title: Adverse events in cancer patients with sickle cell trait or disease: case reports.
abstract: OBJECTIVE
  Given the relatively high prevalence of sickle cell trait and disease among African Americans and established racial disparities in cancer outcomes, we reviewed the literature regarding adverse events in cancer patients with these hematologic genotypes. Erythrocyte sickling can result from extreme hypoxia and other physiologic stressors, as might occur during cancer therapy. Further, tumoral hypoxia, a poor prognostic and predictive factor, could lead to a cycle of local sickling and increased hypoxia.
  
  
  METHODS
  A search of PubMed produced 150 publications, most of which were excluded because of incidental relevance. Eleven case reports of patients diagnosed from 1993 to 2013 were reviewed.
  
  
  RESULTS
  Two reports of patients with sickle cell trait describe an abundance of sickled erythrocytes within tumors, and a third report describes sickling-related events requiring multiday hospitalization. Eight reports of patients with sickle cell disease delineated multiorgan failure, vaso-occlusive crises, and rapid renal deterioration. Hypothesized triggers are delayed clearance of anticancer agents attributable to baseline kidney damage, activation of vasoadherent neutrophils from treatment to counter chemotherapy-induced neutropenia, hypoxia from general anesthesia, and intratumoral hypoxia.
  
  
  CONCLUSIONS
  Clinical implications include pretreatment genotyping for prophylaxis, dose adjustment, and enhanced patient monitoring. With the current lack of high-quality evidence, however, the scope of poor outcomes remains unknown.
authors.affiliation: Department of Community Medicine, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
authors.forename: Helen
authors.initials: H
authors.lastname: Swede
authors.affiliation: Lea's Foundation Center for Hematologic Disorders, Division of Hematology/Oncology, Connecticut School of Medicine, Farmington, Connecticut, USA.
authors.forename: Biree
authors.initials: B
authors.lastname: Andemariam
authors.affiliation: Department of Community Medicine, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
authors.forename: David I
authors.initials: DI
authors.lastname: Gregorio
authors.affiliation: Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut, USA.
authors.forename: Beth A
authors.initials: BA
authors.lastname: Jones
authors.affiliation: Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California, USA.
authors.forename: Dejana
authors.initials: D
authors.lastname: Braithwaite
authors.affiliation: Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York, USA.
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Rohan
authors.affiliation: Department of Community Medicine, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
authors.forename: Richard G
authors.initials: RG
authors.lastname: Stevens
mesh_terms: D000293:Adolescent; D000755:Anemia, Sickle Cell / Q000139:chemically induced* / Q000188:drug therapy; D000970:Antineoplastic Agents / Q000009:adverse effects*; D000986:Antisickling Agents / Q000627:therapeutic use; D002648:Child; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000188:drug therapy; D012805:Sickle Cell Trait / Q000139:chemically induced* / Q000188:drug therapy
chemical_list: D000970:Antineoplastic Agents; D000986:Antisickling Agents