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Akademisyen hocalarımız ile dayanışma içerisinde yaptığımız çalışmalar meyvelerini vermeye başladı.

Lale OLCAY hocamız ile uzun zamandır yaptığımız çalışmalardan bir tanesi daha yayımlanmış bulunmaktadır.

Sayın Lale hocama ve tüm yazarlara emeklerinden dolayı tebrik ediyorum ve başarılı çalışmalarının devamını diliyorum.

lale hoca 1

lale hoca 2

Summary: In the literature, studies on the oxidant effects of nontransferrin
bound iron [NTBI (eLPI assay)] during chemotherapy of
acute lymphoblastic leukemia and acute myeloblastic leukemia are
lacking. We established NTBI and oxidative stress determinants
(OSD), iron parameters, high-sensitive C-reactive protein (hs-CRP)
levels, liver tests, cumulative chemotherapeutic doses, and transfused
blood in 36 children with acute leukemia throughout chemotherapy.
These parameters were determined at the beginning and end of chemotherapy
blocks (11 time points) and in 20 healthy children using
enzyme-linked immunosorbent assay, and colorimetric and fluorometric
enzymatic methods. In acute lymphoblastic leukemia, NTBI,
OSD, and hs-CRP were higher than controls at 4/11, 7/11, and 9/11
time points (P< 0.05). At 3 time points, NTBI and OSD concurrently increased. Ferritin, soluble transferrin receptor, serum iron, and transferrin saturation were higher than in controls at 5 to 11/11 time points (P< 0.05). Those with NTBI had higher iron parameters than those without NTBI (P< 0.05), but showed similar OSD, hs-CRP, liver enzymes, cumulative chemotherapeutics, and transfused blood (P> 0.05). OSD did not correlate with NTBI, but correlated with hsCRP.
In conclusion, NTBI is a poor predictor of OSD in acute leukemia
possibly because of the heterogeneity of NTBI and chronic
inflammation. Further studies are needed to delineate the
pathophysiology of these diseases.
Key Words: acute lymphoblastic/myeloblastic leukemia, iron
overload, nontransferrin bound iron, lipid peroxidation, protein
oxidation, hs-CRP, soluble transferrin receptor

The Impact of Iron Overload in Acute Leukemia: Chronic
Inflammation, But Not the Presence of Nontransferrin
Bound Iron is a Determinant of Oxidative Stress
Lale Olcay, MD,* Mustafa Serteser, MD,w Murat Kolay, MSc,w
Havva F. Balcı, MD,* U¨lku¨ M. Yıldırım, MD,* Sibel A. Tekgu¨ndu¨z, MD,z
Tuncay Hazırolan, MD,y and Yunus K. Terzi, MD8
Summary: In the literature, studies on the oxidant effects of nontransferrin
bound iron [NTBI (eLPI assay)] during chemotherapy of
acute lymphoblastic leukemia and acute myeloblastic leukemia are
lacking. We established NTBI and oxidative stress determinants
(OSD), iron parameters, high-sensitive C-reactive protein (hs-CRP)
levels, liver tests, cumulative chemotherapeutic doses, and transfused
blood in 36 children with acute leukemia throughout chemotherapy.
These parameters were determined at the beginning and end of chemotherapy
blocks (11 time points) and in 20 healthy children using
enzyme-linked immunosorbent assay, and colorimetric and fluorometric
enzymatic methods. In acute lymphoblastic leukemia, NTBI,
OSD, and hs-CRP were higher than controls at 4/11, 7/11, and 9/11
time points (P< 0.05). At 3 time points, NTBI and OSD concurrently increased. Ferritin, soluble transferrin receptor, serum iron, and transferrin saturation were higher than in controls at 5 to 11/11 time points (P< 0.05). Those with NTBI had higher iron parameters than those without NTBI (P< 0.05), but showed similar OSD, hs-CRP, liver enzymes, cumulative chemotherapeutics, and transfused blood (P> 0.05). OSD did not correlate with NTBI, but correlated with hsCRP.
In conclusion, NTBI is a poor predictor of OSD in acute leukemia
possibly because of the heterogeneity of NTBI and chronic
inflammation. Further studies are needed to delineate the
pathophysiology of these diseases.
Key Words: acute lymphoblastic/myeloblastic leukemia, iron
overload, nontransferrin bound iron, lipid peroxidation, protein
oxidation, hs-CRP, soluble transferrin receptor
(J Pediatr Hematol Oncol 2017;39:425–439)
Iron overload is a major complication of acute lymphoblastic
leukemia (ALL) and acute myeloblastic leukemia
(AML) therapy.1 There are many reports on the development
of iron overload in hematologic malignancies before,
during, immediately stopping chemotherapy, after cessation,
and after transplantation.1–7
Iron overload increases the propensity for infection and the
proliferation of neoplastic cells by causing quantitative and/or
qualitative abnormalities in T, B, natural killer cells or monocyte/macrophages,7–14
as well as causing thrombosis,15 and
atherogenesis.16 Elevated pretransplantation serum ferritin levels
were shown to be strongly associated with lower survival.17
The human body is incapable of excreting excess
iron.18 Free iron (nontransferrin bound iron; NTBI) can
freely enter cells when iron storage capacity of the organism
is exceeded.19,20 This causes the development of reactive
hydroxyl radicals, which lead to lipid peroxidation and
protein oxidation through Fenton and Haber-Weiss reactions,21
thereby damaging the cell membrane, organelles,
and DNA. Iron is deposited mainly in the liver, spleen,
myocardia, and endocrine organs, eventually giving rise to
liver problems (fibrosis, hepatocellular cancer, and cirrhosis),
heart disease, diabetes mellitus, and growth and
developmental retardation.18,22,23
However, in the literature, studies pertaining to the
relationship between NTBI and chemotherapy are limited2–7;
moreover, issues with these studies are as follows:
(1) Patients with hematologic malignancies and/or were
prescribed chemotherapy drugs that were administered
before or at the time of evaluation were not homogenous.
Iron overload developing in different sections of the same
chemotherapy block was also not evaluated.
(2) In studies pertaining to childhood leukemia, there is no
information about NTBI follow-up from the beginning
to the end of therapy.
(3) There is no adequate study about the damage done to
cells by NTBI itself in leukemia patients. In only 1
study6 was it shown that NTBI-containing plasma
stimulated ox-brain phospholipid peroxidation. The
quantity of protein oxidation products was also higher
in samples with NTBI than those without NTBI in a
cohort of ALL children, without giving any detail about
the patients and the chemotherapy drugs that they
received until evaluation.
(4) There is no study indicating the threshold NTBI level
after which cell damage (protein oxidation and lipid
peroxidation) begins.
(5) Leukemia patients who received heavier chemotherapy or
for shorter durations displayed heavier iron overload.1
Therefore, the development of oxidant substances is
expected because of not only NTBI, but chemotherapy
itself. In the literature, there is no study examining
the role of chemotherapy drugs and NTBI separately on
the emergence of oxidant injury in patients with acute
leukemia.
Received for publication July 30, 2016; accepted April 21, 2017.
From the *Unit of Pediatric Hematology, A.Y. Ankara Oncology
Training and Research Hospital; zUnit of Pediatric Oncology, Sami
Ulus Children’s Hospital; yDepartment of Radiology, Hacettepe
University; 8Department of Medical Genetics, Bas¸kent University
Faculty of Medicine, Ankara; and wDepartment of Biochemistry,
Acıbadem University, I˙stanbul, Turkey.
Present address: Lale Olcay, MD, Bas¸kent University Faculty of
Medicine, Department of Pediatrics, Unit of Pediatric Hematology
Oncology, Mares¸al Fevzi C¸ akmak Caddesi, S¸ehit Temel Kug˘uluog˘lu
Sokak, No:24, 06490, Bahc¸elievler, Ankara.
Supported by Tu¨bitak as project 113S041.
The authors declare no conflict of interest.
Reprints: Lale Olcay, MD, Unit of Pediatric Hematology, A.Y. Ankara
Oncology Training and Research Hospital, Ankara, Turkey
(e-mails: lolcay@baskent.edu.tr; laleolcay@hotmail.com.tr).
Supplemental Digital Content is available for this article. Direct URL
citations appear in the printed text and are provided in the HTML
and PDF versions of this article on the journal’s Website,

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