This action might not be possible to undo. Are you sure you want to continue?
1865 : Trousseau recommends cod liver oil and
sunlight as treatment for rickets. He also recognises and identifies osteomalacia as the adult form of rickets. 1919: Sir Edward Mellanby proposes that rickets is due to the absence of a fat-soluble dietary factor. 1925 McCollum and co-workers discovered vitamin D. Hess and Weinstock show that vitamin D activity is produced in the skin by ultraviolet irradiation. 1936 Windaus identifies the structure of vitamin D in cod liver oil.
Vitamin D deficiency (Ricket)
Consequences of Vit-D deficiency
In Children 1. Causes poor mineralization of the collagen matrix in
young children’s bones leading to growth retardation and bone deformities (refer to picture) In Adults 1. Induces secondary hyperparathyroidism, which causes a loss of matrix and minerals, thus increasing the risk of osteoporosis and fractures 2. Poor mineralization can lead to painful osteomalacia 3. Causes muscle weakness
According to Holick, M.F 2005, some scientific
research showed a link between vitamin D deficiency and certain diseases; a)Diabetes b)Multiple sclerosis c) Rheumatoid arthritis d)Hypertension e)Cardiovascular disease f) Colon, breast, pancreas, prostate and ovary cancers
Vitamin D encompasses 2 molecule; ergocalciferol (D2) &
Fat soluble vitamin where it needs the presence of bile and fats in
the GUT to be absorbed by the body.
Supplements containing vitamin D3 (cholecalciferol) are obtained
from animal sources (usually as a by-product of wool fat).
Vitamin D2 (ergocalciferol) is obtained from food supplements.
Causes of Vit-D deficiency:
Homebound elderly Women in veil Strict vegan Severe renal impairment (unable to convert to its active
GUT problem (eg: coeliac disease, Crohn’s disease, short
Classification of Vit-D deficiency:
Mild vitamin D deficiency: Serum 25-OHD levels in the
range 25–50 nmol/L, mild deficiency leads to increased parathyroid hormone secretion and high bone turnover
Moderate vitamin D deficiency: Serum 25-OHD levels of
12.5–25 nmol/L, moderate deficiency has been associated with reduced bone density, high bone turnover and increased risk of hip fracture in older people
Severe vitamin D deficiency: Serum 25-OHD levels of <
12.5 nmol/L, resulting in osteomalacia may present with bone and muscle pains, weakness and pseudofractures. Cortical thinning occurs because of secondary hyperparathyroidism
Note: 25-hydroxyvitamin D (25-OHD),
Treatment of established osteoporosis Prevention of corticosteroid induced osteoporosis Treatment of hypocalcaemia in hypoparathyroidism Rickets Renal osteodysthrophy Secondary hyperparathyroidism Psoriasis (calcipotriol)
Hypercalcaemia Hyperphosphatemia Hypervitaminosis D Artheriosclerosis or cardiac function impairment Renal function impairment
Note:Pregnancy and breast-feeding; No problems reported with normal intakes. There is a risk of hypercalcaemic tetany in breast fed infants whose mothers take excessive doses of vitamin D.
Production of Vit-D:
•Vitamin D ingested or made
from the skin will be transported to the liver. •Metabolised to 25hydroxyvitamin D (25-OHD) which is a major circulating form in the body. •Next, hydroxylation in the kidney will form the biological active form 1,25dihydroxyvitamin D3. •UVB is resposible for the conversion of 7dehydrocholesterol into previtamin D3.
Mode of action:
Vit-D is essential for promoting the absorption and
utilisation of calcium and phosphorus and normal calcification of the skeleton
Along with parathyroid hormone and calcitonin, it
regulates serum calcium concentration by altering serum calcium and phosphate blood levels as needed, and mobilising calcium from bone cellular processes, including the immune system and insulin production proliferation of skin cells
It maintains neuromuscular function and various other
Calcipotriol: induces differentiation and suppresses
Initial dosing: Adult and children >20kg needs 1µg od. <20kg needs 0.05µg/kg/day. Neonates: 0.1µg/kg/day Maintenance dosing: 0.25-2µg od
Post-menopausal: 0.25µg bd Renal osteodysthrophy: Initial: 0.25µg od and increase by 0.25µg over 2-4 weeks (range:0.5-1.oµg) until satisfactory serum calcium is achieved Hypoparathyroidism/rickets: 0.25µg od
Note : Always start on the lowest possible dose : During initial phase of the medication, serum calcium should be determined twice weekly. Subsequently, monitoring should also be undertaken at 2-4 weeks and 2-3 monthly intervals thereafter.
Generally well tolerated. Toxicity can occur with large dose (10,000units) for six
Early signs & symptoms: Anorexia, constipation,
diarrhoea, dry mouth, fatigue, headache, nausea and vomiting, thirst and weakness bone pain, cardiac arrhythmias, hypertension, renal damage (increased urinary frequency, decreased urinary concentrating ability; nocturia, proteinuria), psychosis (rare) and weight loss.
Later symptoms: calcification of soft tissues and include
Anticonvulsants (phenytoin, barbiturates or primidone): may
reduce effect of vit-D by accelerating its metabolism
Calcitonin: effect of calcitonin may be antagonised by vit-D Colestyramine, colestipol: may reduce intestinal absorption
Digoxin as hypercalcaemia can potentiate effect of digoxin
Liquid paraffin: reduce intestinal absorption of vit-D Sucralfate: may reduce intestinal absorption of vit-D. Thiazide diuretics: may increase risk of hypercalcaemia. Magnesium containing antacid: hypermagnesaemia
Absorption is the best taken with fatty meals May be dropped directly into the mouth or mixed
with cereal, fruit juice, or other food
Avoiding concurrent use of nonprescription
medications or dietary supplements containing calcium, phosphorus, or vitamin D, unless otherwise directed by health care professional
Untapped potential of Vitamin D:
Role in infection particularly tuberculosis Autoimmune disease (eg: rheumatoid arthritis, multiple
sclerosis and inflammatory bowel diseases, including ulcerative colitis and Crohn’s disease)
Age-related macular degeneration Maternal pre-eclampsia Cardiovascular diseases (exposure to UVB decrease blood
pressure and decrease inflammatory marker eg:tumour necrosis factor which involves in artherosclerosis)
Diabetes (insufficiency predispose to type 2 diabetes)
Stock available: a) 1-α calcidol (0.25µg, 1.0µg) b) Calcitriol (0.25µg) c) Calcipotriol cream/ointment 50mcg/g One International Unit of vitamin D is defined as the activity of 0.025 μg of
cholecalciferol. Thus: 1 μg vitamin D = 40 units vitamin D
A suitable dose of vitamin D in most cases is 10 μg (400 units) daily For prevention of fracture in older people, there is evidence that a higher
dose of 20 μg (800 units) with calcium 1200 mg daily is required
Dietary supplements , viewed 16/06/09
Ann Rev Pharmacol Toxicol 2001; 41: 421–442 Nutrition 2005; 135:2739S-2748S
Guyton K, Kensler T, Posner G. Cancer chemoprevention using natural vitamin D and synthetic analogs. Holick, M.F. The Influence of Vitamin D on Bone Health Across the Life Cycle. American Society for Parekh N, Chappell RJ, Millen AE, et al. Association between vitamin D and age-related macular
degeneration in the Third National Health and Nutrition Examination Survey, 1988 through 1994. Arch Ophthalmol 2007; 125: 661–669. preeclampsia. J Clin Endocrinol Metab 2007; 92: 3517–3522.
response. Science 2006; 311: 1770–1773.
Bodnar LM, Catov JM, Simhan HN, et al. Maternal vitamin D deficiency increases the risk of
Liu PT, Stenger S, Li H, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial Schauber J, Dorschner RA, Coda AB, et al. Injury enhances TLR2 function and antimicrobial peptide expression
through a vitamin D-dependent mechanism. J Clin Invest 2007; 117: 803–811.
Diamond, T.H et al. Vitamin D and adult bone health in Australia and New Zealand: a position statement.
Medical Journal of Australia. 2005; 182: 281–285
Zitterman A. Vitamin D and disease prevention with special reference to cardiovascular disease. Prog
Biophys Mol Biol 2006; 92: 39–48
Pittas AG, Lau J, Hu FB, Dawson-Hughes B. The role of vitamin D and calcium in type 2 diabetes. A
systematic review and meta-analysis. J Clin Endocrinol Metab 2007; 92: 2017–2029
Gombart AF, Borregaard N, Koeffler HP. Human cathelicidin antimicrobial peptide (CAMP) gene is a
direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25dihydroxyvitamin D3. Faseb J 2005; 19: 1067–1077.
Dr Upfal, J 2007, The Australian drug guide, Black Inc Melbourne Australian Medicine Handbook (2007)
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.