Background Vitamin D deficiency is still thought to be widespread in the UK and in recent years the number of cases of rickets reported in children has increased. In this study, the distribution of vitamin D and the prevalence of vitamin D deficiency have been determined for a multi-ethnic population from the inner-city area of Birmingham, UK, where a vitamin D testing service has been readily available for over 10 years.Methods Serum 25-hydroxyvitamin D concentration was determined using an automated platform (Nichol's Advantage Speciality System) for 830 outpatient samples collected randomly at the end of summer (September).Results In our total study population, prevalence of vitamin D deficiency, defined as a 25-hydroxyvitamin D concentration o10 mg/L, was high (24%): one in eight Caucasians, one in four Black Afro-Caribbeans and one in three Asians were found to be deficient. Levels of deficiency were much higher in Asian women, with almost one in two individuals (43%) found to have a vitamin D level below 10 mg/L. ConclusionOur study has shown that widespread vitamin D deficiency in a UK inner-city population remains an issue. In concordance with other studies, we found a high prevalence of vitamin D deficiency in Afro-Caribbean and Asians, and, in particular, women. It is clear that more routine screening of vitamin D is needed.
Background: We have developed a new thiopurine S-methyltransferase (TPMT) phenotyping method that measures TPMT activity in whole blood. To evaluate this assay, we compared it with conventional TPMT phenotyping, which uses a red blood cell (RBC) lysate and genotyping for analysis of common TPMT mutations.
Background: Thiopurine S-methyltransferase (TPMT) phenotype analysis, expressed as TPMT activity, is established as a routine pharmacogenomic test to screen patients prior to initiating thiopurine drug therapy. Conventionally measured TPMT activity is corrected for red blood cell (RBC) parameters. Here we present evidence that supports the simplification of the TPMT assay: by expressing TPMT activity in mU/L whole blood, without undertaking any haemoglobin (Hb) correction. Methods: Hb concentrations were compared in consecutive samples that had been received for TPMT phenotype analysis and which were stratified into samples with high (n ¼ 111) and samples with normal (n ¼ 50) Hb-corrected enzyme activity. TPMT activity was also measured in samples received for full blood count determination, stratified into those with low (n ¼ 50) and normal (n ¼ 50) Hb. A reference interval for TPMT activity in mU/L was derived from a correlation between activity expressed in conventional units and that expressed in mU/L (n ¼ 1563), supported by comparison with associated genotype (n ¼ 201). Results: In the high TPMT activity group, 83% of specimens had a low Hb concentration compared with 14% of specimens in the normal TPMT group. Samples with a low Hb concentration were found to have significantly higher Hb-corrected TPMT activity than samples with a normal Hb concentration: 83 versus 44 nmol 6-methyl thioguanine /g Hb/h, P , 0.0001. These results strongly suggest that misleading high Hb-corrected TPMT activity is found in anaemic patients. Based on the reference interval for enzyme activity of 70-150 mU/L, phenotype-genotype concordance compared well with the conventional approach (88% versus 89%). Furthermore, distribution of TPMT phenotypes with activity expressed in mU/L was identical: 0.5% deficient, 11% low, 86% normal and 2.5% high, to when it was expressed in conventional units. Conclusion: Expressing TPMT activity in mU/L can overcome misleading high Hb-corrected TPMT results occurring in patients with anaemia, which could lead to inappropriate treatment. Removing the need to measure RBC indices further simplifies TPMT phenotyping, leading to a more robust assay, with reduced turn-around time and cost.
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