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      Assessment of splenic function

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          Abstract

          Hyposplenic patients are at risk of overwhelming post-splenectomy infection (OPSI), which carries mortality of up to 70%. Therefore, preventive measures are warranted. However, patients with diminished splenic function are difficult to identify. In this review we discuss immunological, haematological and scintigraphic parameters that can be used to measure splenic function. IgM memory B cells are a potential parameter for assessing splenic function; however, more studies are necessary for its validation. Detection of Howell–Jolly bodies does not reflect splenic function accurately, whereas determining the percentage of pitted erythrocytes is a well-evaluated method and seems a good first-line investigation for assessing splenic function. When assessing spleen function, 99mTc-labelled, heat-altered, autologous erythrocyte scintigraphy with multimodality single photon emission computed tomography (SPECT)-CT technology is the best approach, as all facets of splenic function are evaluated. In conclusion, although scintigraphic methods are most reliable, they are not suitable for screening large populations. We therefore recommend using the percentage of pitted erythrocytes, albeit suboptimal, as a first-line investigation and subsequently confirming abnormal readings by means of scintigraphy. More studies evaluating the value of potentially new markers are needed.

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          Human blood IgM "memory" B cells are circulating splenic marginal zone B cells harboring a prediversified immunoglobulin repertoire.

          The human peripheral B-cell compartment displays a large population of immunoglobulin M-positive, immunoglobulin D-positive CD27(+) (IgM(+)IgD(+)CD27(+)) "memory" B cells carrying a mutated immunoglobulin receptor. By means of phenotypic analysis, complementarity-determining region 3 (CDR3) spectratyping during a T-independent response, and gene-expression profiling of the different blood and splenic B-cell subsets, we show here that blood IgM(+)IgD(+)CD27(+) cells correspond to circulating splenic marginal zone B cells. Furthermore, analysis of this peripheral subset in healthy children younger than 2 years shows that these B cells develop and mutate their immunoglobulin receptor during ontogeny, prior to their differentiation into T-independent antigen-responsive cells. It is therefore proposed that these IgM(+)IgD(+)CD27(+) B cells provide the splenic marginal zone with a diversified and protective preimmune repertoire in charge of the responses against encapsulated bacteria.
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            Risk of infection and death among post-splenectomy patients.

            The true incidence of post-splenectomy sepsis remains undetermined. An English literature review on post-splenectomy sepsis was undertaken by means of databases of MEDLINE for the period 1966-96. The data registered included age at splenectomy, indication for splenectomy, incidence of infection and death, interval between splenectomy and infection, and microbial aetiology. The reports include 19 680 patients having undergone splenectomy with a median follow up of 6.9 years. The incidence of infection after splenectomy was 3.2% and the mortality rate was 1.4%. Only 6942 reports were sufficiently detailed to allow useful analysis. The incidence of infection among children and adults was similar, 3.3% and 3.2%, respectively. However, the death rates among children were higher than adults (1.7% vs. 1.3%). The incidence of infection was highest among patients with thalassemia major (8.2%), and sickle-cell anaemia (7.3%). The highest mortality rates were observed among patients with thalassaemia major (5.1%), and sickle-cell anaemia (4.8%). The incidence of sepsis among post-splenectomy patients is low, however, it carries a high mortality rate especially among children with hematological disorders. Copyright 2001 The British Infection Society.
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              Memory B cells from human tonsils colonize mucosal epithelium and directly present antigen to T cells by rapid up-regulation of B7-1 and B7-2.

              Human memory B cells that carry mutated IgV region genes were isolated from tonsils by negative selection of IgD+ naive B cells and CD38+ germinal center B cells and plasma cells. They were mainly found within the intraepithelial areas, but not in the B cell follicles of human tonsils. Memory B cells but not naive B cells have the capacity to present antigen directly to T cells, owing to the constitutive expression of the accessory molecules B7-1/CD80 and B7-2/CD86. Signals through antigen receptors and CD40 antigen result in these two molecules being further up-regulated more rapidly and strongly on memory B cells than on naive B cells. The unique anatomical localization of memory B cells beneath the surface of mucosa, together with their strong APC capacity, may explain the well-known prompt and robust secondary antibody responses.
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                Author and article information

                Contributors
                +31-20-5662067 , +31-20-6977192 , alexander.deporto@student.uva.nl
                Journal
                Eur J Clin Microbiol Infect Dis
                European Journal of Clinical Microbiology & Infectious Diseases
                Springer-Verlag (Berlin/Heidelberg )
                0934-9723
                1435-4373
                19 September 2010
                19 September 2010
                December 2010
                : 29
                : 12
                : 1465-1473
                Affiliations
                [1 ]Department of Infectious Diseases, Tropical Medicine and AIDS, G2-105, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands
                [2 ]Department of Nuclear Medicine, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, Netherlands
                [3 ]Department of Internal Medicine, Nephrology Unit, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, Netherlands
                [4 ]Department of Internal Medicine, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, Netherlands
                Article
                1049
                10.1007/s10096-010-1049-1
                2995208
                20853172
                8faaffe1-073a-48a8-98c3-c29c748a3a3e
                © The Author(s) 2010
                History
                : 24 June 2010
                : 17 August 2010
                Categories
                Review
                Custom metadata
                © Springer-Verlag 2010

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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