Objective:This study aimed to describe and compare the nutritional status of adult patients submitted to allogeneic hematopoietic stem cell transplantation at two different time points (admission and discharge).Methods:A retrospective, descriptive and quantitative study was performed based on clinical, laboratory and nutritional data obtained from medical records of adult patients of both genders submitted to allogeneic hematopoietic stem cell transplantation in a bone marrow transplantation reference center in Rio de Janeiro in the period from 2010 to 2013. Statistical analysis was performed using the SPSS software (version 22.0).Results:Sixty-four patients were evaluated. The mean age was 42.1 ± 3.2 years and the most prevalent disease was acute myeloid leukemia (39%). There was a high prevalence of gastrointestinal symptoms including nausea (100%), vomiting (97%) and mucositis (93%). Between admission and discharge there was a significant decrease in the median weight (−2.5 kg; 71.5 vs. 68.75 kg; p-value < 0.001), body mass index (−0.9kg/m2; 24.8 vs. 24.4kg/m2; p-value < 0.001), and serum albumin levels (−0.2g/dL; 3.7 vs. 3.6g/dL; p-value = 0.024). The survival time after hematopoietic stem cell transplantation correlated negatively with C-reactive protein at discharge (CC = −0.72; p-value < 0.001) and positively with serum albumin levels (CC = 0.56; p-value = 0.004) and with high total protein level at discharge (CC = 0.53; p-value = 0.006).Conclusion:Our results suggest that patients submitted to allogeneic hematopoietic stem cell transplantation have compromised nutritional status during the hospital stay for transplantation.

A hiper-homocisteinemia é um fator de risco independente para as doenças vasculares oclusivas. Os mecanismos exatos pelos quais a hiper-homocisteinemia favorece o desenvolvimento dessas doenças não são totalmente compreendidos. Sugere-se que o dano ao endotélio vascular, promovido pelas espécies de oxigênio reativas, oriundas da oxidação da homocisteína, seja a causa dos eventos tromboembólicos. Estudos indicam que a homocisteína interfere em vários mecanismos anticoagulantes mediados pelo endotélio vascular, tais como: redução da ativação da proteína C, inibição da trombomodulina e supressão da expressão do sulfato de heparan. Sabe-se que os níveis de homocisteína são influenciados por diversos fatores, dentre eles destaca-se a deficiência de vitaminas do complexo B (especialmente folato, cobalamina e piridoxina). A suplementação de folato, isoladamente ou em combinação com a cobalamina e piridoxina, reduz os níveis de homocisteína plasmática mesmo em pessoas que não apresentam deficiência dessas vitaminas. Esta revisão tem como objetivos abordar os possíveis mecanismos pelos quais a hiper-homocisteinemia poderia levar ao desenvolvimento de eventos tromboembólicos e o tratamento nutricional da hiper-homocisteinemia.

Hyper-homocysteinemia is an independent risk factor for occlusive vascular disease. The exact mechanisms by which hyperhomocysteinemia promotes the development of these diseases are still unclear. It has been suggested that damage to the vascular endothelium caused by reactive oxygen species produced during the auto-oxidation of homocysteine, may be the cause of the thrombo-embolic events. Studies have indicated that homocysteine interferes in various anticoagulant mechanisms mediated by the vascular endothelium, for example, reduction in protein C activation, inhibition of thrombomodulin and suppression of heparan sulfate expression. It is known that many factors influence the homocysteine levels including deficiency of the vitamin B complex (mainly folate, pyridoxine and cobalamin). Folate supplementation, alone or combined with pyridoxine and cobalamin, reduces plasmatic homocysteine levels even in people who are not vitamin deficient. This paper will address the possible mechanisms by which hyper-homocysteinemia could favor the development of thrombo-embolic events as well as addressing its nutritional treatment.