vitamin d | benifits of vitamin d | detail explain about vitamin d

 

LESIONS IN VITAMIN D DEFICIENCY. 

Deficiency of vitamin D may result from:

i) reduced endogenous synthesis due to inadequate exposure to sunlight;
ii) dietary deficiency of vitamin D;
iii) malabsorption of lipids due to lack of bile salts such as in intrahepatic biliary obstruction, pancreatic insufficiency and malabsorption syndrome;
iv) derangements of vitamin D metabolism as occur in kidney disorders (chronic renal failure, nephrotic syndrome, uraemia), liver disorders (diffuse liver disease) and genetic
disorders; and
v) resistance of end-organ to respond to vitamin D.
Deficiency of vitamin D from any of the above
mechanisms results in 3 types of lesions:
1. rickets in growing children;
2. osteomalacia in adults; and
3. hypocalcaemic tetany due to neuromuscular dysfunction.

RICKETS.

 The primary defects in rickets are:
interference with mineralisation of bone; and
deranged endochondral and intramembranous bone
growth.
The pathogenesis of lesions in rickets is better understood
by contrasting them with sequence of changes in normal bone
growth as outlined in Table 9.5.

MORPHOLOGIC FEATURES. 

Rickets

Rickets occurs in growing children from 6 months to 2 years of age. The disease has
the following lesions and clinical characteristics Skeletal changes. These are as under:

i) Craniotabes is the earliest bony lesion occurring due to small round unossified areas in the membranous bones of the skull, disappearing within 12 months of birth. The
skull looks square and box-like.
ii) Harrison’s sulcus appears due to indrawing of soft ribs on inspiration.
iii) Rachitic rosary is a deformity of chest due to cartilaginous overgrowth at costochondral junction.
iv) Pigeon-chest deformity is the anterior protrusion of sternum due to action of respiratory muscles.
v) Bow legs occur in ambulatory children due to weak bones of lower legs.
vi) Knock knees may occur due to enlarged ends of the femur, tibia and fibula.
vii) Lower epiphyses of radius may be enlarged.
viii) Lumbar lordosis is due to involvement of the spine and pelvis.

Biochemical changes. These are as follows:

i) Lowered levels of active metabolites of vitamin D (25- hydroxy vitamin D and 1, 25-dihydroxy vitamin D).

ii) Plasma calcium levels are normal or slightly low.

iii) Plasma phosphate levels are lowered.

iv) Plasma alkaline phosphatase is usually raised due to osteoblastic activity.

Vitamin D-dependent rickets is an autosomal dominant disorder of vitamin D. The disease responds rapidly to administration of 1,25-dihydroxy vitamin D.

OSTEOMALACIA

Osteomalacia is the adult counterpart of rickets in which there is failure of mineralisation of the osteoid matrix. 

It may occur following dietary deficiency, poor endogenous synthesis of vitamin D, or as a result of conditioned deficiency.

MORPHOLOGIC FEATURES.

Osteomalacia 

 Due to deficiency of vitamin D, osteoid matrix laid down fails to get mineralised.

In H and E stained microscopic sections, this is identified by widened and thickened osteoid seams (stained pink) and decreased mineralisation at the borders between osteoid and bone (stained basophilic).

 von Kossa’s stain for calcium may be employed to mark out the wide seams of unstained osteoid while the calcified bone is stained black. In addition, there may be increased

osteoclastic activity and fibrosis of marrow.

Clinical features. (Sign and symptoms)

Osteomalacia is characterised by:

i) muscular weakness;

ii) vague bony pains;

iii) fractures following trivial trauma;

iv) incomplete or greenstick fractures; and

v) looser’s zones or pseudofractures at weak places in bones.

Biochemical changes. 

These are:

i) normal or low serum calcium levels;

ii) plasma phosphate levels lowered; and

iii) raised serum alkaline phosphatase due to increased osteoblastic activity.

It may be worthwhile to note here that another chronic disorder of skeleton seen in elderly, osteoporosis, is clinically similar but biochemically different disease (Chapter 28).

HYPERVITAMINOSIS D. 

Very large excess of vitamin D may cause increased intestinal absorption of calcium and

phosphorus, leading to hypercalcaemia, hyperphosphataemia and increased bone resorption. 

These changes

may result in the following effects:

i) increased urinary excretion of calcium and phosphate;

ii) predisposition to renal calculi;

iii) osteoporosis; and

iv) widespread metastatic calcification, more marked in the

renal tubules, arteries, myocardium, lungs and stomach.