Background: Poland has one of the highest cervical cancer mortality rates in Europe. It is related to the problem of late diagnosis and low attendance rate in screening programs. The objective of the study has been to assess the annual production loss due to the cervical cancer morbidity and mortality in Poland in 2012. The outcomes have been to provide comprehensive information on cervical cancer's influence on population's ability to work and its overall economic burden for the society. The study has also provided the methodological framework for disease-related production losses in Polish settings. Material and Methods: The human capital method was used. The production losses were calculated in both monetary and quantitative terms (working days lost) due to 4 following reasons: 1) temporary disability to work, 2) permanent disability, 3) informal care, and 4) mortality. Results: Cervical cancer resulted in approx. 702 964 working days lost in 2012 due to absence at work for both patients and care givers and a total number of 957 678 working days lost due to patients' mortality. The total value of production lost was assessed at 111.4 million euros. More than 66% of this value was attributed to women's mortality. Conclusions: The calculation of production lost due to cervical cancer burden provides strong evidence to support adequate health promotion and disease prevention actions. Actions promoting cervical cancer screening should be intensified including workplace health promotion activities. Med Pr 2016;67(3):289-299Key words: screening, cost of illness, indirect costs, cervical neoplasm, gross domestic product (GDP), economic burden Streszczenie Wstęp: Polska ma jeden z najwyższych w Europie wskaźników umieralności kobiet z powodu nowotworu szyjki macicy. Niewiele kobiet uczestniczy w programach przesiewowych, a u wielu choroba jest późno diagnozowana. Celem badania było oszacowanie produkcji utraconej z powodu występowania nowotworu szyjki macicy w Polsce w 2012 r., a tym samym ocena wpływu choroby na zdolność populacji do pracy. Analizę można traktować również jako przykład metodyki szacowania strat produkcyjnych z powodu występo-wania określonej jednostki chorobowej przy wykorzystaniu dostępnych w Polsce danych. Materiał i metody: Wykorzystano metodę kapitału ludzkiego i oszacowano produkcję utraconą z 4 powodów -1) czasowej niezdolności do pracy, 2) trwałej niezdolności do pracy, 3) opieki członków rodziny nad osobą chorą i 4) umieralności -w kategoriach monetarnych i ilościowych (dni utraconej produkcji). Wyniki: Nowotwór szyjki macicy spowodował w 2012 r. utratę 702 964 dni produkcji z powodu chorobowości i 957 678 dni z powodu umieralności. Całkowitą produkcję utraconą oszacowano na 111,4 mln euro, z czego ponad 66% było spowodowanych zgonami osób chorych na nowotwór. Wnioski: Oszacowanie produkcji utraconej z powodu nowotworu szyjki macicy dostarcza silnych argumentów w procesie alokacji zasobów w sektorze zdrowia na rzecz prewencji nowotworów. Należy zintensyfikować również działania z zak...
Introduction: Annual vaccination against influenza can prevent 59% of influenza-related illness in healthy individuals. However, influenza vaccination coverage rate in Poland remains low, and at a rate of around 3% it is significantly below most other European Union countries, and in particular the United Kingdom (UK), where it is above 60%. The objective of this study is to analyze the potential savings for the Polish health care system based on the assumption that the influenza coverage rate in Poland would be the same as in the UK. Material and methods: The total number of influenza and influenza-like infections in 2016 in Poland stood at 4.3 million. Based on the data from the Sentinel System, we classified 41% of them as confirmed influenza cases. Influenza vaccination coverage among the general population in this period was 3.4% in Poland and 61.1% in the UK. The literature gives six categories of potential costs associated with a diagnosis of influenza. Because of poor availability of health care cost data, this study captures only part of the real influenza cost in Poland. Our model evaluated two types of potential savings associated with higher influenza vaccines rate: avoided productivity loss and avoided costs of pulmonary hospitalization connected with the influenza virus. Results: In the hypothetical scenario in which influenza coverage rate in Poland would be the same as in the UK, Poland could avoid almost 35% of current influenza incidence, which equals over 617 thousand cases in 2016. The yearly cost of pulmonary hospitalization due to influenza in Poland was PLN 7.1 million, while the cost of productivity loss due to influenza was estimated at PLN 161.6 million. These costs added to PLN 168.7 million, or PLN 94.68 per an infected individual. We estimate the savings connected with lower productivity loss and pulmonary hospitalization frequency for Polish society, if the influenza coverage rates were on the UK level, at PLN 58.4 million. Conclusions: The results of our analysis demonstrate that an increase in influenza vaccination coverage would generate significant economic savings for the Polish health care and social security system.
Introduction. Our previous flow cytometry-based comparison of HIV(+) and HIV(-) autologous hematopoietic stem cell transplant (auto-HSCT) recipient immunomes at 56, 180 and 365 days post-transplant to each other and to healthy controls (HCs) showed that both sets of auto-HSCT recipient immunomes approached HCs over time, but retained significant differences. HIV(+), but not HIV(-), auto-AHCT recipients retained pro-inflammatory features consistent with chronic HIV infection. Here, we report the results of a quantitative and functional analysis of immune reconstitution in HIV(+) patients treated with allogeneic hematopoietic stem cell transplant (allo-HSCT), in comparison with HIV(+) auto-HSCT recipients and HCs. Methods. Blood samples were collected for analysis at days 56, 180 and 365 post-transplant from HIV(+) transplant recipients and at 1 time point from HCs. Whole blood analysis was performed by five-color flow cytometry across 100 immune marker combinations. Comparisons were made between HIV(+) allo-HSCT recipients (n=17, acute myeloid leukemia, acute lymphocytic leukemia, myelodysplastic syndrome, Hodgkin and non-Hodgkin lymphoma that received myeloablative or reduced intensity conditioning on the BMT-CTN-0903/AMC-080 trial), HIV(+) auto-HSCT recipients (n=36, aggressive B cell non-Hodgkin lymphoma or Hodgkin lymphoma that received myeloablative conditioning on the BMT-CTN-0803/AMC-071 trial) and 71 HCs. Unsupervised principal component analysis (PCA) examined differences in immune cell proportions, identified by flow cytometry across 100 cell subsets at each time point. Wilcoxon rank-sum tests compared median absolute counts and median proportions of cell subsets. An independent feature importance score analysis (FIS) identified contributions of immune cell populations expressing specific immune marker combinations to the differences between HIV(+) auto-HSCT recipients, HIV(+) allo-HSCT recipients and HCs. Functional responsiveness of HIV(+) allo-HSCT recipients' T cells to stimulation with CD3- and CD28-directed antibodies, NK cells to stimulation with IL-12 and IL-18 and monocytes to stimulation with lipopolysaccharide (LPS) was assessed in a preliminary mass cytometry on peripheral blood mononuclear cells isolated at the same time points (n=2) and compared to HCs (n=2). Results. PCA showed that immunomes of HIV(+) allo-HSCT recipients and HIV(+) auto-HSCT recipients clustered together with each other, but away from HCs at all time points throughout the post-transplant year. FIS identified: 1) 13 cell subsets that defined the difference between HIV(+) allo-HSCT recipients (all visits) and HCs, and 2) 11 immune cell subsets that defined the difference between HIV(+) auto-HSCT recipients (all visits) and HCs; in both of these comparisons, activated CD3+/HLA-DR+ T cells had the greatest impact on the difference between HIV(+) and HC immunomes. At 1 year, both HIV(+) transplant recipient cohorts had higher absolute numbers of activated T cells, effector T cells and CD8+ T cells than HCs (Wilcoxon rank-sum test, p<0.0031). HIV(+) autologous and allogeneic HSCT recipients also had lower numbers of CD4+ T cells, naïve T cells and activated NK cells compared to HCs (p<0.0031). FIS also identified 20 immune cell subsets that defined the difference between HIV(+) autologous and allogeneic HSCT recipients immunomes at 1 year, with CD8+/CD27- effector T cell subset exerting the highest impact on the difference. Preliminary functional mass cytometry analysis of 2 HIV(+) allo-HSCT recipients and 2 HCs showed that: 1) IFNʏ production by CD8+ T cells was increased above that of HCs at all time points. 2) Expanded populations of CD4+/T-bet+ cytotoxic cells expressing granzyme B and perforin, and CD8+ cytotoxic T cells expressing granzyme B and perforin, persisted in HIV(+) allo-HSCT recipients at all time points, but not in HCs. 3) NK cells retained an ability to produce IFNʏ in response to stimulation with IL-12 and IL-18 in HIV(+) allo-SCT recipients. 4) Monocytes showed an enhanced production of TNFα in response to stimulation with LPS in HIV(+) allo-HSCT recipients compared to HCs at 1 year post-HSCT. Conclusion. Chronic HIV infection confers the pro-inflammatory immune features on the phenotypic and functional profiling of the T lymphocyte immunome of stem cell transplant recipients, irrespective of allogeneic or autologous stem cell donor source. Disclosures Devine: Bristol Myers: Other: Grant for monitoring support & travel support; Kiadis Pharma: Other: Protocol development (via institution); Magenta Therapeutics: Other: Travel support for advisory board; My employer (National Marrow Donor Program) has equity interest in Magenta. Noy:Janssen: Consultancy; Medscape: Honoraria; Prime Oncology: Honoraria; NIH: Research Funding; Pharamcyclics: Research Funding; Raphael Pharma: Research Funding. Popat:Bayer: Research Funding; Incyte: Research Funding; Jazz: Consultancy. Hofmeister:Celgene: Honoraria; Janssen: Membership on an entity's Board of Directors or advisory committees; Nektar: Honoraria, Membership on an entity's Board of Directors or advisory committees; Karyopharm: Membership on an entity's Board of Directors or advisory committees; Imbrium: Membership on an entity's Board of Directors or advisory committees; Oncopeptides: Membership on an entity's Board of Directors or advisory committees. Navarro:Atara Biotherapeutics: Employment, Equity Ownership. Behbehani:Fluidigm corporation: Other: Travel funding. Lozanski:Boehringer Ingelheim: Research Funding; Beckman Coulter: Research Funding; Stemline Therapeutics Inc.: Research Funding; Genentec: Research Funding. Baiocchi:Prelude: Consultancy.
Intratumor heterogeneity (ITH) results from accumulation of somatic mutations in the fractions of successive cancer cell generations. We aimed to use deep sequencing to investigate ITH in colorectal tumors with particular emphasis on variants in oncogenes (ONC) and tumor suppressor genes (TSG). Samples were collected from 16 patients with colorectal cancer and negative or positive lymph node status (n = 8 each). We deep‐sequenced a panel of 56 cancer‐related genes in the central and peripheral locations of T3 size primary tumors and healthy mucosa. The central region of T3 tumors has a different frequency profile and composition of genetic variants. This mutation profile is capable of independently discriminating patients with different lymph node status (p = 0.028) in the central region. We noted an increasing number of mutations outside of the central region of the tumor and a higher number of mutations in tumors from node‐positive patients. Unexpectedly, in the healthy mucosa, we identified somatic mutations with variant allele frequencies, characteristic not only of heterozygotes and homozygotes but also of other discrete peaks (e.g., around 10%, 20%), suggestive of clonal expansion of certain mutant alleles. We found differences in the distribution of variant allele frequencies in TSGs when comparing node‐negative and node‐positive tumors (p = 0.029), as well as central and peripheral regions (p = 0.00399). TSGs may play an important role in the escape of the tumor toward metastatic colonization.
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