A large variety of platelet dysfunctions has been described in chronic myeloproliferative disorders. These abnormalities may be due to deficiency of platelet granules, arahidonic acid metabolism defects or platelet membrane glycoproteins abnormalities. In this study we intend to detect the incidence of platelet function defects in 76 patients with various types of chronic myeloproliferative disorders. The platelet activity was studied in vitro by measuring platelet aggregation in response to ADP, epinephrine, collagen, arachidonic acid and ristocetin. These results were subsequently correlated with bleeding time and clinical aspects (bleeding or thrombosis). We found complex changes in platelet response with all agonists, in varied proportions. These abnormalities include absent, decreased or abnormal platelet aggregation response. In a few cases we found a markedly decreased, almost absent platelet response to all agonists while in some patients a normal platelet aggregation was noted. The correlation between these results and template bleeding time, thrombotic or hemorrhagic events and the type of diseases was difficult to establish and sometimes conflictual. Despite this fact, we consider that investigating platelet aggregation may be useful not only for the assesment of the hemostatic balance in chronic myeloproliferative disorders but also for a better insight into cell abnormalities occuring in these pathologic conditions.

Type 2 diabetes mellitus represents a major public health challenge, due to the continuously growing prevalence and the complexity of the diabetic complications. Hyperglycemia seems to be the main mechanism for the disease progression. During erythrocyte's long life span, erythrocyte membranes are affected by the chronic exposure to glucose, which triggers several biochemical modifications that lead to both structural and functional disruption, which are further involved in the physiopathology of diabetes and its complications. Non-enzymatic protein glycation of red blood cell membrane proteins occur in two phases: early glycation, characterized by Schiff bases and Amadouri compounds formation, and advanced glycation, characterized by advanced glycation end products (AGEs). These products could be valuable tools for early diagnosis or biomarkers for disease progression, depending on how advanced they are in the glycation process. Advanced glycated end products were linked with diabetic complications. Also, lipid peroxidation and decreased activity of the enzyme pumps occur in the erythrocyte membrane of the diabetic patients. The investigation of lipid rafts and erythrocyte membrane fatty acids are a valuable tool for longterm monitoring of metabolic status. Further investigation of the erythrocyte membrane could provide novel biomarkers for monitoring of diabetes and its complications.

Eosinophils are leukocytes with multiple functions in physiologic and pathologic circumstances. Eosinophilia is typically associated with reactive conditions (helmintic infections, allergic or drug reactions and atopic disorders) and sometimes with hematologic and non-hematologic malignancies. Evaluation of a patient with eosinophilia requires numerous imaging investigations and laboratory tests (19.55 vs. 4.93 ng/mL, p<0.05). Within patients with eosinophilia, the clonal eosinophilia group showed a significantly higher median ECP value compared to the median ECP values of the non-clonal eosinophilia groups -(30.15 vs. 19.5 ng/mL, p<0.05 and respectively 30.15 vs. 13.3 ng/mL, p<0.05). Also patients having non-clonal eosinophilia with malignancy had a significantly higher median ECP value compared to those of reactive eosinophilia and inflammation (19.5 vs. 13.3 ng/mL, p<0.05

The first description of microparticles dates back to 1967, when Wolf reported platelet membrane fragments in human plasma

Acute myeloid leukemia (AML) is a heterogeneous disorder characterized by a wide range of genetic defects. Cytogenetics, molecular and genomic technologies have proved to be helpful for deciphering the mutational landscape of AML and impacted clinical practice. Forty-eight new AML patients were investigated with an integrated approach, including classical and molecular cytogenetics, array-based comparative genomic hybridization and targeted next generation sequencing (NGS). Various genetic defects were identified in all the patients using our strategy. Targeted NGS revealed known pathogenic mutations as well as rare or unreported variants with deleterious predictions. The mutational screening of the normal karyotype (NK) group identified clinically relevant variants in 86.2% of the patients; in the abnormal cytogenetics group, the mutation detection rate was 87.5%. Overall, the highest mutation prevalence was observed for the NPM1 gene, followed by DNMT3A, FLT3 and NRAS. An unexpected co-occurrence of KMT2A translocation and DNMT3A-R882 was identified; alterations of these genes, which are involved in epigenetic regulation, are considered to be mutually exclusive. A microarray analysis detected CNVs in 25% of the NK AML patients. In patients with complex karyotypes, the microarray analysis made a significant contribution toward the accurate characterization of chromosomal defects. In summary, our results show that the integration of multiple investigative strategies increases the detection yield of genetic defects with potential clinical relevance.