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Australian Journal of Pharmacy : November 2006
pharmacy ed counselling casebook • approved CPE vegetables (spinach, broccoli, sprouts, etc), apricots, melon and pumpkin. In supranutritional amounts, vitamin A is toxic and may cause headache, nausea, diarrhoea, dry itchy skin, hair loss, loss of appetite, fatigue, irregular menstruation, bone pain, enlarge- ment of liver and spleen and may lead to birth defects.3–6 Medication implementations: Additive toxic effects with combi- nations of vitamin A and acitretin, etretinate and isotretinoin. Supplemtation may be required with long term orlistat.10 Vitamin D: The natural substance, cholecalciferol (D3) is the main active component of the various forms of vitamin D. The natural and most usual source of cholecalciferol is by the action of short wavelength ultraviolet light (sunlight) converting 7-dehy- drocholesterol to cholecalciferol. Food sources include fish liver oils, fatty fish (sardines, herring, mackerel, tuna, salmon, pilchards), fortified margarines, fortified infant milk formulas, eggs and liver.3–6 Deficiency in children causes abnormal bone development (rickets) and, in adults, osteomalacia, causing backache, muscle weakness, bone pain, and fractures. Long-term deficiency leads to low blood levels of calcium and phosphorus, which results in softening of the bones.3–6 lem in Australia. unusual thirst, increased urination, GIT disturbances, depression and retarded growth in children.3–6,10 Medication implementations: Additional vitamin D may be required for patients taking bisphosphonates, isoniazid, rifamp- icin and phenytoin. Vitamin D deficiency is a major prob- A recent Australian study (2006) showed that vitamin D defi- ciency has re-emerged as a significant paediatric health issue, with complications including hypocalcaemic seizures, rickets, limb pain and fracture. A major risk factor for infants is maternal vitamin Ddeficiency. For older infants and children, risk factors include dark skin colour, cultural practices, prolonged breastfeeding, restricted sun exposure and certain medical conditions. To prevent vitamin D deficiency in infants, pregnant women, especially those who are dark-skinned or veiled, should be screened and treated for vita- min D deficiency, and breastfed infants of dark-skinned or veiled women should be supplemented with vitamin D for the first 12 months of life. Regular sunlight exposure can prevent vitamin D deficiency, but the safe exposure time for children is unknown. Vitamin D deficiency cases mirror recent immigration trends. Since birth or residence in Australia does not appear to be pro- tective, screening of at risk immigrant families should be imple- mented through public health policies.8 Older people in residential care can reduce their incidence of falls if they take a vitamin Dsupplement for two years even if they are not initially classically vitamin D deficient.9 Causes of vitamin D deficiency are summarised in Table Two. Vitamin D in the forms of calcitriol, cholecalciferol (D3) and ergocaliferol (D2) are all indicated in supranutritional doses for prevention and treatment of vitamin D deficiency; hypocal- caemia in hypoparathyroidism, hypophosphataemic rickets, renal osteodystrophy, chronic renal dialysis, treatment of osteo- porosis and prevention of corticosteroid-induced osteoporosis.10 Vitamin D is toxic in supranutritional doses causing symptoms primarily due to the effects of hypercalcaemia, such as weakness, 68 ? THE AUSTRALIAN JOURNAL OF PHARMACY VOL.87 NOVEMBER 2006 Vitamin E: a-tocopherol is the most active of eight very simi- lar compounds with vitamin E activity. It is found in all cell mem- branes, being an antioxidant, it is thought to reduce peroxida- tion of unsaturated fatty acids by free oxygen radicals and protects cell walls from chemical injury. Deficiency (rare) may occur in fat malabsorption. Food sources include vegetable oils (wheat germ oil is the rich- est), margarine, mayonnaise, nuts and seeds, some vegetables, cereals, eggs, butter and fruits. Due its antioxidant properties, vitamin E has been promoted as a ‘magic potion’ for a number of conditions. However, little evidence exists as has been shown by a number meta-analysis and systematic reviews.11–13 The seven-year HOPE trial found that in patients with vascu- lar disease or diabetes mellitus, long-term vitamin E supplemen- tation did not prevent cancer or major cardiovascular events and may have increased the risk for heart failure.13 concluded that high-dosage (> or =400 IU/d) vitamin E supple- ments may in fact increase rather than decrease all-cause mor- tality and should be avoided.14 However, one study found an association between low circulating levels of vitamin E and the presence of frailty.15 Another study demonstrated equivocal results regarding the benefits of vitamin E in Parkinson’s disease, tardive dyskinesia and cataracts; however, the statistical methods employed were questionable.16 Another trial concluded that vitamin E supplements should not be recommended for primary or secondary prevention of Table Two: Causes of vitamin D deficience 3–6,8,9 Reduced intake or synthesis of vitamin D3 • Being born to a vitamin D-deficient mother; most commonly veiled or dark-skinned women, or women of Asian background who actively avoid exposure to sunlight • Prolonged breastfeeding • Dark skin colour • Reduced sun exposure—veiled or modest clothing, chronic illness or hospitalisation, intellectual disability, and excessive use of sunscreen • Low intake of foods containing vitamin D Abnormal gut function or malabsorption • Small-bowel disorders (for example, coeliac disease) • Pancreatic insufficiency for example, cystic fibrosis) • Biliary obstruction (for example, biliary atresia) Reduced synthesis or increased degradation of 25-OHD or 1,25- (OH)2D • Chronic liver or renal disease • Drugs: rifampicin, isoniazid and some anticonvulsants, for example, phenytoin A meta-analysis