Hypersplenism: History and current status

Lv, Yunfu; Lau, Wan Yee; Li, Yejuan; Deng, Jie; Han, Xiaoyu; Gong, Xuezhong; Liu, Ning; Wu, Huimeng

doi:10.3892/etm.2016.3683

Cited by 68 publications

(76 citation statements)

References 45 publications

(48 reference statements)

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“…Hypersplenism is related to spleen size and phagocytic capacity of splenic macrophages. 34 A larger spleen size, which indicates more blood cells stored, and a higher phagocytic capacity of splenic macrophages would result in lower peripheral blood cell counts, and thus a more obvious increase in peripheral blood cell counts after splenectomy. In 15.9% (62/390) of patient-times with peripheral cytopenia, the blood cells counts increased but they did not reach normal, indicating that in addition to hypersplenism other factors were involved.…”

Section: Discussionmentioning

confidence: 99%

Causes of peripheral cytopenia in hepatitic cirrhosis and portal hypertensive splenomegaly

Lau

et al. 2017

Exp Biol Med (Maywood)

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Impact statementFor a long time, the development of peripheral cytopenias as a complication to cirrhotic portal hypertension has been attributed to hypersplenism; however, this has never been fully demonstrated. Dameshek summarized that hypersplenism should be diagnosed by the presence of four conditions: (a) mono-or multi-lineage peripheral cytopenias; (b) compensatory hyperplasia of bone marrow; (c) splenomegaly; and (d) correction of cytopenias after splenectomy. We retrospectively analyzed the clinical data from 183 surgical patients, and found that 80.5% of peripheral cytopenias was caused by hypersplenism, 16% by a combination of factors, and 3.5% by other factors unrelated to hypersplenism. As the first quantitative findings in this field, our results verify that hypersplenism is a major, but not exclusive, cause of peripheral cytopenias, and provides important clinical evidence for investigating the cause of peripheral cytopenias. AbstractThe clinical data of 183 patients with hepatitic cirrhosis and portal hypertensive splenomegaly complicated by peripheral cytopenia were retrospectively analyzed to investigate the causes of peripheral cytopenia, as well as the proportion of the causes in these patients. All patients underwent splenectomy. Before operation, these patients had one or more types of peripheral cytopenia (cumulative cytopenia: 390 patient-times). After splenectomy, blood counts in 79.2% (309/390) returned to normal, while in 15.9% (62/390) they increased but failed to reach to normal levels, and in 4.9% (19/390) they became lower than before the operations. For the last group of patients (n ¼ 19), long-term follow-up showed that blood counts returned to normal in five patients. In other words, in 80.5% [(309 þ 5)/390 or 314/ 390] of patient-times, the peripheral cytopenia was due to hypersplenism, in 15.9% it was due to a combination of factors, and in 3.6% [14/390] it had nothing to do with the hypersplenism. Thus, hypersplenism is a major cause, but not the only cause, of peripheral cytopenia in patients with hepatic cirrhosis and portal hypertensive splenomegaly, and splenectormy is an effective treatment for these patients.

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Section: Discussionmentioning

confidence: 99%

Causes of peripheral cytopenia in hepatitic cirrhosis and portal hypertensive splenomegaly

Lau

et al. 2017

Exp Biol Med (Maywood)

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“…Thus, we believe the specific decreases in B and T cells in circulation in MPKCδKO/ ApoE −/− mice were mainly due to the function of splenomegaly, which is known to increase the uptake and clearance of circulating blood cells, likely due to increased monocytes or macrophages in the red pulp of the spleen to cause increased retention of all cell types, even platelets. In multiple studies have shown the surgical removal of the enlarged spleen will rapidly return the circulatory cells to normal levels 39 . It is commonly found that bone marrow progenitor cells of these circulatory cells are not abnormal unless the basic pathogenesis of the disease also affected those bone marrow stem cells, such as those involved in autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Macrophage Apoptosis and Atherosclerosis by Lipid-Induced PKCδ Isoform Activation

Park

Xia

et al. 2017

Circulation Research

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Rationale: Activation of monocytes/macrophages by hyperlipidemia associated with diabetes and obesity contributes to the development of atherosclerosis. PKCδ expression and activity in monocytes were increased by hyperlipidemia and diabetes with unknown consequences to atherosclerosis. Objective: To investigate the effect of PKCδ activation in macrophages on the severity of atherosclerosis. Methods and Results: PKCδ expression and activity were increased in Zucker diabetic rats. Mice with selective deletion of PKCδ in macrophages were generated by breeding PKCδ flox/flox mice with LyzM-Cre and ApoE−/− mice (MPKCδKO/ApoE−/− mice) and studied in atherogenic (AD) and very high fat diet (HFD). Mice fed AD and HFD exhibited hyperlipidemia, but only HFD fed mice had insulin resistance and mild diabetes. Surprisingly, MPKCδKO/ApoE−/− mice exhibited accelerated aortic atherosclerotic lesions by 2-fold vs. ApoE−/− mice on AD or HFD. Splenomegaly was observed in MPKCδKO/ApoE−/− mice on AD and HFD, but not on regular chow. Both the AD or HFD increased macrophage numbers in aortic plaques and spleen by 1.7 and 2-fold, respectively, in MPKCδKO/ApoE−/− vs. ApoE−/− mice due to decreased apoptosis (62%) and increased proliferation (1.9 fold), and not due to uptake, with parallel increased expressions of inflammatory cytokines. Mechanisms for the increased macrophages in MPKCδKO/ApoE−/− were associated with elevated phosphorylation levels of pro-survival cell signaling proteins, Akt and FoxO3a, with reduction of pro-apoptotic protein Bim associated with PKCδ induced inhibition of P85/PI3K. Conclusion: Accelerated development of atherosclerosis induced by insulin resistance and hyperlipidemia may be partially limited by PKCδ isoform activation in the monocytes, which decreased its number and inflammatory responses in the arterial wall.

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“…Compensatory bone marrow hyperplasia is also observed (Lv et al . ). Hypersplenism can generally be classified into either primary or secondary hypersplenism.…”

Section: Discussionmentioning

confidence: 97%

“…Mechanisms causing hypersplenism include retention of blood cells within the spleen, phagocytosis and autoimmunity (Lv et al . ). To the authors’ knowledge, hypersplenism has not been described in horses, but should be considered in clinical cases of pancytopenia in which other causes are eliminated.…”

Section: Introductionmentioning

confidence: 97%

Suspected case of hypersplenism as a cause of anaemia, thrombocytopenia and leucopenia in a Miniature Horse gelding

Ruby

Wong

Sponseller

et al. 2018

Equine Veterinary Education

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Summary A 23‐year‐old Miniature Horse gelding was presented to the Lloyd Veterinary Medical Center with a 3‐week history of decreased appetite, lethargy and mild intermittent colic. A complete blood count revealed leucopenia, characterised by neutropenia and lymphopenia, as well as anaemia, thrombocytopenia and hyperproteinaemia whereas hypertriglyceridaemia was noted on serum biochemistry profile. Bone marrow evaluation was nondiagnostic and the horse was negative for antiplatelet antibody testing, Coombs test, equine infectious anaemia virus and Anaplasma phagocytophilum. The horse was hospitalised for 36 days and received supportive care, antibiotics, corticosteroids, dextrose‐containing fluids and a whole blood transfusion. Following initial improvement and stabilisation, the horse became severely anaemic and acutely recumbent on Day 36 and was subjected to euthanasia. Post‐mortem examination provided a diagnosis of hypersplenism with a markedly enlarged spleen along with histiocytic phagocytosis of erythrocytes and platelets. Examination of bone marrow showed appropriate erythroid hyperplasia and no evidence of myelopthisis or neoplasia. This report describes the first presumptive case of primary hypersplenism in an equid as a cause of pancytopenia.

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Hypersplenism: History and current status

Cited by 68 publications

References 45 publications

Causes of peripheral cytopenia in hepatitic cirrhosis and portal hypertensive splenomegaly

Causes of peripheral cytopenia in hepatitic cirrhosis and portal hypertensive splenomegaly

Regulation of Macrophage Apoptosis and Atherosclerosis by Lipid-Induced PKCδ Isoform Activation

Suspected case of hypersplenism as a cause of anaemia, thrombocytopenia and leucopenia in a Miniature Horse gelding

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