Abdulkadir Basturk

Neutrophil to lymphocyte ratio--not an independent prognostic factor in patients with the myelodysplastic syndrome.

PURPOSEnNeutrophil-to-lymphocyte ratio (NLR) was evaluated as a potential prognostic factor in patients with myelodysplastic syndrome (MDS).nnnMATERIALS AND METHODSnBetween December 2009 and April 2014, 14 female (35%) and 26 male (65%) MDS patients who were followed up in our hematology clinic were included in the study for NLR during diagnosis. Division was into two groups according to the NLR, and the correlation with mortality was evaluated. The prognostic significance of NLR regarding treatment outcome was also evaluated with adjustment for known confounding risk factors.nnnRESULTSnThe mortality rate of the patient group was 55%, and median survival was 18 months. There was no significant correlation between mortality and NLR at a median value of 1.8 (p=0.75). Thrombocytopenia was observed to increase mortality (p=0.027), and there was a significant correlation between mortality and pancytopenia (p=0.017).nnnCONCLUSIONSnThis first study of NLR and mortality did not show any significant correlation . In centres with limited access to genetic evaluation for the presence of pancytopenia and/or thrombocytopenia at the time of diagnosis, a platelet level less than 50?109/l may be poor prognostic markers in MDS patients.

Pseudothrombocytosis due to microerythrocytosis: a case of beta thalassemia minor complicated with iron deficiency anemia.

as well as bone marrow examination were done and chronic myeloproliferative disorders were ruled out. A month after iron and vitamin B 12 replacement therapy, the CBC revealed Hb 8.8 g/dl, MCV 52.4 fl and platelet count 3,223 × 10 9 /l. Peripheral smear examination revealed similar findings and thrombocytosis was still not evident. After completion of the second month of therapy, the CBC revealed Hb 8.4 g/dl, MCV 54.9 fl and platelet count 164 × 10 9 /l ( table 1 ). Since there was an insufficient increase in the Hb level, a further examination with Hb electrophoresis with high-performance liquid chromatography was done and β-thalassemia minor was detected. When all the peripheral smears were re-examined together, many microerythrocytes in each highpower field could be noticed. It was understood that these microerythrocytes were spuriously counted as platelets by the blood counter. The normalization of platelet count after 2 months which was associated with increased erythrocyte volume as a result of therapy supported our observation. The first case of pseudothrombocytosis in the literature was reported by Stass et al. [4] in a case of hairy cell leukemia in 1977. In our literature search, we could identify several cases of pseudothrombocytosis, some of which are summarized in table 2 [4–12] . This phenomenon has also been reported with fungal contamination, accidental Thalassemia minor and iron deficiency anemia are the two major causes of microerythrocytosis. Reactive thrombocytosis is frequently observed in iron deficiency anemia. The normal erythrocyte and thrombocyte volumes are 80–96 and 7–10 fl, respectively. In microcytic anemias like iron deficiency, the erythrocyte volume can be reduced to 30 fl, whereas in diseases like chronic myeloproliferative disorders or May-Hegglin anomaly, the platelet volume can be enlarged up to 30–80 fl [1–3] . Volume changes in blood cells may result in erroneous analysis in the automatic blood counters. Thus, abnormal complete blood count (CBC) results should be evaluated with caution. A 35-year-old female patient was admitted to the outpatient clinics with fatigue. At the physical exam she had pale conjunctiva, subicteric sclera and palpable liver and spleen below the costal margins. Her laboratory examination revealed hemoglobin (Hb) 5.3 g/dl, mean corpuscular volume (MCV) 41.8 fl, white blood cells 4.36 × 10 6 /l, platelet count 5,074 × 10 9 /l (normal range 150–450 × 10 9 /l), red cell distribution width 26.2%, ferritin 2.16 ng/ ml, and vitamin B 12 134.9 pg/ml. In the peripheral smear, hypochromia, microcytosis, anisocytosis and target cells were observed. The platelets were large and seen as aggregates without any evidence of thrombocytosis ( fig. 1 ). Investigation for JAK2 mutation and BCR-ABL1 fusion Received: July 16, 2012 Accepted after revision: November 21, 2012 Published online: March 8, 2013

Paraoxonase and arylesterase activities in adults with vitamin B12 deficiency

Objective: The purpose of this study was to investigate paraoxonase (PON) and arylesterase (ARES) enzyme activity in adults with vitamin B12 deficiency, and specific changes in the activities of these enzymes following vitamin B12 treatment. Methods: A total of 46 patients with vitamin B12 deficiency (aged 18–82 years) and 45 healthy volunteer controls (aged 19–64 years) participated in this study. Venous blood samples were collected, and serum vitamin B12, homocysteine (HCY), methylmalonic acid, PON1, and ARES levels were measured. Results: Paired comparison showed that pre- and post-treatment values for PON and ARES were similar between patients and controls (both P > 0.05). There was no statistically significant relationship between patients’ pre-/post-treatment PON or HCY levels and serum vitamin B12 levels, compared with those of the control group (P > 0.05). Discussion: The results of the present study do not support the hypothesis that the antioxidant enzymes PON and ARES have an underlying role in vitamin B12 deficiency and related hyperhomocysteinemia. Our findings suggest that PON and ARES do not play a role in the systemic effects of vitamin B12 deficiency.

Evaluation of Inflammation Parameters in Philadelphia Negative Chronic Myeloproliferative Neoplasia Patients.

BACKGROUNDnChronic myeloproliferative diseases are clonal stem cell diseases which occur as a result of uncontrollable growth and reproduction of hematopoietic stem cells, which are the myeloid series source in bone marrow. Recent studies have suggested that chronic inflammation can be a triggering factor in the clonal change in chronic myeloproliferative neoplasia (CMPN). In our study, we evaluated the existence of a chronic inflammation process in our Philadelphia negative (Ph-)CMPN patients using inflammation parameters in combination with demographic, laboratory and clinical characteristics of the patients.nnnMATERIALS AND METHODSnDemographic characteristics, clinical and laboratorial data, and thrombosis histories of 99 Ph-CMPN patients, who were diagnosed at our outpatient clinic of hematology in accordance with WHO 2008 criteria, were analyzed retrospectively,with 80 healthy individuals of matching gender and age included as controls. Complete blood counts, sedimentation, C reactive protein (CRP), JAK V617F gene mutations, abdomen ultrasound images and previous thrombosis histories of these patients were retrospectively analyzed.nnnRESULTSnPh-CMPN and healthy control groups included 99 and 80 cases, respectively. PV, ET and MF diagnoses of patients were 43 (%43.4), 44 (44.4%) and 12 (12.1%), respectively. JAK V617F gene mutation was found to be positive in 64 (71.1%) of all cases and in 27(65.8%), 32 (82%), 5 (50%) of the cases in PV, ET and PMF groups, respectively. Thrombosis was determined as 12 (12%) in the entire group, 12.5% in the JAK V617F negative and 15.3% in the positive patients, with no statistical significance (p=0.758). No significant difference was observed between patients with and without previous thrombosis history in respect to hemogram parameters, sedimentation and CRP (p>0.05), neutrophil to lymphocyte ratio (NLR), erythrocyte distribution width (RDW), mean platelet volume (MPV) and sedimentation levels of the patient.