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Antioxidant vitamins C and E supplementation increases markers of haemolysis in sickle cell anaemia patients: a randomized, double‐blind, placebo‐controlled trial
Author(s) -
Arruda Martha M.,
Mecabo Grazielle,
Rodrigues Celso A.,
Matsuda Sandra S.,
Rabelo Iara B.,
Figueiredo Maria S.
Publication year - 2013
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.12185
Subject(s) - haemolysis , placebo , medicine , antioxidant , vitamin c , oxidative stress , gastroenterology , vitamin e , red blood cell , anemia , randomized controlled trial , vitamin , sickle cell anemia , fetal hemoglobin , hemoglobin , immunology , biology , biochemistry , pathology , pregnancy , disease , alternative medicine , fetus , genetics
Summary Erythrocytes from sickle cell anaemia ( SCA ) patients continuously produce larger amounts of pro‐oxidants than normal cells. Oxidative stress seems to primarily affect the membrane and results in haemolysis. The use of antioxidants in vitro reduces the generation of pro‐oxidants. To evaluate the impact of vitamins C ( V it C ) and E ( V it E ) supplementation in SCA patients, patients over 18 years were randomly assigned to receive V it C 1400 mg + V it E 800 mg per day or placebo orally for 180 d. Eighty‐three patients were enrolled (44 vitamins, 39 placebo), median age 27 (18–68) years, 64% female. There were no significant differences between the two groups regarding clinical complications or baseline laboratorial tests. Sixty percent of the patients were V it C deficient, 70% were V it E deficient. Supplementation significantly increased serum V it C and E . However, no significant changes in haemoglobin levels were observed, and, unexpectedly, there was a significant increase in haemolytic markers with vitamin supplementation. In conclusion, V it C + V it E supplementation did not improve anaemia and, surprisingly, increased markers of haemolysis in patients with SCA and S ‐β 0 ‐thalassaemia. The exact mechanisms to explain this findings and their clinical significance remain to be determined.