Secondary Deficiency

This is caused by compromised absorption, increased excretion or increased demands or losses. Inadequate absorption can occur in malabsorption syndromes such as coeliac and Crohn's disease, with long-term use of certain medications such as phenytoin, sulfasalazine, cimetidine, antacids and OCP, in congenital malabsorption states and in blind loop syndrome (Beers et al 2003), especially when combined with suboptimal dietary intake (Carmel 2006). Significantly impaired absorption has also been observed in HIV patients (Revell et al 1991).

Besides impaired absorption, inadequate use can occur with concurrent vitamin B12 or C deficiency or chronic alcoholism. A genetic variation in folate requirement has also been identified, as a congenital enzyme deficiency exists in approximately 13% of the Western population (Ma et al 1994). In these cases, total or partial absence of the enzyme responsible for the final step in converting folate to its major active metabolite (methylene tetrahydrofolate reductase) results in decreased plasma levels (Kumar & Clarke 2002). Therefore, these individuals have a higher folate requirement than others without this congenital enzyme deficiency and display increased susceptibility to folate deficiency. Folate 469

A number of pharmaceutical drugs, such as folic acid antagonists (e.g. methotrexate), can affect folic acid status by interfering with absorption, use and conversion to its active forms. In such cases, oral folic acid supplements are sometimes given to reduce side-effects, although it may marginally reduce drug efficacy (Kumar & Clarke 2002, Strober & Menon 2005).

Additionally, there are several subpopulations with increased demands for folic acid, such as pregnant and lactating women, the elderly and patients with malignancies, haemolytic anaemias such as sickle cell disease, chronic exfoliative skin disorders, or achlorhydria (Gropper et al 2005). Extra losses have also been reported in haemodialysis patients.

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