompaning rickets
? Serum ionized calcium concentration falls
below 3-4mg/dl
? Muscular irritability
? Diagnosis based on the combined presence of
rickets,low serum calcium concentration,and
symptoms of tetany
Hypervitaminosis D
? Excessive amounts of Vitamin D intake,usually develop
after 1-3 mo of excessive intake
? Anorexia,irritability,constipation,polydipsia
? Chemical examination,Hypercalcemia and
hypercalciuria
? radiographs,metastatic calcification and generalized
osteopetrosis in long bone
? Treatment,discontinuing vitamin D intake and
decreasing calcium intake
科
医
院
徐
秀
Vitamin D deficiency
Provitamin D3
Ultraviolet light
In the
skin,7-dehydrocholesterol
Vitamin D3
(an inactive form)
25-hydroxy vitamin D3
Hydroxylation
In the
Liver:
foods
1,25-hydroxy vitamin D3
(active form)
Hydroxylation
In the
kidneys:
Vitamin D Synthesis and Activation
Vitamin D roles
? Facilitate intestinal absorption of
calcium and phosphorus
? Promote renal reabsorption of
phosphorus
? Direct effect on bone deposition and
reabsorption of calcium and phosphorus
? Maintain calcium and phosphorus
homeostasis
Ca,P
Homeostasis
+1,25(OH)2D
+PTH
-CT
+1,25(OH)2D
-PTH
-CT
+1,25(OH)2D
Bone
Intestine
Kidneys
Parathormone
(PTH)
Calcitonin
(CT)1,25(OH)2D
Ca,P
Homeostasis
Causes of Vitamin D deficiency
?Inadequate direct exposure to sunlight
?Inadequate vitamin D intake
?Higher requirement
?Some diseases,which interfere with
vitamin D absorption or metabolic and
activation
Vitamin D-Deficient Rickets
Epidemiology:
? rare in industrialized countries
? Common in China
20% in the South of China
30-40% in the North of China
Vitamin D deficiency
Osteoid tissue
failure to
mineralize
Osteoid tissue
accumulation
Less Ca absorbed from the intestine
Urine phosphorus
increased
Parathormone secreted
Serum AKP increased
Mobilized
bone Ca,P
Vitamin D-deficient
Rickets
Serum Ca concentration decrease
Low serum
phosphorus
Pathophysiology of Vitamin D-deficient Rickets
Normal or slight decrease in
serum calcium concentration
? General manifestations,irritability,temporary
teeth eruption delayed,anterior fontanel
closure delayed
?Muscles lack of tone
?Head,craniotabes,Ping-Pong ball,caput quadratum
?Chest,beading of the ribs,
pigeon breast deformity,Harrison groove
?Limb,Thickening of the wrists and ankles
Bow-legs,knock-knees
Cliniacl manifestations
Caput
quadratum
Pigeon breast
deformity
The beaning of
ribs (Rachitic
rosary)
Harrison groove
Thicking of the wrists
boxlegsknock-knees
Thicking of the ankles
Biochemical changes
?Normal or low serum calcium
?Serum phosphorus level less than 4mg/dl
?Serum AKP level elevated
?Low serum 25-hydroxycholecalciferol
?Active rickets,Distal ends,cupping and
fraying of the radius and ulna
?Healing rickets,Zones of preparatory
calcificaiton (ZPC); rachitic metaphysis
calcification taken place
Radiographic findings
? Based on:
? a history of inadequate intake of
vitamin D,inadequate exposure to
sunlight
? Characteristic clinical signs of rickets.
? Confirmed by:
Chemical and radiographic examination
Diagnosis
Differential Diagnosis
?Cretinism
?Chondrodystrophy
?Hydrocephalus
?Vitamin D-resistant Rickets
Vitamin D-resistant Rickets
? Familial Hypophosohatemia
(X-linked Hypophosphatemia)
?Vitamin D-Dependent Rickets
(Hypocalcemic Vitamin D-Resistant Rickets)
?Rickets Associated with Renal Tubular Acidosis
?Renal Rickets
Treatment
? Both natural and artificial light of the
appropriate wavelength are effective
therapeutically
?Oral adiministration of Vitamin D is
preferred,5,000-10,000IU/d;
?300,000IU im; repeat one months later,if
needed.
Prevention
? Adequate exposure to ultraviolet light
? Oral administration of Vitamin D
400IU daily
Tetany of Vitamin D Deficiency
(infantile tetany)
? Accompaning rickets
? Serum ionized calcium concentration falls
below 3-4mg/dl
? Muscular irritability
? Diagnosis based on the combined presence of
rickets,low serum calcium concentration,and
symptoms of tetany
Hypervitaminosis D
? Excessive amounts of Vitamin D intake,usually develop
after 1-3 mo of excessive intake
? Anorexia,irritability,constipation,polydipsia
? Chemical examination,Hypercalcemia and
hypercalciuria
? radiographs,metastatic calcification and generalized
osteopetrosis in long bone
? Treatment,discontinuing vitamin D intake and
decreasing calcium intake
