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Homocysteine is associated with microvascular abnormalities in sickle cell disease (827.13)
Author(s) -
Samarron Sandra,
Green Ralph,
Miller Joshua,
Lin Xin,
Wun Ted,
Cheung Anthony
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.827.13
Subject(s) - medicine , homocysteine , creatinine , gastroenterology , anemia , vitamin b12 , sickle cell anemia , disease , b vitamins , pathophysiology , hemoglobin , endocrinology , physiology
The pathophysiology of sickle cell disease (SCD) includes anemia as well as vasculopathy affecting both the micro‐ and macrovasculature. Elevated plasma homocysteine (HCY) is common in SCD patients and may be associated with increased risk of vascular complications. Microvascular characteristics in the bulbar conjunctiva were assessed in 38 SCD patients (19 pediatric, 19 adult) using computer‐assisted intravital microscopy. A severity index (SI), on a scale of 0‐15, was computed to quantify the degree of microvasculopathy in each subject. Serum folate, B12, and creatinine, and plasma pyridoxal‐5'‐phosphate and HCY were determined for each subject. Associations with SI were assessed by multiple regression analysis, controlling for age and sex. Age was strongly correlated with microvasculopathy in the SCD patients, with the SI increasing about 0.1 unit per 1 year increase in age (p<0.001). HCY was directly correlated with SI after controlling for age and sex (p=0.002). None of the B vitamins or creatinine was significantly correlated with SI. Age and HCY are independent determinants of microvasculopathy in SCD patients. B vitamin supplementation, specifically folate, B12 and B6, lowers HCY levels. High dose B vitamin therapy started early in life may maintain low blood levels of HCY, and possibly prevent or slow the progression of microvasculopathy and its associated complications in SCD patients. Grant Funding Source : Supported by NIH HL083276