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Browsing by Author "Jovanovic, D. (58721901700)"

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    Publication
    Clinical and epidemiological evaluation of tuberculosis in Serbia, 1990-2004
    (2007)
    Jovanovic, D. (58721901700)
    ;
    Skodric-Trifunovic, V. (23499690800)
    ;
    Markovic-Denic, Ljiljana (55944510900)
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    Stevic, R. (24823286600)
    ;
    Vlajinac, H. (7006581450)
    SETTING: Republic of Serbia, excluding Kosovo. OBJECTIVE: To estimate the clinical and epidemiological pattern of tuberculosis (TB) in Serbia during the period 1990-2004. DESIGN: A retrospective analysis of clinical and epidemiological data on TB patients registered in annual TB reports. RESULTS: During the 15-year period, TB incidence levelled off in Serbia. The slightly decreasing trend occurred in both total pulmonary TB (PTB) and laboratory confirmed PTB (PTB+) incidence (P > 0.05), while the trend of extra-pulmonary TB (EPTB) incidence increased slightly (P > 0.05). During the same period, TB mortality showed a significantly decreasing trend (P < 0.05). The mean annual proportion of PTB+ cases among newly reported PTB cases was 62.7%. The mean proportion of EPTB cases among total TB cases was 6.1%. The mean percentage of cases with resistance to at least one anti-tuberculosis drug was 4.8%. CONCLUSION: Thanks to the good organisation and efficient work of anti-tuberculosis dispensaries in Serbia, as well as to the low incidence of AIDS and low frequency of Mycobacterium tuberculosis resistant strains, TB incidence did not increase during the period observed and TB mortality significantly decreased, despite markedly deteriorated socio-economic conditions during the 1990s. © 2007 The Union.
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    Health-related quality of life in lung cancer patients in Serbia: Correlation with socio-economic and clinical parameters
    (2010)
    Maric, D. (57196811444)
    ;
    Jovanovic, D. (58721901700)
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    Golubicic, I. (6603074739)
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    Dimic, S. (57208444020)
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    Pekmezovic, T. (7003989932)
    The objective of this study was to assess health-related quality of life (HRQoL) in patients with advanced non-small cell lung cancer (NSCLC). In Serbia, there is the lack of available data on HRQoL in lung cancer patients. The special attention in our study has been paid on relationships between socio-economic factors and HRQoL. This cross-sectional study was undertaken in group of 100 NSCLC patients with advanced stage diseases. HRQoL was measured using three standard instruments: 36-item Short Form Health Survey, EORTC QLQ-C30 and its Lung Cancer module (EORTC QLQ-LC13). Unexpected, highly educated patients reported significantly worse social functioning (P = 0.044), and higher degree of financial difficulties (P = 0.047), in comparison with less-educated. Also unusual, unemployed patients had significantly better HRQoL in all domains and significantly lower symptom distress. Significantly better overall HRQoL (P = 0.043), social (P = 0.024), emotional (P = 0.001) and mental functioning (P = 0.011) were observed in patients treated with chemotherapy in comparison with newly diagnosed ones. In addition, the most prominent side effects of chemotherapy were nausea and vomiting, and all QoL domains correlated significantly with them. Patients who undergo active treatment improve their HRQoL but chemotherapy-induced emesis adversely affects many HRQoL domains. Additionally, HRQoL is highly dependent on patient's socio-economic characteristic. © 2009 Blackwell Publishing Ltd.
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    Oxidative stress and inflammation parameters-novel biomarkers for idiopathic pulmonary fibrosis
    (2022)
    Roksandic Milenkovic, M. (56033494500)
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    Klisic, Aleksandra (56160473800)
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    Ceriman, V. (57204881031)
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    Kotur Stevuljevic, J. (6506416348)
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    Savic Vujovic, K. (57217857650)
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    Mirkov, D. (57214282798)
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    Gajic, M. (57204877678)
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    Ilic, B. (56806538200)
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    Dimic, N. (57460624900)
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    Samardzic, N. (56033770200)
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    Jovanovic, D. (58721901700)
    Objective: The pathophysiological mechanisms of idiopathic pulmonary fibrosis (IPF) are not well elucidated. It is assumed that oxidative stress and inflammation are the key underlying culprits for its onset and progression. To gain deeper insight into these processes, we have evaluated several oxidative stress parameters, inflammation markers [i.e., high sensitivity C-reactive protein (hsCRP), serum amyloid A1 (SAA1)], soluble programmed cell death-ligand 1 (sPD-L1), and 25-hydroxyvitamin D [25(OH)D] in IPF patients. Patients and Methods: Biochemistry analyses were done in 30 consecutive IPF patients and 30 age and gender-matched healthy control group (CG). Results: IPF patients had significantly higher advanced oxidation protein products (p<0.001), pro-oxidant-antioxidant balance (p=0.010), total oxidative status (p<0.001), and ischemia modified albumin (p<0.001) compared to CG. Lower total antioxidant status and total sulfhydryl groups (tSGH) and significantly higher sPD-L1, hsCRP (p<0.001 for all), SAA1 proteins (p=0.014) and [25(OH)D] severe deficiency [11.0 (9.6-15.1) nmol/L] in IPF patients compared to CG were observed. Paraoxonase 1 activity and hsCRP level were lower, while tSHG and sPD-L1 were higher in IPF patients with more severe disease (i.e., II+III stage compared to I stage, p<0.05 for all). Conclusions: IPF patients are in a state of profound oxidative stress compared to healthy people. The inflammatory component of the disease was confirmed by higher hsCRP and SAA1, but lower [25(OH)D] in IPF than in healthy people. Also, higher levels of sPD-L1 in patients with IPF compared to healthy individuals suggest that sPD-L1 may have a significant role in immune response in IPF. © 2022 Verduci Editore s.r.l. All rights reserved.
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    The prothrombin factor II G20210A mutation with pulmonary thromboembolism and a normal level of fibrin degradation products
    (2009)
    Nagorni-Obradovic, Lj. (59602283800)
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    Miljic, P. (6604038486)
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    Djordjevic, V. (7005657086)
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    Pešut, D. (55187519500)
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    Jovanovic, D. (58721901700)
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    Stojsic, J. (23006624300)
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    Stevic, R. (24823286600)
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    Radojkovic, D. (6602844151)
    Diagnosis of pulmonary thromboembolism (PTE) usually includes clinical pretest probability assessment, testing for specific degradation products of cross-linked fibrin (D-dimer) and imaging studies. Patients with radiological findings attributable to pulmonary infarction and normal D-dimer level, may present a diagnostic and therapeutic challenge. A 37-year-old Caucasian female had episodes of hemoptysis, and bilateral pulmonary nodular infiltrates on chest radiograph and computerized tomography. The plasma D-dimer level was normal, perfusion lung scan was not conclusive and histological examination of an open lung biopsy revealed recent thrombotic pulmonary infarction. She deteriorated and more perfusion defects were detected on perfusion lung scan. Genetic analysis revealed her to be a carrier of the prothrombin factor II (FII) G20210A mutation.
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    Publication
    The prothrombin factor II G20210A mutation with pulmonary thromboembolism and a normal level of fibrin degradation products
    (2009)
    Nagorni-Obradovic, Lj. (59602283800)
    ;
    Miljic, P. (6604038486)
    ;
    Djordjevic, V. (7005657086)
    ;
    Pešut, D. (55187519500)
    ;
    Jovanovic, D. (58721901700)
    ;
    Stojsic, J. (23006624300)
    ;
    Stevic, R. (24823286600)
    ;
    Radojkovic, D. (6602844151)
    Diagnosis of pulmonary thromboembolism (PTE) usually includes clinical pretest probability assessment, testing for specific degradation products of cross-linked fibrin (D-dimer) and imaging studies. Patients with radiological findings attributable to pulmonary infarction and normal D-dimer level, may present a diagnostic and therapeutic challenge. A 37-year-old Caucasian female had episodes of hemoptysis, and bilateral pulmonary nodular infiltrates on chest radiograph and computerized tomography. The plasma D-dimer level was normal, perfusion lung scan was not conclusive and histological examination of an open lung biopsy revealed recent thrombotic pulmonary infarction. She deteriorated and more perfusion defects were detected on perfusion lung scan. Genetic analysis revealed her to be a carrier of the prothrombin factor II (FII) G20210A mutation.

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