Vitamin D is a group of fat-soluble prohormones. Two major forms of which are vitamin D 2 (or ergocalciferol) and vitamin D 3 (or cholecalciferol). Production is greatest in the stratum basale and stratum Produced in skin spinosum . exposed to sunlight, specifically
Functions of Vitamin DRegulates the calcium and phosphorus levels in the blood by promoting their absorption from food in the intestines.Promotes bone formation and mineralization .Inhibits parathyroid hormone secretion from the parathyroid gland.Affects the immune system by promoting immunosuppression, phagocytosis, and anti-tumor activity
Dietary sources ofvitamin-D Fortified foods especially dairy products, cereals and vit. Supplements. Fish, liver, oils, egg yolk & butter. Infants: obtain vit D supplement from mothers milk, infant formulas, cow milk .
Why Vitamin D deficiency occurs? Due to:-Inadequate sunlight exposure.Poor access to micronutrients rich food.Disorder that limit its absorption.Deficient soil quality.Impaired conversion into active metabolites.Possible role of dietary fibers.
These lead to:- Learning disability Impaired work capacity. Increased susceptibility to infection
Deficiency causes:- In children :- RICKETS:- Bone softening diz., deformity of long bones occur. In adults :- OSTEOMALACIA :- Bone thinning disorder,proximal muscle weakness & bone fragility. OSTEOPOROSIS:-Decrease bone minerilzation & inc. Bone fragility.
RICKETS:- Rickets is characterized by bone deformities due to incomplete mineralization, resulting in soft & pliable bones and delay in teeth formation. The weight bearing bones are bent to form bow legs
Risk factors Breast-fed infants whose mothers are not exposed to sunlight . Breast-fed infants who are not exposed to sunlight . Lactose intolerant. Individuals with red hair have a decreased risk for rickets due to their greater production of vitamin D in sunlight.
Pathogenesis of Rickets Appears to develop in 3 stages:- 1 st stage Absence of adequate stores In supply of 1,25 dihydroxy vit D Intestinal absorption of Ca & P Release of parathyroid hormone 1,25 (OH)2 vit D3 25(OH) vit D (in kidney) Absorption of Ca & P Mobilization of Ca & P from bone
Treatment:- Natural & artificial light are effective therapeutically but oral administration preferred. Administration of 15,000ugm or 6,00,000 IU of vit.D 3 orally or I.M. induces rapid healing. If healing lines of rickets is not seen on x- ray plate of bone within 3-4 weeks of therapy, the above dose may be repeated . Cases who respond to this therapy are further put on 400 units or 10ugm of vitamin D 3 per
Requirement Body needs are met entirely by conversion of 7 dehydrocholesterol to vit D 3 in skin Or in absence of exposure to UV light, it can be met entirely by ingestion of Vit D The recommended dietary intake for vit D by infants has been accepted as 200IU/day and children 400IU/day
Hypervitaminosis – D Signs & symptoms - similar to idiopathic hypercalcemia. Symptoms include:- Hypotonia, anorexia, irritability, constipation, polyuria, pallor Aortic stenosis, vomiting Hypertension Retinopathy Urine shows proteinuria Metastatic calcification as revealed by x- rays Generalized osteoporosis T/t includes discontinuation of vit D &
References :- Essential Pediatrics by O . P . GhaiTextbook of Preventive & social medicine by K . Park www.mc.vanderbilt.edu