Background: Chronic myeloproliferative diseases are clonal stem cell diseases which occur as a result ofuncontrollable growth and reproduction of hematopoietic stem cells, which are the myeloid series source inbone marrow. Recent studies have suggested that chronic inflammation can be a triggering factor in the clonalchange in chronic myeloproliferative neoplasia (CMPN). In our study, we evaluated the existence of a chronicinflammation process in our Philadelphia negative (Ph-)CMPN patients using inflammation parameters incombination with demographic, laboratory and clinical characteristics of the patients. Materials and
Methods:Demographic 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 analyzedretrospectively,with 80 healthy individuals of matching gender and age included as controls. Complete bloodcounts, sedimentation, C reactive protein (CRP), JAK V617F gene mutations, abdomen ultrasound images andprevious thrombosis histories of these patients were retrospectively analyzed.
Results: Ph-CMPN and healthycontrol 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%) ofall cases and in 27(65.8%), 32 (82%), 5 (50%) of the cases in PV, ET and PMF groups, respectively. Thrombosiswas determined as 12 (12%) in the entire group, 12.5% in the JAK V617F negative and 15.3% in the positivepatients, with no statistical significance (p=0.758). No significant difference was observed between patients withand 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) andsedimentation levels of the patient.