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      Splenic torsion in a cat with chronic anemia

      case-report
      ,
      JFMS Open Reports
      SAGE Publications
      Splenectomy, splenitis, non-regenerative anemia, extramedullary hematopoiesis

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          Abstract

          Case summary

          A 4-year-old female spayed domestic shorthair cat with chronic anemia was evaluated for acute-onset lethargy, vomiting, abdominal distension, and a palpably enlarged and firm spleen. Abdominal ultrasound confirmed marked splenomegaly and concern for a splenic infarct, prompting exploratory abdominal surgery, where splenic torsion was diagnosed. A splenectomy was performed, and the cat recovered uneventfully. Splenitis was diagnosed on histopathology. Anemia improved postoperatively. The role of chronic anemia and other concurrent findings in the development of splenic torsion in this case remains unknown.

          Relevance and novel information

          Splenic torsion has not been previously reported in cats, making this the first case of its kind. In cases of splenomegaly and abnormal splenic blood flow, splenic torsion should be considered a differential diagnosis in cats.

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          Most cited references24

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          Extramedullary hematopoiesis: a new look at the underlying stem cell niche, theories of development, and occurrence in animals.

          Extramedullary hematopoiesis (EMH) is the formation and development of blood cells outside the medullary spaces of the bone marrow. Although widely considered an epiphenomenon, secondary to underlying primary disease and lacking serious clinical or diagnostic implications, the presence of EMH is far from incidental on a molecular basis; rather, it reflects a well-choreographed suite of changes involving stem cells and their microenvironment (the stem cell niche). The goals of this review are to reconsider the molecular basis of EMH based on current knowledge of stem cell niches and to examine its role in the pathophysiologic mechanisms of EMH in animals. The ability of blood cells to home, proliferate, and mature in extramedullary tissues of adult animals reflects embryonic patterns of hematopoiesis and establishment or reactivation of a stem cell niche. This involves pathophysiologic alterations in hematopoietic stem cells, extracellular matrix, stromal cells, and local and systemic chemokines. Four major theories involving changes in stem cells and/or their microenvironment can explain the development of most occurrences of EMH: (1) severe bone marrow failure; (2) myelostimulation; (3) tissue inflammation, injury, and repair; and (4) abnormal chemokine production. EMH has also been reported within many types of neoplasms. Understanding the concepts and factors involved in stem cell niches enhances our understanding of the occurrence of EMH in animals and its relationship to underlying disease. In turn, a better understanding of the prevalence and distribution of EMH in animals and its molecular basis could further inform our understanding of the hematopoietic stem cell niche.
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            Splenic complications in malaria: case report and review.

            Clinicians are increasingly confronted with diagnosis and management of malarial complications. In nonfalciparum malaria, severe complications usually involve the spleen, most notably among them the condition termed spontaneous splenic rupture. A case of infection due to Plasmodium malariae resulting in a symptomatic splenic hematoma is presented. Malarial splenic enlargement and pathology are reviewed, as well as splenic complications such as spontaneous rupture, hematoma, hyperreactive malarial syndrome, hypersplenism, ectopic spleen, torsion, and formation of cysts. Also evaluated are the 11 reported cases of spontaneous splenic rupture in malaria in the English-language literature from 1960 to 1991. Most cases of spontaneous splenic rupture in malaria occur during acute infection and are associated with Plasmodium vivax. Lack of prior immunity to malaria appears to be a major predisposing factor. Increasingly, splenic complications are managed by supportive care and spleen-conserving procedures to avoid postoperative and asplenic morbidity.
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              Hypersplenism.

              Cytopenias in liver disease are a common finding. In the past they have mostly been attributed to pooling and/or destruction of blood cells in the enlarged spleen, leading to the term 'hypersplenism'. With recent advances in the understanding of the physiology of blood formation, in particular with the discovery of several haematopoietic growth factors, new insight into the pathophysiology of blood cell derangements in liver disease has been obtained. Recombinant haematopoietic growth factors present new opportunities for support of the haematopoietic system, which is required because of toxic antiviral therapies or surgical interventions in these patients.
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                Author and article information

                Journal
                JFMS Open Rep
                JFMS Open Rep
                JOR
                spjor
                JFMS Open Reports
                SAGE Publications (Sage UK: London, England )
                2055-1169
                31 January 2024
                Jan-Jun 2024
                : 10
                : 1
                : 20551169231216405
                Affiliations
                [1-20551169231216405]Center for Integrative Mammalian Research, Ross University School of Veterinary Medicine, Basseterre, St Kitts, West Indies
                Author notes
                [*]Melissa C Bucknoff DVM, DACVECC, Center for Integrative Mammalian Research, Ross University School of Veterinary Medicine, P.O. Box 334, Basseterre, St Kitts, West Indies Email: MeBucknoff@ 123456rossvet.edu.kn
                Author information
                https://orcid.org/0009-0009-2502-9305
                https://orcid.org/0000-0002-4660-5676
                Article
                10.1177_20551169231216405
                10.1177/20551169231216405
                10832429
                38304753
                e9a1eeeb-712c-4f88-8b8d-3dbb2e57c552
                © The Author(s) 2024

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Funding
                Funded by: school of veterinary medicine, ross university, FundRef https://doi.org/10.13039/100021039;
                Categories
                Case Report
                Custom metadata
                January-June 2024
                ts1

                splenectomy,splenitis,non-regenerative anemia,extramedullary hematopoiesis

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