RESUMO
OBJECTIVE: To evaluate for disparities in surgical care among US children with hepatoblastoma (HB) and hepatocellular carcinoma (HCC). STUDY DESIGN: In this retrospective National Cancer Database study (2004-2015), children aged <18 years with HB or HCC were included. Multivariable mixed-effects logistic regression was used to evaluate the association of sociodemographic factors (age, sex, race and ethnicity, insurance status, income, proximity to treating hospital) with the odds of undergoing surgical treatment after adjusting for disease-related factors (tumor size, metastasis, comorbidities) and hospital-level effects. Subgroup analyses by tumor histology were performed. RESULTS: A total of 811 children were included (HB: 80.9%; HCC: 19.1%), of which 610 (75.2%) underwent surgical treatment. Following adjustment, decreased odds of undergoing surgical treatment were associated with Black race (OR: 0.46 vs White, 95% CI [95% CI]: 0.26-0.80, P = .01), and having Medicaid (OR: 0.58 vs private, 95% CI: 0.38-0.88, P = .01) or no insurance (OR: 0.33 vs private, 95% CI: 0.13-0.80, P = .02). In children with HB, Black race was associated with decreased odds of undergoing surgical treatment (OR: 0.47 vs White, 95% CI: 0.25-0.89, P = .02). In children with HCC, Medicaid (OR: 0.10 vs private, 95% CI: 0.03-0.35, P < .001), or no insurance status (OR: 0.10 vs private, 95% CI: 0.01-0.83, P = .03) were associated with decreased odds of undergoing surgical treatment. Other than metastatic disease, no additional factors were associated with likelihood of surgical treatment in any group. CONCLUSIONS: Black race and having Medicaid or no insurance are independently associated with decreased odds of surgical treatment in children with HB and HCC, respectively. These children may be less likely to undergo curative surgery for their liver cancer.
Assuntos
Carcinoma Hepatocelular , Disparidades em Assistência à Saúde , Hepatoblastoma , Neoplasias Hepáticas , Humanos , Hepatoblastoma/cirurgia , Carcinoma Hepatocelular/cirurgia , Neoplasias Hepáticas/cirurgia , Neoplasias Hepáticas/patologia , Masculino , Feminino , Criança , Estudos Retrospectivos , Pré-Escolar , Lactente , Estados Unidos , Disparidades em Assistência à Saúde/estatística & dados numéricos , Disparidades em Assistência à Saúde/etnologia , Adolescente , Fatores Sociodemográficos , Medicaid/estatística & dados numéricos , Fatores Socioeconômicos , Bases de Dados FactuaisRESUMO
Biliary atresia (BA) is a neonatal T cell-mediated, inflammatory, sclerosing cholangiopathy. In the rhesus rotavirus (RRV)-induced neonatal mouse model of BA (murine BA), mice lacking B cells do not develop BA, and the lack of B cells is associated with loss of T-cell and macrophage activation. The aim of this study was to determine the mechanism of B cell-mediated immune activation (antigen presentation versus cytokine production) in murine BA. Normal neonatal B cells in the liver are predominantly at pro-B and pre-B cellular development. However, BA mice exhibit a significant increase in the number and activation status of mature liver B cells. Adoptively transferred B cells into RRV-infected, B cell-deficient mice were able to reinstate T-cell and macrophage infiltration and biliary injury. Nonetheless, neonatal liver B cells were incompetent at antigen presentation to T cells. Moreover, 3-83 immunoglobulin transgenic mice, in which B cells only present an irrelevant antigen, developed BA, indicating a B-cell antigen-independent mechanism. B cells from BA mice produced a variety of innate and adaptive immune cytokines associated with immune activation. In vitro trans-well studies revealed that BA B cells secreted cytokines that activated T cells based on increased expression of T-cell activation marker cluster of differentiation 69. Conclusion: Neonatal liver B cells are highly activated in murine BA and contribute to immune activation through production of numerous cytokines involved in innate and adaptive immunity; this work provides increased knowledge on the capacity of neonatal B cells to contribute to an inflammatory disease through cytokine-mediated mechanisms, and future studies should focus on targeting B cells as a therapeutic intervention in human BA.