5 research outputs found
Markers of oxidative stress in umbilical cord blood from G6PD deficient African newborns
<div><p>Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked disorder that affects as many as 400 million people worldwide, making it the most common enzymatic defect. Subjects with G6PD deficiency are more likely to develop neonatal hyperbilirubinemia potentially leading to kernicterus and are at increased risk for acute hemolytic anemia when exposed to pro-oxidant compounds such as anti-malarial drugs. We collected umbilical cord blood from 300 males born in Uganda to assess for novel markers of systemic oxidative stress. We determined that 10.7% of the samples collected were G6PD A- deficient (G202A/A376G) and when these were compared with unaffected controls, there was significantly higher 8-hydroxy-2’-deoxyguanosine (8-OHdG) concentration, elevated ferritin, increased leukocyte count and higher small molecule antioxidant capacity. These data suggest increased baseline oxidative stress and an elevated antioxidant response in umbilical cord blood of patients with G6PD deficiency.</p></div
Markers of oxidative stress/inflammation in G6PD deficient UCB from male neonates.
<p>(A) Levels of plasma 8-OHdG, n = 32 G6PD deficient, n = 35 Normal samples. (B) Pearson’s correlation analysis of plasma 8-OHdG levels and absolute lymphocyte counts. (C) Comparison of G6PD deficient UCB lymphocyte counts between high and low 8-OHdG levels determine by the median 8-OHdG value (31.9 nM). (D) Plasma ferritin concentration in UCB. (E) Plasma small molecule antioxidant capacity expressed in equivalents of Trolox. (F) Plasma protein carbonylation as nmol/mg. (G) Plasma catalase activity in UCB. See also <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0172980#pone.0172980.s001" target="_blank">S1 Table</a>. Columns indicate the mean values and standard deviation. P-values in two-way comparisons were derived from a Student’s t-test.</p
Complete blood count indices in G6PD deficient UCB from male neonates.
<p>(A-E) Total white blood cell (WBC), neutrophil, lymphocyte, platelet counts and hemoglobin were in G6PD deficient samples (n = 32) compared to normal controls (n = 240). Columns indicate the mean values and standard errors. P-values in two-way comparisons were derived from a Student’s t-test. Platelet values are from 23 G6PD deficient and 136 normal controls due to equipment malfunction. See also <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0172980#pone.0172980.s001" target="_blank">S1 Table</a>.</p
Recommended from our members
Outcomes after Second Hematopoietic Cell Transplantation in Children and Young Adults with Relapsed Acute Leukemia.
Children with acute leukemia who relapse after hematopoietic cell transplantation (HCT) have few therapeutic options. We studied 251 children and young adults with acute myelogenous or lymphoblastic leukemia who underwent a second HCT for relapse after their first HCT. The median age at second HCT was 11 years, and the median interval between first and second HCT was 17 months. Most of the patients (n = 187; 75%) were in remission, received a myeloablative conditioning regimen (n = 157; 63%), and underwent unrelated donor HCT (n = 230; 92%). The 2-year probability of leukemia-free survival (LFS) was 33% after transplantation in patients in remission, compared with 19% after transplantation in patients not in remission (P = .02). The corresponding 8-year probabilities were 24% and 10% (P = .003). A higher rate of relapse contributed to the difference in LFS. The 2-year probability of relapse after transplantation was 42% in patients in remission and 56% in those in relapse (P = .05). The corresponding 8-year probabilities were 49% and 64% (P = .04). These data extend the findings of others showing that patients with a low disease burden are more likely to benefit from a second transplantation. Late relapse led to a 10% decrement in LFS beyond the second year after second HCT. This differs from first HCT, in which most relapses occur within 2 years after HCT