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Vitamin – C

  1. Ascorbic acid is essential for formation of collagens and intracellular matrix in teeth, bones and capillaries.
  2. Involved in tyrosine metabolism.
  3. Help in maintenance of vascular integrity through prostacyclin
  4. Reduce oxidation of LDL and prevent deposition at atheromatous plaques.
  5. lnvolved in adrenal cortical functioning and electron transport.
  6. Help in storage and absorption of iron.  



* Citrus fruits and vegetables.


* Vitamin c destroyed in cooking.


* Adrenal glands and lens have particularly high contents of vitamin c. Q


Daily doses:

  1. Term infants     -30 mg/day
  2. Preterm infants -50 mg/day
  3. Older children    -40mg/day

The need for vitamin C is increased by febrile illness particularly infectious and diarrheal diseases, iron def, cold exposure, smoking, Hypoproteinemia.


Clinical features of deficiency

  1. Majority of cases occur between 6 - 24 month.
  2. Irritability, digestive disturbances and loss of appetite appear early.
  3. Generalized tenderness especially in leg. Pain result in pseudo paralysis and legs assume the typical frog position.
  4. Hemorrhages occur under the periosteum of long bones.
  5. Costochondral junction becomes prominent and appear sharp and angular.
  6. Gums are swollen and may bleed.
  7. Petechial hemorrhages may occur in skin and mucus membrane.
  8. Anemia
  9. Wound healing is delayed
  10. Hematuria, melena, and orbital or subdural hemorrhages may be found.  

Diagnosis- based on clinical, radio logical and lab findings

X-ray appearance

  1. → mainly seen at knee.
  2. Ground glass appearance of medulla
  3. Pencil thinning of cortex
  4. Ring shape epiphysis [Wimberger sign) Q
  5. White line of Fraenkel, a zone of calcification at metaphysis
  6. A zone of rarefaction or destruction appears proximal and parallel to the white line [white line of scurvy)
  7. Pulken spur
  8. Subperiosteal hemorrhages Q 

Lab diagnosis   

  1. Blood plasma level> 0.6 mg% exclude scurvy                      
  2. Better assessed in buffy coat.
  3. After a test dose 80% of it can be found in urine            
  4. Tyrosine loading test
  5. PT is prolonged 


  1. Sources → fish, liver, oil, egg yolk.      
  2. Dosages.
    1. Infants 200 IU/day        
    2. Children 400 IU/day


Changes in Vit D deficiency

Deficiency of vit D → less calcium absorbs from intestine → . S Calcium → stimulate PTH which brings certain changes

            → Mobilization of calcium/phosphorus from bone

↑ PTH     ↑ excretion of phosphorus in urine.

            →  ↑ Alkaline phosphatase [due to  osteoblastic activity]



Failure of mineralization of growing bone or osteoid tissue


Failure of mature bone to mineralize is called osteomalacia.


  1. Calcium def. with secondary Hyper parathyroid ism
    1. Lack of Vit D * Lack of exposure to sun light
      1. Dietary def. of Vit D
      2. Congenital
    2. Malabsorption of Vit D
    3. Hepatic disease.
    4. Anticonvulsant drug.
    5. Renal osteodystrophy.
    6. Vit D dependent rickets Type I  
  2. Primary phosphate def. No. secondary Hyperparathyroidism.
    1. Primary Hypophosphatemia                
    2. Phosphate deficiency or malabsorption
    3. Fanconi syndrome                        
    4. RTA type II
    5. Oncogenic hyposphatemia  

3. End organ resistance to 1,25 (OH)2 D3

  • Vit D dependent type II

Vitamin D levels in serum

                                                         25 (OH)D level (ng /ml)


Less than 10


10 – 20


20-60 Q




Greater than 90


Clinical manifestations


Usually manifest in later half of first year

  1. Craniotabes - earliest manifestation Q
  2. Anterior fontanelle large and closure delayed
  3. Bossing of frontal and parietal bone.
  4. Rachitic rosary
  5. Pigeon breast chest
  6. Harrisons groove
  7. Eruption of primary teeth delayed
  8. Moderate degree of scoliosis, kyphosis, lordosis
  9. Epiphyses of long bones are widened
  10. Bowing of leg! knock kneel coxa vera
  11. Pot belly abdomen - visceroptosis
  12. B/IL lamellar cataract
  13. ↑ Sweating over fore head 



By clinical, lab and radiological feature.

  1. Lab finding       
    1. Serum calcium normal or ↓
    2. Serum phosphorus ↓
    3. Alkaline phosphatase ↑
    4. Urinary c-amp level is elevated.
  2. X-rays changes observed in lower ends of radius and ulna (Cupping – Splaying – Fraying).Q
    1. A cup shaped or saucer like depression at growing end of the bone
    2. Epiphyseal plate appear widened  

Clinical variants

  1. Vitamin D dependent rickets
    1. It is Autosomal recessive (AR) disorder
    2. Enzyme activity of J ex Hydroxylase is deficient resulting in low level of 1,25 (OH)2 D3 even in presence of   Hypocalcemia, and High PTH.        
    3. These patients have aminoaciduria, glucosuria and RT A.
    4. Treatment → with massive dose of vitamin D2 or with 1,25 (OH)2 D3.
  2. Vit D dependent rickets Type II
    1. Patient who fail to respond to above therapy are labeled as having vitamin D dependent rickets type II. The defect lies in marked reduction of binding of 1,25' (OH)2 D3 to its Nuclear receptor and defective nuclear translocation.
    2. This may be associated with short stature and alopecia total is. 
  3. Familial Hxpophosphatemia
    [Vitamin D resistant Rickets] Q
    1. Most common non. Nutritional from of rickets
    2. X- linked dominant condition.
    3. Defect in proximal tubular reabsorption of phosphate conversion of 0,25 (OH)2 D3 to 1,25 (OH)2 D3 [evidenced by low serum level of 1,25 (OH)2 DJ despite hypophosphatemia] 

Clinical features

  1. Bowing of lower extremities, coxa vera, genu valgum, short stature.
  2. Tetany, myopathy, rachitic rosary and Harrison grove, characteristic of calcium def. rickets' are not evident.
  3. Pulp deformities [Intraglobular dentin] more common where as in calcium def rickets enamel deformities are more common.

Treatment → oral phosphate with vitamin D3


Description: scan0005


Fig: Biochemical evaluation of a child with refractory rickets

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