Non-Fasting Total Serum Homocysteine (tHcy) Levels in Folate-Supplemented Omani Arabs with Sickle Cell Disease in the Steady State and in Crisis
Huxley Knox-Macaulay, David Gravell, Gavin Ross, Fehmida Zia, Anil Pathare, Salam Al Kindi
Asian Hematology Research Journal · pp. 67–76 · Published 31 May 2018
Abstract
The aim of this investigation is to determine tHcy levels in SCD Omani Arabs in (i) the steady state (ii) crisis (iii) relative to non-SCD subjects as such values might help clarify the role of tHcy in SCD. Serum tHcy concentrations and other laboratory analyses including serum folate and cobalamin measurements were performed on non-fasting blood samples in 287 non-smoking predominantly adult subjects comprising 133 SCD (SCDstst and SCDcr) patients, 23 HbAS individuals and 131 volunteers acting as controls. Serum tHcy concentration was measured by the Abbott IMx Analyzer using a competitive fluorescence polarization immunoassay (FPIA) while serum folate was determined using the Abbott IMx folate reagent kit based on ion capture technology and serum cobalamin by the Abbott IMx B12 microparticle enzyme intrinsic factor immunoassay (MEIA). Other investigations performed included detailed blood cell counts and variant hemoglobin analyses. Blood counts of the whole cohort whose ages ranged from 8-50 years were essentially normal; nevertheless, hypochromic microcytic red cells were found in about 80% of cases suggestive of α thalassemia trait. Serum folate and cobalamin values post-fortification were normal. Serum tHcy levels were lower in SCD patients than in HbAS and normal volunteers who acted as controls while SCDstst tHcy concentration was higher than that of SCDcr. Our results in Omani Arabs showed the tHcy levels in SCD patients during steady state are higher than those in crisis and are at variance with those obtained in African-Americans and Nigerians in whom tHcy values in the steady state are lower than in a crisis. However, differences in assay methods and varying proportions in SCD haplotypes (50% Benin, 25% Bantu and 25% Arab Indian) amongst the Omani SCD patients are likely to explain this variance. Folate and cobalamin supplementation facilitated vaso-occlusion. The nature of the βs haplotype and the prevalence of α thalassemia appear to militate against the development of stroke in our SCD Omani patients.
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