Background Pregnant women are more prone to oxidative stress. Iron deficiency anemia not only affects hematological parameters but also disturbs body oxidative balance, which impairs pregnancy outcome. Besides, iron therapy may generate harmful oxygen species. Objectives The aim of this study was to investigate the effect of the nature of oral iron supplementation (ferrous vs. ferric) in pregnant women with iron deficiency on oxidative stress and its correlation with peripheral systemic inflammatory response markers. Patients and methods A clinical trail study involves study included 30 healthy and 50 anemic pregnant women in their 20th-36th gestational weeks who fulfilled the inclusion criteria. They were randomly distributed to receive either ferrous sulfate or ferric polymaltose complex. Outcome was assessed after 8 weeks of iron supplementation and included hematological parameters, neutrophil : lymphocyte ratio, platelet : lymphocyte ratio, mean platelet volume, serum malondialdehyde (MDA), total antioxidant capacity (TAC), iron, and ferritin. Results Anemic pregnant women have increased oxidative stress with high levels of MDA and TAC, both at baseline and following iron supplementation (P < 0.001). Following 8 weeks of iron supplementation, there were a significant increase (P < 0.001) in hemoglobin and serum ferritin, and a significant decrease (P < 0.001) in the peripheral inflammatory markers neutrophil: lymphocyte ratio, platelet: lymphocyte ratio, mean platelet volume, and absolute lymphocyte counts. Conclusion Iron polymaltose complex was as effective as ferrous sulfate as both were able to correct hematologic parameters in parallel to a decrease in MDA and peripheral inflammatory markers together with an increase in TAC levels to maintain oxidative balance.

Objectives To assess the relationship between iron treatments and to gain weight in the female patients. Materials and methods This study was conducted prospectively between 2013 and 2014 to assess the relationship between iron treatments and to gain weight in the female patients who were admitted to hematology clinic, Ministry of Health İstanbul Research Hospital with a diagnosis of iron deficiency anemia and iron therapy between the ages of 18 and 50 and signed informed consent. Results After 3 months of iron therapy, significant hemoglobin (Hgb) increase was observed in 30 of 33 patients. Weight gain and Hgb increase have not been found in three patients. Hgb increases in patients who gained weight more than 3 kg were found to be statistically significant than patients who gained weight 3 kg or less (P = 0.008). Conclusion Obesity and metabolic syndrome are current health problems in terms of mortality and morbidity. Weight gain related to iron therapy is a common problem in female patients with iron deficiency anemia. Patients under iron therapy should be counseled in terms of weight gain complication and benefits of diet and followed up serum ferritin and Hgb levels to prevent prolonged iron therapy. Physicians should pay attention to patients who do not gain weight without dieting.

Background Thalassemia is associated with the generation of labile iron in the red blood cells, which promotes the formation of reactive oxygen species, leading to cumulative cell damage. Ischemia modified albumin (IMA) is now suggested to reflect generalized oxidative stress. Objectives The aim of this study was to evaluate IMA in children with transfusion-dependent (TD) β-thalassemia and its relation with serum ferritin and iron chelation therapies. Patients and methods A total of 60 children with TD thalassemia were divided into three groups on the basis of the type of iron chelation therapy received: group A received oral deferiprone (DFP), group B received effervescent deferasirox (DFX), and group C did not receive any type of iron chelation therapy. A total of 20 age-matched and sex-matched healthy children were included as controls. Serum ferritin and IMA were determined for all participants. Results There were significant increases in serum ferritin and IMA levels in thalassemic children than in controls (P < 0.001 for each). Children on DFP and DFX had significantly lower IMA levels compared with children not receiving any iron chelation therapy (P < 0.001 and 0.01, respectively). Serum ferritin had a positive significant association with IMA (r = +0.27 and P = 0.03). Conclusion IMA was higher in children with TD thalassemia than in controls. Moreover, its level in thalassemic children on either DFP or DFX was significantly lower than its level in children not receiving any chelation therapy. Therefore, IMA may be a possible marker of iron-induced oxidative stress in β-thalassemia.

Background Hemostasis is a dynamic process resulting from the balance between procoagulant and anticoagulant factors. The liver plays a key role in blood coagulation, being the site of synthesis of almost all coagulation factors and inhibitors. In addition to synthesis, the hepatic reticuloendothelial system is also involved in the clearance of activated coagulation factors as well as enzyme-inhibitor complexes. Plasma levels of fragment D-dimer represent an accurate marker of fibrinolytic activity. Thus, coagulation abnormality is a predictable feature of acute and chronic liver diseases. Aim The aim of the study was to evaluate fibrinolytic activity in patients with various degrees of liver parenchymal damage and its relation to the synthetic function of hepatic coagulation. Patients and methods We studied 40 patients with liver cirrhosis, who were classified into two groups according to Child-Pugh classification: group I, comprising patients with Child class A or B (n = 17), and group II, comprising patients with Child class C (n = 23). In addition, there was a control group (group III) (n = 15). Results Platelet count was significantly low in group II compared with groups I and III (P = 0.001); platelet distribution width was significantly high in group II compared with groups I and III (P = 0.009). There was nonsignificant difference between the studied groups as regards the mean platelet volume (P = 0.4). Fibrinogen and factor VII were significantly decreased in group II when compared with group I and group III (P = 0.01 and 0.001, respectively). D-dimer was significantly increased in group II when compared with group I and group III (P = 0.04). In group II (Child class C) there was significant positive correlation between fibrinogen level, prothrombin concentration, and factor VII (r = 0.53 and 0.58; P = 0.009 and 0.004, respectively) and significant negative correlation between fibrinogen level, activated partial thromboplastin time, and D-dimer concentration (r = −0.50 and −0.39; P = 0.01 and 0.05, respectively). There was significant negative correlation between D-dimer concentration and prothrombin concentration (r = −0.59; P = 0.003). Conclusion Patients with liver cirrhosis suffer from complex coagulation changes. There is a state of hyperfibrinolysis in decompensated cirrhosis. Abnormal fibrinolytic activity is a major hemostatic defect in patients with liver parenchymal damage.

Background/aim Diffuse large B-cell lymphoma (DLBCL) constitutes the largest subtype of B-cell non-Hodgkin's lymphomas. The prognostic ability of the International Prognostic Index in the era of immunochemotherapy is modest. New prognostic biomarkers are mandatory to provide new insights into the risk stratification of DLBCL. Nowadays, serum-free light chain (sFLC) assay is being applied to hematologic non-plasma cell B-cell lymphoid malignancies. The aim of our work was to investigate the prevalence and prognostic value of elevated sFLC (monoclonal and polyclonal) in DLBCL and their impact on event-free survival (EFS) and overall survival (OS). Patients and methods This cohort study included 58 patients with DLBCL. Pretreatment serum samples were taken to detect κ and λ sFLCs with enzyme-linked immunosorbent assay. Patients were followed up every 3 months and computed tomographic scan was done every 6 months for 24 months after treatment. EFS and OS were estimated. Results Twenty-four patients (41.38%) had elevated κ or λ sFLC. Thirteen patients (22.41%) and 11 patients (18.97%) had monoclonal and polyclonal elevated sFLC, respectively. EFS and OS significantly decreased in patients with elevated sFLC and in those with abnormal sFLC ratio (monoclonal elevated sFLC). OS significantly decreased in patients with monoclonal elevated sFLC when compared with those with polyclonal elevated sFLC, but there was no difference between monoclonal and polyclonal elevated sFLC patients as regards EFS. Conclusion Elevated sFLC and abnormal sFLC ratio (monoclonal elevated sFLC) correlate with disease outcome (EFS and OS). There was no difference between monoclonal and polyclonal elevated sFLC as regards EFS but there was significant difference as regards OS.

Background The interest in glutathione-S-transferase (GST) isoenzymes has increased because of their regulatory role in the interaction with critical kinases involved in controlling stress response, apoptosis, and proliferation. GSTP1 is of particular interest with regard to cancer, because many tumors are characterized by high GSTP1 expression. Aim of the work We aimed at evaluating the role of GSTP1 genetic polymorphisms in chronic myeloid leukemia (CML) patients. Patients and methods We genotyped 40 CML patients and 30 healthy individuals of matched age and sex. Results Wild GSTP1 was found in 15/40 CML patients (37.5%) and in 21/30 (70%) controls, whereas mutant allele (homozygous and heterozygous) was present in 25/40 (62.5%) and 9/30 (30%) CML patients and controls, respectively. The odds ratio for GSTP1 was 3.889 (95% confidence interval, 1.417-10.674; P = 0.009*) with four-fold increased risk for CML. No significant difference in genotype frequency was present between wild and mutant genotypes when age of onset, sex, white blood cell count over 100×10 ⁹ /l at presentation, or smoking status were considered. Conclusion These data indicate that GSTP1 mutant allele may contribute significantly to the susceptibility to CML in a sample of the Egyptian patients. These results should be considered preliminary and must be confirmed in studies with larger sample sizes.

Background Little is known about the prognostic importance of coexpression of CD49d and CD38 in chronic lymphocytic leukemia (CLL) patients. Aim This study aimed to investigate the coexpression of both CD38 and CD49d as prognostic and survival markers in CLL patients. Patients and methods Fifty-two patients with newly diagnosed B-cell CLL were included in the study. Twenty age-matched and sex-matched healthy control participants were also included in the study. Patients were subjected to a clinical examination and abdominal ultrasonography and chest radiography. Laboratory investigations including complete blood count, β2 microglobulin, cytogenetic analysis, and immunophenotyping by flow cytometer (B-lymphocyte markers and the expression of CD38 and CD49d) were performed. Results There was a significant decrease in hemoglobin concentration and platelet counts in patients who coexpressed CD49d+/CD38+ compared with patients who expressed CD49+ alone, whereas white blood cell and lymphocyte counts, lactate dehydrogenase, and β2 microglobulin were significantly higher. In addition, CD49d+/CD38+ coexpression was significantly high in advanced stages of CLL. A positive correlation was detected between CD49d expression and poor prognostic parameters in CLL. The median treatment-free time was shorter in CD49d+ patients (32 months) compared with CD49d- patients (98 months). The median treatment-free duration was shorter in CD38+ patients (28 months) compared with CD38- patients (102 months). In the concordant cases of CD49d+/CD38+, the median treatment-free survival was shorter (24 months) in patients with CD49+/CD38+ patients compared with disconcordant cases of CD49d+/CD38- patients (62 months). Conclusion CD38 and Cd49d expressions are considered prognostic markers for CLL patients and they should be assessed to decided on the patient's therapy and to determine disease prognosis. These molecules should also be tested in a large-scale study to determine their potential in preventing frequent relapses and development of resistance to chemotherapy in CLL.

Background Acute lymphoblastic leukemia (ALL) is the most common form of childhood cancer with a cure rate approaching 80%. Neuron-specific enolase (NSE) is known to be a cell-specific isoenzyme of the glycolytic enzyme enolase. The expression of NSE is a late event in neural differentiation, thus making it a useful index of neural maturation. It is a highly specific marker for neurons and peripheral neuroendocrine cells. NSE in cerebrospinal fluid (CSF) is a reliable marker of neuronal damage. It is believed to signal for brain damage after hypoxic-ischemic and traumatic injury. Objective and methods This study aimed to measure CSF levels of NSE as a neurochemical marker for brain damage in response to chemotherapy at diagnosis and during induction using the enzyme-linked immunosorbent assay method. Thirty newly diagnosed ALL patients were enrolled in this study, comprising 19 male and 11 female patients. Results NSE level in the CSF samples increased from 9.3 ± 2.1 μg/l on day 0 (before the start of treatment) to 14.9 ± 1.85 μg/l on day 7 and then gradually decreased to 11.4 ± 1.46 μg/l on day 28. The increase in NSE levels in CSF on days 7 and 28 was considered highly significant when compared with those measured on day 0 (before induction therapy). Conclusion We concluded that the increase in NSE in CSF during induction therapy in children with ALL can be interpreted as an early sign of brain damage.

Background Neuropilin-1 (NRP-1, BDCA-4, or CD304) is a nontyrosine kinase coreceptor for semaphorins and vascular endothelial growth factor, involved in neural development and tumor angiogenesis. Objective The aim of this study was to evaluate NRP-1/CD304 expression in acute leukemia to be used as a potential marker for minimal residual disease (MRD) detection using flow cytometry. Materials and methods This study was conducted on 30 adults with newly diagnosed acute leukemia admitted to the Hematology Unit, Internal Medicine Department, Main Alexandria University Hospitals and Alexandria Research Institute within the period from February 2014 to December 2014, and 10 patients diagnosed with hypersplenism were also included as a control group. The following investigations were carried out for all patients: complete blood picture, bone marrow examination, and immunophenotyping using flow cytometry. Results This study showed that NRP-1/CD304 expression was statistically higher in B-lineage acute lymphoblastic leukemia (ALL) than in the acute myeloid leukemia and the control group (P = 0.002). There was a positive correlation between NRP-1/CD304 percentage expression and blast cell percentage in the bone marrow (P = 0.039). Follow-up of the patients on day 28 of induction chemotherapy revealed that NRP-1/CD304 expression was statistically higher in those who did not achieve complete remission than those who did (P = 0.035). Moreover, we observed that leukemic patients with extramedullary infiltration had statistically higher NRP-1/CD304 expression than those who did not have extramedullary infiltration (P = 0.023). All patients who achieved complete remission on day 28 of induction chemotherapy had negative MRD (<0.001). Conclusion It was observed that NRP-1/CD304 was expressed in almost all B-lineage ALL patients in variable degrees. It might be a useful marker in MRD detection of B-lineage ALL patients.

Introduction Multiple myeloma (MM) is neoplasia of plasma cells characterized by clonal proliferation of malignant plasma cells in the bone marrow. Amplification of 1q21 (CKS1B) is the most common recurrent chromosomal aberration in myeloma. Overexpression of the CKS1B gene upregulates cell cycle processes and leads to a more proliferative malignant plasma cell. This is related to an unfavorable clinical course with poor prognosis and disease progression. Also the deletions of CDKN2C have been identified in 40% of the studied MM cases and hence inactivation of CDKN2C may be an important step in the initiation and progression of MM and could be an important prognostic factor. The aim of the work The aim of the study was to assess the prognostic significance of CKS1B gain and CDKN2C gene deletion in MM patients. Patients and methods This prospective cohort study was carried out on 40 newly diagnosed MM patients who were submitted to routine laboratory investigations, including complete blood count, bone marrow aspiration, blood urea nitrogen, creatinine, calcium, albumin, plasma protein electrophoresis, 24 h urine for total protein, and β2-microglobulin, and to detection of CKS1B/CDKN2C (P18) amplification/deletion by fluorescence in-situ hybridization technique. Results On using fluorescence in-situ hybridization, we found that 25% (10 out of 40) of patients showed CKS1B gain and 20% (eight out of 40) showed positive deletion of the CDKN2C gene. All these patients showed inferior outcome and short survival. Conclusion MM patients with CKS1B/CDKN2C (P18) amplification/deletion had a more aggressive disease with adverse impact on survival, which makes CKS1B and CDKN2C genes valuable prognostic indicators in MM patients.

Purpose Cytomegalovirus (CMV) infection and its associated disease are significant complications of allogeneic hematopoietic stem cell transplantation (HSCT). Many risk factors for CMV infection have been previously identified, including different human leukocyte antigens (HLAs) of donor/recipient pairs. We aimed to investigate the relation of broad HLAs of donor/recipient pairs to the occurrence of postallogeneic HSCT CMV infection and disease. Materials and methods A total of 112 patients undergoing allogeneic HSCT from a matched sibling donor were followed up for occurrence of CMV infection and disease by performing weekly quantitative PCR-CMV-DNA and clinical examination until day 100 after transplantation. Results CMV infection occurred in 58 patients (51.8%), whereas CMV disease occurred in 22 (19.6%). On univariate analysis, acute leukemia diagnosis (P < 0.001), donor/recipient CMV serostatus (P = 0.010), methylprednisolone administration (P = 0.002), fludarabine/cyclophosphamide/antithymocyte globulin-conditioning regimen (P = 0.002), age (P = 0.041), HLA-A1 (P = 0.037), HLA-A3 (P = 0.035), HLA-B15 (P = 0.021), HLA-B16 (P = 0.003), HLA-DR6 (P = 0.002), and HLA-Cw7 (P = 0.003) influenced the occurrence of CMV infection significantly. On multivariate analysis, HLA-A3, HLA-B16, and HLA-Cw7 significantly affected the risk for CMV infection occurrence (P = 0.025, 0.004, and 0.008, respectively). Also, HLA-B16 was associated with reduced risk for CMV disease (P = 0.048). Conclusion HLA-B16 has a protective effect against both CMV infection and disease following allogeneic HSCT.

Background Hematopoietic stem cell transplantation (HSCT) is a procedure that can restore marrow function in patients who have had severe marrow injury. It is either autologous or allogeneic. It has become increasingly important to optimize pretransplant risk assessment to improve hematopoietic cell transplantation (HCT) decision making. Single-organ comorbidity involving the liver, lung, heart, or kidney before HCT has been traditionally found to cause organ toxicity after HCT. The HCT-comorbidity index (HCT-CI) has provided better prediction of HCT-related morbidity and mortality compared with other non-HCT-specific indexes. Aim The aim of this study was to investigate the impact of various pretransplant comorbidities on the outcome of patients who had undergone either allogeneic or autologous HSCT in relation to treatment-related mortality, disease-related mortality, and overall survival. Patients and methods A retrospective study was conducted at the Bone Marrow Transplantation Unit, Ain Shams University, on 119 patients who were transplanted either using autologous or allogeneic HSCT. All of them were older than 18 years and had different types of hematologic diseases. The most frequent hematologic disease was acute myeloid leukemia (34.4%), followed by multiple myeloma (17.6%), acute lymphoblastic leukemia (16.8%), and lymphoma (10.9%), whereas aplastic anemia, myelodysplastic syndrome, chronic myeloid leukemia, and biphenotypic leukemia collectively represented 20.1%. They were either incomplete or partial remission. They were categorized on the basis of the HCT-CI as follows: mild score (0), 43 (36.2%) patients; moderate score (1-2), 60 (50.4%) patients; and severe score (΃3), 16 (13.4%) patients. The study data were collected from medical notes, pathology reports, and laboratory data. Results There was a statistically significant relation between the HCT-CI and overall survival (P = 0.012), disease-free survival (P = 0.007), mortality (P = 0.047), and the incidence of graft failure (P = 0.034). Conclusion We concluded that the HCT-CI is a better predictor for detecting the influence of comorbidity in patients with hematologic disorders on mortality, overall survival, and disease-free survival after HCT.

Introduction Acute myeloid leukemia (AML) is a heterogenous disorder that results from a block in the differentiation of hematopoietic progenitor cells along with uncontrolled proliferation. Cytogenetics represents the most valuable predictor for a poor outcome in patients with AML, and the cytogenetic profile of AML at diagnosis consistently remains a highly influential prognostic factor. Of these cytogenetic aberrations, patients with complex karyotype anomalies show very low complete remission rates and short leukemia-free and overall survival. Case presentation We report a case of AML in a 50-year-old female patient who presented with morphologic and immunophenotypic features of AML-M1. The patient's karyotyping and fluorescence in-situ hybridization of cultured bone marrow cells revealed a unique complex karyotype: 49, XX, +1, +8, +21. The patient's condition deteriorated rapidly and she died shortly after induction from fatal infectious complications. Conclusion Reports of trisomy 1 in AML are rare, and, to the best of our knowledge, the present case is the only one reported with the occurrence of trisomy 1 in addition to trisomy 8 and 2. Treatment outcomes of complex karyotype AML patients receiving chemotherapy are very poor; the yet unreported complex karyotype observed in this case seems to be correlated with an adverse prognosis. Single case reports as well as large scale studies are necessary to provide further insights on karyotypic changes taking place in human malignancies.