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      Pleural empyema due to Salmonella in a patient with bronchogenic carcinoma: the first case report from a cancer hospital in Egypt

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          Abstract

          Background

          Salmonella species are motile, Gram-negative facultative anaerobic bacilli, which belong to the family Enterobacteriaceae . The most common clinical presentations of Salmonella infection are gastroenteritis and enteric fever. Detection of Salmonella organisms in empyema is very rare.

          Case presentation

          We report the case of a 66-year-old female patient with bronchogenic carcinoma who developed empyema, and Salmonella was identified from the culture of pleural fluid. After antimicrobial therapy and other therapeutic measures, including the insertion of an intercostal tube, oxygen supplementation, frequent suction of respiratory secretions, and chest physiotherapy, the patient's condition improved. To the best of our knowledge, this is the first case to be reported in Egypt.

          Conclusions

          Our case sheds light on the role of Salmonella in immunocompromised patients in general and cancer patients in specific. We recommend further study of this role, since it may lead to a better understanding of the pathogenicity of this organism in these patients.

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          Most cited references32

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          New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1).

          Assessment of the change in tumour burden is an important feature of the clinical evaluation of cancer therapeutics: both tumour shrinkage (objective response) and disease progression are useful endpoints in clinical trials. Since RECIST was published in 2000, many investigators, cooperative groups, industry and government authorities have adopted these criteria in the assessment of treatment outcomes. However, a number of questions and issues have arisen which have led to the development of a revised RECIST guideline (version 1.1). Evidence for changes, summarised in separate papers in this special issue, has come from assessment of a large data warehouse (>6500 patients), simulation studies and literature reviews. HIGHLIGHTS OF REVISED RECIST 1.1: Major changes include: Number of lesions to be assessed: based on evidence from numerous trial databases merged into a data warehouse for analysis purposes, the number of lesions required to assess tumour burden for response determination has been reduced from a maximum of 10 to a maximum of five total (and from five to two per organ, maximum). Assessment of pathological lymph nodes is now incorporated: nodes with a short axis of 15 mm are considered measurable and assessable as target lesions. The short axis measurement should be included in the sum of lesions in calculation of tumour response. Nodes that shrink to <10mm short axis are considered normal. Confirmation of response is required for trials with response primary endpoint but is no longer required in randomised studies since the control arm serves as appropriate means of interpretation of data. Disease progression is clarified in several aspects: in addition to the previous definition of progression in target disease of 20% increase in sum, a 5mm absolute increase is now required as well to guard against over calling PD when the total sum is very small. Furthermore, there is guidance offered on what constitutes 'unequivocal progression' of non-measurable/non-target disease, a source of confusion in the original RECIST guideline. Finally, a section on detection of new lesions, including the interpretation of FDG-PET scan assessment is included. Imaging guidance: the revised RECIST includes a new imaging appendix with updated recommendations on the optimal anatomical assessment of lesions. A key question considered by the RECIST Working Group in developing RECIST 1.1 was whether it was appropriate to move from anatomic unidimensional assessment of tumour burden to either volumetric anatomical assessment or to functional assessment with PET or MRI. It was concluded that, at present, there is not sufficient standardisation or evidence to abandon anatomical assessment of tumour burden. The only exception to this is in the use of FDG-PET imaging as an adjunct to determination of progression. As is detailed in the final paper in this special issue, the use of these promising newer approaches requires appropriate clinical validation studies.
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            OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis.

            The tumour-necrosis-factor-family molecule osteoprotegerin ligand (OPGL; also known as TRANCE, RANKL and ODF) has been identified as a potential osteoclast differentiation factor and regulator of interactions between T cells and dendritic cells in vitro. Mice with a disrupted opgl gene show severe osteopetrosis and a defect in tooth eruption, and completely lack osteoclasts as a result of an inability of osteoblasts to support osteoclastogenesis. Although dendritic cells appear normal, opgl-deficient mice exhibit defects in early differentiation of T and B lymphocytes. Surprisingly, opgl-deficient mice lack all lymph nodes but have normal splenic structure and Peyer's patches. Thus OPGL is a new regulator of lymph-node organogenesis and lymphocyte development and is an essential osteoclast differentiation factor in vivo.
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              Amphiregulin enhances regulatory T cell-suppressive function via the epidermal growth factor receptor.

              Epidermal growth factor receptor (EGFR) is known to be critically involved in tissue development and homeostasis as well as in the pathogenesis of cancer. Here we showed that Foxp3(+) regulatory T (Treg) cells express EGFR under inflammatory conditions. Stimulation with the EGF-like growth factor Amphiregulin (AREG) markedly enhanced Treg cell function in vitro, and in a colitis and tumor vaccination model we showed that AREG was critical for efficient Treg cell function in vivo. In addition, mast cell-derived AREG fully restored optimal Treg cell function. These findings reveal EGFR as a component in the regulation of local immune responses and establish a link between mast cells and Treg cells. Targeting of this immune regulatory mechanism may contribute to the therapeutic successes of EGFR-targeting treatments in cancer patients. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Access Microbiol
                Access Microbiol
                acmi
                acmi
                Access Microbiology
                Microbiology Society
                2516-8290
                2020
                15 July 2020
                15 July 2020
                : 2
                : 9
                : acmi000151
                Affiliations
                [ 1] departmentDepartment of Clinical pathology , National Cancer Institute, Cairo University , Cairo, Egypt
                [ 2] departmentDepartment of Clinical pathology , Shefaa Al Orman Hospital , Luxor, Egypt
                [ 3] departmentDepartment of Clinical and Chemical Pathology , Faculty of Medicine, Cairo University , Cairo, Egypt
                [ 4] departmentDepartment of Clinical Oncology , Faculty of Medicine, Ain Shams University , Cairo, Egypt
                [ 5] departmentDepartment of Medical Oncology , Shefaa Al Orman Hospital , Luxor, Egypt
                Author notes
                *Correspondence: Ahmed Samir Abdelhafiz, ahmed.samir@ 123456nci.cu.edu.eg
                Author information
                https://orcid.org/0000-0003-4564-8073
                Article
                000151
                10.1099/acmi.0.000151
                7656189
                e8e910a3-b5e6-4472-8760-d4baf712e3a3
                © 2020 The Authors

                This is an open-access article distributed under the terms of the Creative Commons Attribution License. The Microbiology Society waived the open access fees for this article.

                History
                : 05 March 2020
                : 17 June 2020
                Categories
                Case Report
                Custom metadata
                0

                salmonella,empyema,cancer,bronchogenic carcinoma
                salmonella, empyema, cancer, bronchogenic carcinoma

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