Infection in sickle cell disease: a review.

By C. Booth, B. Inusa, S. Obaro. 2010

329 citations recorded by the source corpus.

Infection is a significant contributor to morbidity and mortality in sickle cell disease (SCD). The sickle gene confers an increased susceptibility to infection, especially to certain bacterial pathogens, and at the same time infection provokes a cascade of SCD-specific pathophysiological changes. Historically, infection is a major cause of mortality in SCD, particularly in children, and it was implicated in 20-50% of deaths in prospective cohort studies over the last 20 years. Worldwide, it remains the leading cause of death, particularly in less developed nations. In developed countries, measures to prevent and effectively treat infection have made a substantial contribution to improvements in survival and quality of life, and are continually being developed and extended. However, progress continues to lag in less developed countries where the patterns of morbidity and mortality are less well defined and implementation of preventive care is poor. This review provides an overview of how SCD increases susceptibility to infections, the underlying mechanisms for susceptibility to specific pathogens, and how infection modifies the outcome of SCD. It also highlights the challenges in reducing the global burden of mortality in SCD.

Subfields: Genetics, Hematology

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1. D. Wagner
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Citations in the corpus

• Counterfactual Normalization: Proactively Addressing Dataset Shift and Improving Reliability Using Causal Mechanisms (2018, neutral): “We include seven conditions (such as chronic liver disease and sickle cell disease) C affecting INR that are risk factors for sepsis (Goyette et al., 2004; Booth et al., 2010).”
• Extracellular DNA traps promote thrombosis (2010, background): “RBC adhesion to NETs could also play a role in sickle-cell disease, where a lethal crisis is often precipitated by infection (38).”