Clinical Nutrition Case Study
The Case of Rose: Potential Vitamin D Deficiency and Drug-Nutrient Interactions.
Vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). Vitamin D3 constitute as the two main forms of vitamin D, D3 being the form produced in the cutaneous layer of the skin as a result of ultraviolet B radiation. D3 can also be achieved through the diet and/or supplementation of synthetically produced means. D2 and D3 are both converted to 25-hydroxyvitaminD (25(OH)2D) in the liver: the serum level determines the status of the vitamin (though only as an approximate indicator of supply). Thereafter, 25(OH)2D is further hydroxylated to 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in the liver, the biologically active form which acts in the small intestine and on bone cells to increase calcium absorption, via effects on gut mucosal cells (Thatcher, T. D. and Clarke, B, L. 2011).
Whereas once the presence of related conditions such as rickets or osteomalacia confirmed chronic deficiency of vitamin D, now serum values of 25(OH2)D below 10 ng/mL (or 24.96 nmol/L) may act as a cut off point as at risk for associated diseases of insufficiency and recent research uses the term ‘vitamin D insufficiency’ to explain low serum 25(OH2)D as a cause of related disease: not solely rickets and osteomalacia but in cancer, cardiovascular disease, diabetes and asthma amongst others (Thatcher, T. D. and Clarke, B, L. 2011). However, whilst the use of 25(OH2)D serum level as a marker for describing sufficiency or inadequacy is still a topic under discussion, table 1 offers a basic classification of the vitamin status, as is classified and recently advised by the Institute of Medicine (IOM, 2011), although SACN (2007) advises there is evidence which indicates that vitamin D may be important for many more health outcomes other than those related to bone metabolism, and that 25(OH2)D levels several times more than the required 25nmol/l may be necessary to maintain adequate health.
Potential Clinical Outcomes of Chronic Vitamin D Deficiency
Rickets, as shown in infants, children and adolescents, is the ‘clinical consequence of impaired mineralization of the bone matrix throughout a growing skeleton’ (White, M. P. and Thakker, R. V. 2013). Upon occurrence in adulthood, the term osteomalacia is used which results from this same disturbance after growth plates have fused (ibid). Osteomalacia, as presented in adults, may generate symptoms which are non-specific and difficult to identify, including skeletal deformities and fractures and also muscle weakness (Chalmers, J. et al. 1967). Bone pain can present in parts of the axial skeleton, for example the shoulders, vertebrate and ribs (Feroze, A. et al. 2010), and also a more acute, localized pain may be felt upon touch as a result of concealed yet detectable ‘Looser’s zones’, also known as ‘pseudofractures’, which are often evident upon x-ray (Feroze, A. et al. 2010). These bone infarctions are...