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Published in: BMC Hematology 1/2016

Open Access 01-12-2016 | Debate

Hypersplenism in liver disease and SLE revisited: current evidence supports an active rather than passive process

Authors: John M. Gemery, Andrew R. Forauer, Anne M. Silas, Eric K. Hoffer

Published in: BMC Hematology | Issue 1/2016

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Abstract

Background

Active and passive theories have been advanced to explain splenomegaly and cytopenias in liver disease. Dameshek proposed active downregulation of hematopoiesis. Doan proposed passive trapping of blood components in a spleen enlarged by portal hypertension. Recent findings do not support a passive process.

Discussion

Cytopenias and splenomegaly in both liver disease and systemic lupus erythematosus (SLE) poorly correlate with portal hypertension, and likely reflect an active process allocating stem cell resources in response to injury. Organ injury is repaired partly by bone-marrow-derived stem cells. Signaling would thus be needed to allocate resources between repair and routine marrow activities, hematologic and bone production. Granulocyte-colony stimulating factor (G-CSF) may play a central role: mobilizing stem cells, increasing spleen size and downregulating bone production. Serum G-CSF rises with liver injury, and is elevated in chronic liver disease and SLE. Signaling, not sequestration, likely accounts for splenomegaly and osteopenia in liver disease and SLE. The downregulation of a non-repair use of stem cells, bone production, suggests that repair efforts are prioritized. Other non-repair uses might be downregulated, namely hematologic production, as Dameshek proposed.

Summary

Recognition that an active process may exist to allocate stem-cell resources would provide new approaches to diagnosis and treatment of cytopenias in liver disease, SLE and potentially other illnesses.
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Metadata
Title
Hypersplenism in liver disease and SLE revisited: current evidence supports an active rather than passive process
Authors
John M. Gemery
Andrew R. Forauer
Anne M. Silas
Eric K. Hoffer
Publication date
01-12-2016
Publisher
BioMed Central
Published in
BMC Hematology / Issue 1/2016
Electronic ISSN: 2052-1839
DOI
https://doi.org/10.1186/s12878-016-0042-z

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