Influence of blood count, cardiovascular risks, inherited thrombophilia, and JAK2 V617F burden allele on type of thrombosis in patients with Philadelphia chromosome negative myeloproliferative neoplasms

Introduction: Thrombosis is the most common complication in Philadelphia chromosome negative (Ph-) myeloproliferative neoplasms patients. ----- Patients and methods: In a cohort of 258 Ph- myeloproliferative neoplasm patients, the difference between patients with and without thrombosis was analyzed according to genetic thrombophilia factors, JAK2 V617F status and burden allele, blood count, cardiovascular risk factors and age. Patients were also divided in polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) subgroups as well as by the type of thrombosis. ----- Results: Analysis of cardiovascular risk factors regarding arterial thrombosis showed that PV patients with thrombosis had higher incidence of diabetes (P = .030), ET patients more often had hypertension (P = .003) and hyperlipidemia (P = .005), while PMF patients had hyperlipidemia (P = .046) and at least one cardiovascular risk factor (P = .044). Moreover, leukocytes > 18 × 109/L and V617F burden allele > 25.7% were statistically significantly different in PV patients (P = .019 and borderline significant at P = .055, respectively), while in ET patients leukocytes > 9.2 × 109/L (P 55 years were statistically significantly different (P = .002). PMF patients with V617F burden allele ≤ 34.8% were more prone to thrombosis (P = .032). When comparing patients with and without venous thrombosis, cutoff value of V617F burden allele > 90.4% was significant for PV patients with thrombosis (P = .036), as was > 56.7% for PMF patients with thrombosis (P = .046). Platelets ≤ 536 × 109/L and age at diagnosis > 54 years showed statistically significant difference for ET patients with thrombosis (P = .015 and P = .041, respectively). ----- Conclusion: On the basis of our results, a new scoring system for thrombosis risk in PV could be made, while PMF prognostic model may be expanded for better recognition of potential thrombotic risk factors

Urban air pollution caused by the emission of PM10 from the small household devices and abatement measures

This paper is focusing on particulate matter (PM10 ) as the one of the main pollutants in the urban environments, and the one of the main sources of PM emissions are small household furnaces. This paper shows a part of the results of the research related to measurements of the ambient concentrations of aerosols and definition of the sources of the pollution in one part of Banja Luka city area, with dominant private households. Spatial and seasonal variability of concentrations indicates a significant contribution of biomass and fossil fuel burning as well as specific meteorological conditions. By using positive matrix factorization, technique chemical composition data for PM10 were analysed in order to identify the possible sources and estimate their contribution to PM mass. A biomass combustion devices were identified as the one of dominant PM10 emission sources during the winter season, because highly determined correlation between PM10 and potassium content. From the other side, the results of the project “Typology of Residential Buildings in Bosnia and Herzegovina”, were used as a tool for prediction and quantification of influence of the household’s appliances on the pollution as well as for definition of the possible measures for reduction for this specific location. This approach took in consideration spatial distribution of buildings, but also their type, which can give the opportunity to estimate their present energy needs and predict improvements, which can lead to reduction of the PM10 pollution at the end. On that base, some recommendations for the improvements were analysed

Assessment of PM2.5 sources in the Banja Luka (Bosnia and Herzegovina) suburban area using nondestructive techniques and positive matrix factorization

The sources of different pollutants contributing to ambient PM2.5 in the Banja Luka (Bosnia and Herzegovina) suburban area were estimated. From January 2016 to March 2017, a total of 140 daily PM2.5 filter samples were collected and analyzed by complementary nondestructive analytical techniques. Concentrations of Na, Mg, Al, Si, S, Cl, K, Ca, Ti, V, Cr, Mn, Fe, Ni, Cu, Zn, Br, Rb, Sr, and Pb were determined by energy dispersive X-ray fluorescence technique while black carbon concentration was estimated using multi-wavelength absorption optical measurements. Evaluation of the emission sources was performed based on the obtained PM2.5 composition data using positive matrix factorization model. The results indicate five main groups of sources contributing to the annual mean PM2.5 concentration (38.7 µg/m3): secondary sulfur/coal combustion 35.4% (11.8 µg/m3), biomass combustion 26.1. % (9.2 µg/m3), road salts/heavy oil 21.2% (7.5 µg/m3), soil dust 1.1% (0.4 µg/m3) and traffic emissions less than 0.05%. Black carbon originating from diesel fuel and biomass burning was differentiated by applied optical technique and included into PMF analysis. The approach and results of the field study are unique and significant contribution to the air quality management in this area.Copyright © 2022 American Association for Aerosol Researc

Association of Appendicitis, Helicobacter Pylori Positive Gastritis and Thrombotic Thrombocytopenic Purpura in an Adolescent

BACKGROUND Thrombotic thrombocytopenic purpura (TTP) in children is a rare life-threatening syndrome, characterized by microangiopathic hemolytic anemia, thrombocytopenia with renal dysfunction, neurologic symptoms, and fever. TTP is usually caused by deficient activity of von Willebrand factor cleaving protease (ADAMTS13), due to either gene mutations or acquired via anti-ADAMTS13 autoantibodies. It can be triggered by bone marrow or solid organ transplantation, cardiothoracic-, abdominal-, and orthopedic surgeries, infections including very rarely Helicobacter pylori infection. CASE REPORT Here we report a case of a 16-year-old male with TTP, who presented with thrombocytopenia before an appendectomy. Seven days after surgery, our patient started to vomit, developed melena, and was admitted to our pediatric intensive care unit (PICU) with clinical presentation of shock. Gastroscopy revealed H. pylori positive hemorrhagic gastritis. The patient was treated by erythrocyte transfusions, fresh frozen plasma, human albumin, glucose-electrolyte solutions, vitamin K, platelet transfusion before implantation of central venous catheter, and antibiotics. After 36 hours, we started plasma exchange (PEX). Blood tests showed deficiency of ADAMTS13. Due to the presence of anti-ADAMTS13 autoantibodies, rituximab was administered. Due to generalized tonic-clonic seizures, he was artificially ventilated. Brain MR angiography showed small ischemic cerebro-vascular insult in the arteria cerebri media region. Despite immunosuppressive therapy and PEX, the patient did not improve completely until the H. pylori infection was eradicated. After which, he recovered completely. CONCLUSIONS We present a rare case of TTP accompanied with appendicitis and gastritis caused by H. pylori, where TTP improvement was dependent on H. pylori infection eradication