The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
The spleen and sickle cell disease: the sick(led) spleen
Abstract
Summary: The spleen has a combined function of immune defence and quality control of senescent or altered red cells. It is the first organ injured in sickle cell anaemia (SCA) with evidence of hyposplenism present before 12 months in the majority of children. Repeated splenic vaso‐occlusion leads to fibrosis and progressive atrophy of the organ (autosplenectomy), which is generally complete by 5 years in SCA. The precise sequence of pathogenic events leading to hyposplenism is unknown. Splenic injury is generally silent and progressive. It can be clinically overt with acute splenic sequestration of red cells, an unpredictable and life‐threatening complication in infants. Splenomegaly, with or without hypersplenism, can also occur and can coexist with loss of function. Hyposplenism increases the susceptibility of SCA children to infection with encapsulated bacteria, which is notably reduced by penicillin prophylaxis and immunization. Whether hyposplenism indirectly increases the risk of vaso‐occlusion or other circulatory complications remains to be determined.
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Citations
Cites
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Prophylaxis with Oral Penicillin in Children with Sickle Cell Anemia
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Improved survival of children and adolescents with sickle cell disease
Quinn, C. T., Rogers, Z. R., McCavit, T. L., & Buchanan, G. R. (2010) · Blood · doi:10.1182/blood-2009-07-233700 · Cited by 907
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Wang, W. C., Ware, R. E., Miller, S. T., Iyer, R. V., Casella, J. F., Minniti, C. P., Rana, S., Thornburg, C. D., Rogers, Z. R., Kalpatthi, R. V., et al. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60355-3 · Cited by 803
Post-splenectomy and hyposplenic states
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A Hemodynamic Study of Pulmonary Hypertension in Sickle Cell Disease
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Functional Asplenia in Sickle-Cell Anemia
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Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy
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Cited by
Rees, D. C., Williams, T. N., & Gladwin, M. T. (2010) · The Lancet · doi:10.1016/s0140-6736(10)61029-x · Cited by 2,504
Self-citationPiel, F. B., Steinberg, M. H., & Rees, D. C. (2017) · New England Journal of Medicine · doi:10.1056/nejmra1510865 · Cited by 1,488
Self-citationKato, G. J., Piel, F. B., Reid, C. D., Gaston, M. H., Ohene-Frempong, K., Krishnamurti, L., Smith, W. R., Panepinto, J. A., Weatherall, D. J., Costa, F. F., et al. (2018) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2018.10 · Cited by 1,501
Piel, F. B., Steinberg, M., & Rees, D. C. (2016) · Spiral (Imperial College London) · doi:10.1056/nejmc1706325#sa6 · Cited by 659
Self-citationBrousse, V., El Hoss, S., Bouazza, N., Arnaud, C., Bernaudin, F., Pellegrino, B., Guitton, C., Odièvre‐Montanié, M., Mames, D., Brouzes, C., et al. (2018) · American Journal of Hematology · doi:10.1002/ajh.25260 · Cited by 25
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Metadata
- Authors
- Brousse, V., Buffet, P., & Rees, D.
- Venue
- British Journal of Haematology
- Publisher
- Wiley
- Published
- 2014-05-26
- Volume
- 166
- Issue
- 2
- Pages
- 165-176
- ISSN
- 0007-1048 (ISSN-L)
- 1365-2141
- OpenAlex
- W2070251534
- Cited by
- 294
- References
- 54
- FWCI
- 7.95
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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