From the Medical Literature
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Hyposplenism is more frequent in lupus than previously thought, associated with an increased risk of severe infections, especially in patients with early onset disease or antiphospholipid syndrome.
Infections are among the leading causes of morbidity and mortality in systemic lupus erythematosus (SLE). While immunosuppressive therapies are known risk factors, the role of hyposplenism has been under-researched. Recently, a team led by Dr. Ludovic Trefond at Sorbonne Université, Paris, addressed this by studying a cohort of 245 SLE patients. They identified impaired spleen function using the presence of Howell-Jolly bodies in peripheral blood smears, alongside clinical, radiological, and laboratory data pertaining to infection occurrences.
Hyposplenism More Frequent than Previously Reported
In this study, 23 participants exhibited hyposplenism, a prevalence of 9.4%, significantly higher than previous findings. Three independent factors were strongly associated with hyposplenism:
Onset of the disease in childhood or adolescence,
Presence of antiphospholipid syndrome (APS), and
General symptoms like fever, fatigue, or weight loss in the medical history.
These correlations suggest that hyposplenism primarily affects patients with pronounced systemic disease involvement. Hematological findings such as neutrophilia, monocytosis, eosinophilia, and thrombocytosis were more frequent in those with hyposplenism. These blood changes could provide clinical indications of previously unrecognized splenic impairment. Radiologically, hyposplenism was notably associated with spleen hypoplasia or atrophy, indicating that splenic damage in SLE might be a dynamic and potentially irreversible process.
Increased Risk of Severe Infections
Over one-third of patients with hyposplenism required hospital treatment due to infections, compared to nearly 6% of those without splenic dysfunction. Even after accounting for potential influencing factors, the risk of severe infections remained significantly elevated. The association with pneumococcal infections was particularly alarming: while these were virtually absent in patients with healthy spleens, they occurred frequently in the hyposplenism group, sometimes leading to intensive care or even death.
The authors hypothesize that chronic damage to the reticuloendothelial system due to immune complexes may contribute to the development of hyposplenism, with a potential vascular origin. The close association with APS suggests repeated microthromboses and micro-infarcts could lead to ongoing structural and functional destruction of splenic tissue.
Overall, these findings underscore the clinical relevance of spleen function in SLE. They advocate for early identification of affected individuals and consistent implementation of preventive measures.
Trefond L et al. RMD Open 2026; 12: e006355; doi: 10.1136/rmdopen-2025-006355
