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Hawai'i Journal of Health & Social Welfare logoLink to Hawai'i Journal of Health & Social Welfare
. 2025 Nov;84(11):261–268. doi: 10.62547/HYLO1221

Hepatocellular Carcinoma in Pacific Islanders vs. Whites

Shelby K Yee 1, Linda L Wong 1,2
PMCID: PMC12818485  PMID: 41567656

Abstract

Pacific Islanders (PI) have amongst the highest incidences of hepatocellular carcinoma (HCC), but large studies characterizing this population are limited. This study explores potential disparities in treatment and outcome by comparison of PIs and Whites with HCC treated at a single center. A prospectively collected database of 1608 patients diagnosed with HCC from 1993–2022 at the only liver disease/transplant center in Hawai‘i identified 252 PI and 338 White patients. Demographic, medical history, laboratory, tumor characteristics, treatment, survival data were collected. Chi-square, t-test, univariate logistic regression analyses and Kaplan-Meier survival analysis were conducted. Compared to Whites, PIs were younger, had lower educational attainment, and were more likely to be born outside the US. PIs also had a 4-fold higher likelihood of Hepatitis B (HBV) infection and higher rates of metabolic comorbidities. In contrast, Whites were 3 times more likely to have Hepatitis C infection, with higher likelihood of history of high-risk behavior (illicit drugs, incarceration, tattoos) and higher rates of presentation with cirrhosis. Of patients with screenable diseases, PIs were less than half as likely to be diagnosed through screening and presented with larger tumors and more advanced disease. Both groups were equally likely to receive treatment (including surgical treatment). Survival was similar between groups. Disparities in HCC screening and presentation seen in PIs may be attributed to high rates of occult HBV infection in this group. Initiatives to further improve outcomes for HCC in PIs should concentrate on expanding screening for chronic viral hepatitis and addressing barriers to care delivery following diagnosis.

Keywords: Hepatocellular carcinoma, HCC, viral hepatitis, HBV, HCV, Pacific Islander, disparities, screening

Introduction

Hepatocellular carcinoma (HCC) is the sixth most common cancer and sixth leading cause of cancer mortality in the US.1 Significant disparities in the incidence, prevalence, treatment, and outcomes of patients with hepatocellular carcinoma have been well documented in the literature, and have been attributed to factors including sex, socioeconomic status, and race/ethnicity.27

Pacific Islanders (PI) remain a population with one of the highest incidences of HCC. Previous studies have demonstrated a 2–8 times higher risk of the development of HCC and a 2–5 fold higher mortality rate in some PI groups compared to non-Hispanic Whites.810 The high burden of disease in this group has been primarily attributed to the high incidence of chronic hepatitis B (HBV).11 However, despite advances in the prevention and delay of HCC with the use of the HBV vaccine and antiviral agents, observable racial disparities continue to exist and thus may represent differences in access to general health care and prevention/screening, as well as variable utilization of treatment modalities.12,13 PIs are a high risk ethnic group with high morbidity and mortality from HCC, yet there is much left unknown about this population, as the majority of previous studies addressing racial disparities have aggregated PIs with Asians/Asian Americans, making it difficult to draw specific conclusions about PIs.

Hawai‘i is the state with the largest Native Hawaiian/Pacific Islander population and is the state with the third highest incidence of HCC in the US.8,14 With a target patient population that spans multiple generations, it is an ideal location to study the underlying risk factors and trends in the development of HCC in PIs. This study uses a well-annotated database of patients with liver cancer in Hawai‘i to compare HCC in PIs to non-Hispanic White patients.

Methods

This is a retrospective study of 1608 HCC cases referred over a 30-year period (1993–2022) to a group of physicians who were associated with the only liver transplant center and liver disease center in Hawai‘i. This center was also the tertiary referral center for the American territories of the Pacific Basin (including Samoa, Guam, and the Northern Mariana Islands) as well as small Pacific Island nations (Tonga, Palau, the Marshall Islands, and the Federated States of Micronesia). Patients also included foreign nationals from Asian countries who sought medical care in the US. This liver center and transplant center were initially affiliated with St. Francis Medical Center (later renamed Hawai‘i Medical Center-East) and Queen’s Medical Center after 2012. These centers cared for approximately 60–70% of the HCC cases in Hawai‘i and included all patients who were referred to these centers during this timeframe. This study was approved by the Institutional Review Board of The University of Hawai‘i at Mānoa and found to follow ethical regulations. All data was deidentified prior to use for the study and thus was exempt from requiring patient consent.

HCC was diagnosed histologically by percutaneous biopsy or at surgery. In the first decade and consistent with the previous United Network for Organ Sharing (UNOS) policy regarding transplant for HCC, patients without histologic confirmation were included if they had a history of chronic liver disease, a mass of at least 2 cm seen on 2 imaging studies (ultrasound, CT scan or MRI), and 1 of the following: (1) vascular blush evident on CT scan or MRI, (2) alpha fetoprotein (AFP) > 200 ng/mL, or (3) arteriogram confirming the tumor. More recently, the diagnosis of HCC was made with imaging alone if a contrast-enhanced study (dynamic CT or MRI) showed typical arterial enhancement with “washout” in the venous phase, as described by the American Association for the Study of Liver Disease (AASLD) guidelines.15,16

Data collected

Information on demographics, medical history, laboratory data, tumor characteristics, treatment, and survival was collected from clinical records. Demographic data included age, sex, birthplace, and the patient’s self-reported ethnicity. Ethnicity was categorized as “White”, “Asian” (East Asians, including Filipinos), “Pacific Islander” (including Native Hawaiians), “Mixed”, or “Other”. For this study, there were 252 patients identified who were of Pacific Islander ethnicity and 338 White patients.

Information was collected on the type of medical insurance and categorized into “Government” insurance (Medicare, Medicaid, Veterans Association), Private insurance, or uninsured. Years of formal education were recorded and categorized into “finished high school” (⩾ 12 years) versus not completing high school (< 12 years).

Medical history recorded included diabetes mellitus, hyperlipidemia, previous malignancy other than HCC, smoking (current and past use but exact date of cessation was not well documented ), and risk factors for HCC including viral hepatitis, significant alcohol use (defined as greater than 2 alcoholic beverages daily for ⩾ 10 years regardless of sex), and other chronic liver diseases. Measured height and weight were used to determine body mass index (BMI). Obesity was defined as BMI ⩾ 30.

The collected laboratory data included bilirubin, albumin, prothrombin time with International Normalized Ratio (INR), creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), platelet count, and AFP. Hepatitis B and C serologies were obtained if this information was not available from pre-existing records. For hepatitis B, it was noted whether patients had only hepatitis B core antibody positivity in the absence of hepatitis B surface antigen. Laboratory data used for the study were obtained within 2 weeks of an initial visit or at the time of the visit. Tumors were stratified to largest tumor diameter ⩾ 10 cm or < 10 cm. Normal AFP was defined as < 20 ng/mL.

Although the Liver Center recommends HCC surveillance in patients with cirrhosis with AFP and liver ultrasound every 6 months, there was no uniform screening protocol used in the cohort. Referring physicians used a combination of AFP and/or imaging (ultrasound, CT scan or MRI) at variable intervals. HCC was deemed to be found on “surveillance” if the patient had a previous imaging study from 3 to 12 months prior to the current study. HCC not found on screening was either found with symptoms (pain, abdominal mass, weight loss, jaundice) or incidentally with imaging done for unrelated reasons.

Treatments

Treatments in the overall cohort included liver resection, transplantation, locoregional therapies (radiofrequency ablation, cryosurgery, percutaneous ethanol injection, transarterial chemoembolization [TACE] or Yttrium90 radioembolization) and systemic therapies. Liver resection was considered in Child’s A patients and early Child’s B patients (Child-Turcotte-Pugh score of 7, without any evidence of ascites or encephalopathy). Liver transplantation was considered in patients with unresectable HCC but who met Milan criteria (single tumor ⩽ 5 cm or 2 to 3 tumors, each ⩽ 3 cm). All liver resections and transplantations were performed by a single surgical group practice.

Statistical Analysis

All analyses were performed using Excel version Office 2021 (Microsoft Corporation, Redmond, WA) and SPSS statistical software version 27 (IBM Corp., Armonk, NY). The cohort was divided into 2 groups of patients for comparison: Pacific Islanders (PIs) and Whites.

Numerical variables were compared using the unpaired t-test, and categorical variables were analyzed using chisquare analysis. Odds-ratios (OR) with 95% confidence intervals (CI) were calculated using univariate and multivariate logistic regression. Variables significant at P=.10 in univariate analyses were included in the multivariate models along with age and sex. Variables significant at P<.05 were considered significant in the multivariate model. Overall survival analysis was conducted using Kaplan-Meier analysis, and Cox regression was utilized for analysis of 1-, 3-, and 5- year survival analyses to evaluate potential influential factors.

Results

Patient demographics and comorbidities

PIs were younger at presentation compared to Whites, with a mean age of 59.8 years compared to 63.2 years (P<.001). Both groups exhibited a male predominance with 79.4% and 82.2% of patients being male in the PI group and White group respectively. PI patients were nearly 10 times as likely to be born outside of the US compared to Whites (OR 9.65, 95% CI 1.33–69.90), and had a lower level of educational attainment, with 72.4% receiving a high school level of education compared to 89.2% of White patients (OR 0.32, 95% CI 0.20–0.52). There was no statistically significant difference between groups with regards to government insurance or uninsured status (Table 1).

Table 1.

Demographics of Pacific Islander and White Hepatocellular Carcinoma Patients from a Hawai‘i Tertiary Referral Center, 1993–2022

Pacific Islander No. (%) White No. (%) P-value/OR, 95% CI
Age in years [mean, (SD)] 59.8 (SD 11.0) 63.2 (SD 8.73) .001
Sex: Male 195 (79.4%) 278 (82.2%) 0.83, 0.55–1.26
Government insurance or uninsured 165 (71.4%) 209 (60.4%) 1.24, 0.88–1.75
Completed high school 138 (72.4%) 255 (89.2%) 0.32, 0.20–0.52
Born outside of the US 88 (37.6%) 19 (5.9%) 9.65, 1.33–69.90

P-values derived from t-test

With regard to comorbidities and risk factors (Table 2), PIs had significantly higher rates of infection with HBV, with 30.7% of patients affected compared to 6.5% of White patients (OR 3.77, 95% CI 2.55–5.55). PIs were less likely to have a history of engaging in high-risk social behaviors that included illicit drug use, incarceration, and having tattoos (OR 0.52, 95% CI 0.37–0.73); and were found to have lower rates of infection with HCV, with 40.9% of patients affected compared to 66.8% of White patients (OR 0.34, 95% CI 0.24–0.48). There were no significant differences between groups with regard to significant alcohol use or smoking history. Of note, PI patients were found to be half as likely to have a history of/concomitant non-HCC malignancy compared to the White group (OR 0.47, 95% CI 0.28–0.80). While there was no significant difference in the rates of NASH/NAFLD between groups, PIs were disproportionately affected by metabolic comorbidities compared to Whites and were about twice as likely to suffer from diabetes mellitus (OR 1.81, 95% CI 1.27–2.59), hyperlipidemia (OR 1.74, 95% CI 1.19–2.55), hypertension (OR 2.00, 95% CI 1.41–2.84), and obesity (OR 2.90, 95% CI 2.02–4.16).

Table 2.

Risk Factors and Comorbidities of Pacific Islander and White Hepatocellular Carcinoma Patients from a Hawai‘i Tertiary Referral Center, 1993–2022

Pacific Islander White OR, 95% CI
Hepatitis B 75 (30.7%) 22 (6.5%) 3.77, 2.55–5.55
Hepatitis C 102 (40.9%) 225 (66.8%) 0.34, 0.24–0.48
NASH/NAFLD 27 (12.0%) 29 (8.6%) 1.44, 0.841–2.47
Other cancer 20 (8.3%) 55 (16.3%) 0.47, 0.28–0.80
Diabetes mellitus 91 (37.3%) 83 (24.7%) 1.81, 1.27–2.59
Hypertension 136 (61.8%) 139 (44.8%) 2.00, 1.41–2.84
Hyperlipidemia 70 (30.3%) 67 (20.0%) 1.74, 1.19–2.55
BMI ≥ 30 112 (50.4%) 83 (25.9%) 2.90, 2.02–4.16
High risk social behavior (illicit drug use, incarceration, tattoos) 80 (32.1%) 161 (47.6%) 0.52, 0.37–0.73
Smoking (current) 46 (28.4%) 65 (29.1%) 0.96, 0.62–1.51
Smoking history 168 (70.0%) 243 (72.8%) 0.88, 0.61–1.26
Alcohol use 145 (59.4%) 194 (57.4%) 1.08, 0.78–1.51

NASH nonalcoholic steatohepatitis, NAFLD nonalcohol fatty liver disease

Tumor characteristics/laboratory studies

PIs presented with larger tumors (Table 3); the mean size of primary tumor was 6.69 cm in the PI group compared to 5.05 cm in Whites, and 25.4% of PI patients presented with a tumor ⩾ 10 cm compared to 13.9% in Whites (OR 2.10, 95% CI 1.38–3.19). Additionally, PI patients were more likely to present with more advanced disease, with 31.7% of patients presenting with stage III/IV disease compared to 24.0% in the Whites (OR 1.53, 95% CI 1.06–2.20). There were no significant differences between groups in the percentage of patients presenting with multiple tumors or bilateral tumors. Despite presenting with larger primary tumors and later stage disease, PI patients were less likely to have cirrhosis (OR 0.64, 95% CI 0.43–0.95), ascites (OR 0.62, 0.41–0.94), and encephalopathy (OR 0.46, 95% CI 0.28–0.74).

Table 3.

Tumor Characteristics of Pacific Islander and White Hepatocellular Carcinoma Patients from a Hawai‘i Tertiary Referral Center, 1993–2022

Pacific Islander White P-value/OR, 95% CI
Mean size of primary tumor (cm) 6.69 (SD 4.67)
*8 diffuse
5.05 (SD 4.22)
*9 diffuse
.001
Size ≥ 10cm 56 (25.4%) 38 (13.9%) 2.10, 1.38–3.19
Multiple tumors 79 (33.0%) 106 (32.1%) 1.04, 0.73–1.49
Bilateral tumors 38 (17.1%) 53 (17.7%) 0.96, 0.61–1.52
Met Milan Criteria 98 (41.0%) 156 (46.3%) 0.81, 0.58–1.12
Cirrhosis 180 (74.6%) 276 (82.1%) 0.64, 0.43–0.95
Ascites 16 (18.7%) 44 (27.0%) 0.62, 0.41–0.94
Encephalopathy 26 (10.8%) 70 (20.8%) 0.46, 0.28–0.74
AJCC Stage 1 140 (55.6%) 197 (58.3%)
2 32 (12.7%) 60 (17.8%)
3 61 (24.2%) 75 (22.2%)
4 19 (7.5%) 6 (1.8%)
Advanced disease (stage III/IV) 80 (31.7%) 81 (24.0%) 1.53, 1.06–2.20

AJCC American Joint Committee on Cancer

P-values derived from t-test

In terms of laboratory studies (Table 4), PI patients had significantly higher bilirubin (2.23 compared to 1.59 mg/dL in Whites, P=.02) and higher creatinine (1.16 compared to 0.94 mg/dL in Whites, P<.001). PI patients also had a significantly higher mean Model for End-stage Liver Disease (MELD) score compared to White patients; 11.8 and 10.7 respectively (P=.009). There was no difference in AFP levels between groups, both when comparing median AFP levels or percentage of patients with abnormal AFP levels (>20 ng/mL).

Table 4.

Laboratory Studies of Pacific Islander and White Hepatocellular Carcinoma Patients from a Hawai‘i Tertiary Referral Center, 1993–2022

Pacific Islander White P-value/OR, 95% CI
Mean Albumin (mg/dL) 3.42 (SD 0.72) 3.53 (SD 0.69) .08
Mean Bilirubin (mg/dL) 2.23 (SD 3.30) 1.59 (SD 3.02) .02
Mean Creatinine (mg/dL) 1.16 (SD 0.56) 0.936 (SD 0.66) .001
Mean Platelets (x103/µl) 180 (SD 98.1) 150 (SD 91.4) .001
Mean INR 1.20 (SD 0.27) 1.22 (SD 0.24) .23
Median AFP (ng/mL) 34.8 28.0 .67
Normal AFP (< 20 ng/mL) 100 (39.9%) 148 (43.7%) 0.86, 0.61–1.19
Mean MELD score 11.8 (SD 4.81) 10.7 (SD 4.68) .009

INR international normalized ratio, AFP alpha fetoprotein, MELD Model for End-stage Liver Disease

P-values derived from t-test

Diagnosis, treatments, and outcomes

In terms of diagnosis of disease, there was no difference in the percentage of patients that were symptomatic at diagnosis between groups. However, of patients with screenable conditions (cirrhosis, chronic viral hepatitis), patients in the PI group were found to be less likely to have been diagnosed on screening compared to White patients (OR 0.45, 95% CI 0.30–0.68) (Table 5). When evaluating screening rates by viral etiology, patients with HBV-associated HCC (HBV-HCC) were found to be screened at significantly lower rates than patients with HCV-associated HCC (HCV-HCC) (OR 0.46, 95% CI 0.29–0.73) (data not shown).

Table 5.

Diagnosis, Treatment, and Outcomes of Pacific Islander and White Hepatocellular Carcinoma Patients from a Hawai‘i Tertiary Referral Center, 1993–2022

Pacific Islander White P-value/OR, 95% CI
Symptomatic at diagnosis 95 (38.6%) 112 (33.7%) 1.24, 0.88–1.74
Diagnosis on screening 43 (22.6%) 107 (39.5%) 0.45, 0.30–0.68
Received treatment 177 (76.0%) 243 (78.6%) 0.86, 0.57–1.29
Surgical intervention (transplant or resection) 48 (19.0%) 73 (21.6%) 0.85, 0.57–1.28
Transplantation 10 (9.6%) 25 (16.1%) 0.56, 0.26–1.22
Liver Resection 37 (14.8%) 41 (12.3%) 1.24, 0.77–2.00
       
Loss to follow up 14 (5.56%) 22 (6.51%) 0.85, 0.42–1.69
1-year survival 145 (62.0%) 207 (66.1%) 0.84, 0.59–1.19
3-year survival 92 (38.4%) 151 (45.2%) 0.76, 0.53–1.08
5-year survival 66 (30.7%) 105 (37.8%) 0.73, 0.50–1.06
Median survival (months) 20.0 29.2 .79

P-values derived from t-test

Patients in the PI and White groups were equally likely to receive any type of treatment (OR 0.86, 95% CI 0.57–1.29), and equally likely to receive curative surgical treatment with either liver transplantation or resection (OR 0.854, 95% CI 0.57–1.28). There was no difference in the proportion of patients who met Milan criteria between groups (Table 3), and 10 PI patients (9.6%) underwent transplantation compared to 25 (16.1%) of White patients (OR 0.56, 95% CI 0.26–1.22). Thirty-seven (14.8%) PI patients underwent liver resection compared to 41 (12.3%) Whites (OR 1.24, 95% CI 0.77–2.00) (Table 5).

With regard to outcomes, 1-, 3-, and 5-year survival were similar between groups, and there was no difference in overall survival with Kaplan Meier analysis (Figure 1). Furthermore, there was no difference in the rates of loss to follow up between the PI group and the White group (OR 0.84, 95% CI 0.42–1.69) (Table 5).

Figure 1.

Figure 1.

Kaplan Meier Survival Curve Comparing Pacific Islanders (PI) to White Patients with HCC from a Hawai‘i Tertiary Referral Center, 1993–2022

Discussion

This study identified clear disparities in presentation and diagnosis between PIs and Whites. PIs presented at younger ages with larger tumors and more advanced disease compared to Whites. Both groups exhibited unique risk factor profiles which illustrate the heterogeneity of HCC and how pathogenesis may potentially differ.

Viral hepatitis was a significant risk factor for development of disease in both PIs and Whites, but each group had a propensity for a particular type of viral hepatitis, likely representing differences in exposures. In the PIs, chronic infection with HBV is the primary risk factor for HCC. In the US, Asian Americans and PIs account for more than 50% of the chronic HBV cases, with most of these cases attributed to foreign-born individuals, a pattern replicated in the current study.1719 Despite the introduction of universal infant HBV vaccination in many US-affiliated Pacific Island territories, limited availability and logistic difficulties of vaccine delivery within 24 hours of birth (eg, storage/transportation, reduced antenatal screening, attendance of medical personnel at birth, added cost) may contribute to a higher prevalence of HBV in non-US born PI patients.20,21 Antiviral agents have reduced the risk of cirrhosis and ultimately HCC and have been available in developed countries for many years.2123 However, limited availability of antivirals in resource-constrained, high endemicity areas has limited their routine usage. Together, these factors may account for observed differences in HBV burden and subsequently, the higher prevalence of HBV-HCC in PIs.

In White patients, HCV infection was the most important risk factor, with this cohort exhibiting a 3-fold higher risk compared to PIs. This pattern was reflected nationally, with the CDC reporting that non-Hispanic Whites had the second highest chronic case rates of HCV over the last 5 years, compared to Asian/PIs with the lowest chronic case rates; although rates in both groups have increased over this time.24 The current study suggests that this difference in prevalence of HCV between groups may be explained by different social behavioral patterns, with White patients found to have a 2 times higher likelihood of previous engagement in high-risk social behaviors (illicit and intravenous drug usage, history of incarceration, and having tattoos).

The pattern of presentation observed in the current study with PIs presenting at younger ages with larger tumors and later stage disease compared to Whites, may be partly attributed to the differences in viral etiology. Previous studies have similarly demonstrated that HBV-HCC is associated with younger ages and larger tumor size compared to HCV-HCC.25,26 The rapid progression of HBV-HCC compared to HCV-HCC may be explained in part by the hepatocarcinogenesis of each type of viral hepatitis. HBV induces carcinogenesis through both direct and indirect mechanisms—by directly integrating into host DNA; and indirectly by enhancing the infiltrative capabilities, inhibiting tumor cell apoptosis, and promoting higher rates of growth.27 These mechanisms are responsible for the rapid progression of malignancy oftentimes without cirrhosis. These patients generally present at younger ages and in the absence of complications of chronic liver disease, and as a result, patients with HBV-HCC may be less likely to undergo screening, a trend observed in the current study. In contrast, HCV induces carcinogenesis indirectly—intra-cellular HCV replication and the subsequent innate immune response creates a chronic inflammatory microenvironment that progresses to hepatic fibrosis, dysplastic nodular changes, and eventual malignant transformation.28 The pathogenesis of disease in HCV-HCC is longer, with cirrhosis developing over a course of nearly 20–30 years and the subsequent rate of development of HCC in these cirrhotic patients nearing 1–4% annually.29

While some of these differences in presentation between groups can be explained by viral mechanisms, another important factor captured in the current study is the lower rate of HCC surveillance in PIs compared to Whites. The reasons for the disparity in screening rates is multifactorial. As discussed above, viral etiology may play a significant role, with lower screening rates observed in HBV-HCC compared to screening rates in cirrhotic patients with HCV-HCC. Financial status, medical insurance, health literacy and language barriers are known factors impacting access to care.13,30,31 Additionally, differences in care-seeking behavior related to cultural beliefs/practices and fear of stigmatization may be barriers to seeking care. 32,33

The current study on HCC in PIs is limited in that it is a single center study done over 3 decades and changes in management may have occurred over this period. Furthermore, although the center cared for the majority of cases of HCC in Hawai‘i in addition to all cases referred there, and thus included cases across the spectrum of disease, it is possible that referral bias may exist, especially for those with advanced disease. Improvements in imaging and referral patterns may likely have affected earlier detection, surveillance, and treatment in the more recent years. Additionally the PI group in itself is heterogenous in origin, and analysis as a single group may contribute to confounding bias.

Conclusion

Despite the limitations, this study has granular detail about liver disease and socioeconomic factors in a large series of PIs, a population which suffers from a high burden of HCC but is often not represented in large administrative databases. This study identified disparities in disease presentation in PIs, which appear to be driven by higher rates of occult chronic HBV infection in this population. This study also demonstrated that if PIs have early HCC, they can have similar opportunities for curative therapies and survival. However, poor outcomes may be driven by late presentation of HCC. Future efforts should address barriers to prompt detection. This may include culturally sensitive outreach events to provide resources/education and discrete screening for viral hepatitis in high-risk communities. Efforts should also be made to educate providers on the need for screening for viral hepatitis in PI patients, treatment and prompt referral to specialists as needed. This would promote early detection of HCC and access to curative therapy, breaking the pattern of high morbidity and mortality from HCC in this population.

Glossary

Abbreviations

AASLD

American Association for the Study of Liver Disease

AFP

alpha fetoprotein

ALT

alanine aminotransferase

AST

aspartate aminotransferase

BMI

body mass index

HBV

hepatitis b virus

HBV-HCC

hepatitis b virus-associated hepatocellular carcinoma

HCC

hepatocellular carcinoma

HCV

hepatitis c virus

HCV-HCC

hepatitis c virus-associated hepatocellular carcinoma

INR

international normalized ratio

NAFLD

nonalcoholic fatty liver disease

NASH

nonalcoholic steatohepatitis

PI

Pacific Islander

TACE

transarterial chemoembolization

UNOS

United Network for Organ Sharing

Conflict of Interest and Disclosures

Dr. Linda L. Wong has served as a speaker for AstraZeneca.

References

  • 1.Liver Cancer Causes, Risk Factors, and Prevention. National Cancer Institute, NIH; 2022. May 18, Accessed April 8, 2023. https://www.cancer.gov/types/liver/what-is-liver-cancer/causes-risk-factors. [Google Scholar]
  • 2.Wong LL, Hernandez B, Kwee S, Albright C, Okimoto G, Tsai N. Healthcare disparities in Asians and Pacific Islanders with hepatocellular cancer. Am J Surg. 2012;203:726–732. doi: 10.1016/j.amjsurg.2011.06.055. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Yang B, Liu JB, So SK, et al. Disparities in hepatocellular carcinoma incidence by race/ethnicity and geographic area in California: Implications for prevention. Cancer. 2018;124(17):3551–3559. doi: 10.1002/cncr.31598. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Danos D, Leonardi C, Gilliland A, et al. Increased risk of hepatocellular carcinoma associated with neighborhood concentrated disadvantage. Front Oncol. 2018;8:375. doi: 10.3389/fonc.2018.00375. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Shebl FM, Capo-Ramos DE, Graubard BI, McGlynn KA, Altekruse SF. Socioeconomic status and hepatocellular carcinoma in the United States. Cancer Epidemiol Biomarkers Prev. 2012;21(8):1330–1335. doi: 10.1158/1055-9965.EPI-12-0124. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Thylur RP, Roy SK, Shrivastava A, LaVeist TA, Shankar S, Srivastava RK. Assessment of risk factors, and racial and ethnic differences in hepatocellular carcinoma. JGH Open. 2020;4(3):351–359. doi: 10.1002/jgh3.12336. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Native Hawaiian/Other Pacific Islander - The Office of Minority Health . US Department of Health and Human Services, HHS; 2019. Accessed April 8, 2023. https://minorityhealth.hhs.gov/omh/browse.aspx?lvl=3&lvlid=65. [Google Scholar]
  • 8.Miller BA, Chu KC, Hankey BF, Ries LA. Cancer incidence and mortality patterns among specific Asian and Pacific Islander populations in the U.S. Cancer Causes Control. 2008;19(3):227–256. doi: 10.1007/s10552-007-9088-3. [published correction appears in Cancer Causes Control. 2008;19(3):257–8] [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.McGlynn KA, Petrick JL, El-Serag HB. Epidemiology of hepatocellular carcinoma. Hepatology. 2021;73(Suppl 1):4–13. doi: 10.1002/hep.31288. Suppl 1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Chang ET, Keegan TH, Gomez SL, et al. The burden of liver cancer in Asians and Pacific Islanders in the Greater San Francisco Bay Area, 1990 through 2004. Cancer. 2007;109(10):2100–2108. doi: 10.1002/cncr.22642. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Harlan LC, Parsons HM, Wiggins CL, Stevens JL, Patt YZ. Treatment of hepatocellular carcinoma in the community: disparities in standard therapy. Liver Cancer. 2015;4(1):70–83. doi: 10.1159/000367729. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Mathur AK, Osborne NH, Lynch RJ, Ghaferi AA, Dimick JB, Sonnenday CJ. Racial/ethnic disparities in access to care and survival for patients with early-stage hepatocellular carcinoma. Arch Surg. 2010;145(12):1158–1163. doi: 10.1001/archsurg.2010.272. [DOI] [PubMed] [Google Scholar]
  • 13.State Cancer Profiles > Incidence Rates Table. National Cancer Institute, NIH; 2017. Accessed April 8, 2023. https://statecancerprofiles.cancer.gov/incidencerates/index.php?stateFIPS=00&areatype=state&cancer=035&race=00&sex=0&age=001&stage=999&year=0&type=incd&sortVariableName=rate&sortOrder=default&output=0#results. [Google Scholar]
  • 14.Heimbach JK, Kulik LM, Finn RS, et al. AASLD guidelines for the treatment of hepatocellular carcinoma. Hepatology. 2018;67(1):358–380. doi: 10.1002/hep.29086. [DOI] [PubMed] [Google Scholar]
  • 15.Roberts LR, Sirlin CB, Zaiem F, et al. Imaging for the diagnosis of hepatocellular carcinoma: A systematic review and meta-analysis. Hepatology. 2018;67(1):401–421. doi: 10.1002/hep.29487. [DOI] [PubMed] [Google Scholar]
  • 16.People Born Outside of the United States and Viral Hepatitis. US Centers for Disease Control and Prevention, CDC; 2020. Sep 24, Accessed April 8, 2023. https://www.cdc.gov/hepatitis/populations/Born-Outside-United-States.htm. [Google Scholar]
  • 17.Hepatitis B. National Institute of Diabetes and Digestive and Kidney Diseases. NIH; 2019. Jan 17, Accessed April 8, 2023. https://www.niddk.nih.gov/health-information/liver-disease/viral-hepatitis/hepatitis-b. [Google Scholar]
  • 18.Hawai‘i Hepatitis B and Liver Cancer Incidence and Mortality Report. Hawai‘i State Department of Health, Harm Reduction Services Branch and Office of Planning, Policy, and Program Development, Hawai‘i DOH; 2023. Accessed April 8, 2023. https://health.hawaii.gov/harmreduction/files/2023/02/Hawaii-Hep-B-and-Liver-Cancer-Mortality-Report-FINAL-1-31-2023.pdf. [Google Scholar]
  • 19.Lasitani S, Hattori C, Elisara T, Araneta MR. Assessing hepatitis b knowledge among Native Hawaiians and Pacific Islanders in San Diego. J Immigr Minor Health. 2021;23(6):1193–1197. doi: 10.1007/s10903-021-01236-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Thursz M, Njie R, Lemoine M. Hepatitis: Global eradication of hepatitis B—feasible or fallacy? Nat Rev Gastroenterol Hepatol. 2012;9(9):492–494. doi: 10.1038/nrgastro.2012.155. [DOI] [PubMed] [Google Scholar]
  • 21.Papatheodoridis GV, Lampertico P, Manolakopoulos S, Lok A. Incidence of hepatocellular carcinoma in chronic hepatitis B patients receiving nucleos(t)ide therapy: a systematic review. J Hepatol. 2010;53(2):348–356. doi: 10.1016/j.jhep.2010.02.035. [DOI] [PubMed] [Google Scholar]
  • 22.Wong RJ, Jain MK, Therapondos G, Niu B, Kshirsagar O, Thamer M. Antiviral therapy reduces risk of cirrhosis in noncirrhotic HBV Patients among 4 urban safety-net health systems. Am J Gastroenterol. 2021;116(7):1465–1475. doi: 10.14309/ajg.0000000000001195. [DOI] [PubMed] [Google Scholar]
  • 23.2005–2020 Rates of Acute Hepatitis C Cases by Ethnicity. US Centers for Disease Control and Prevention, CDC; 2022. Oct 10, Accessed April 8, 2023. https://www.cdc.gov/hepatitis/statistics/2020surveillance/hepatitis-c/figure-3.6.htm. [Google Scholar]
  • 24.Dohmen K, Shigematsu H, Irie K, Ishibashi H. Comparison of the clinical characteristics among hepatocellular carcinoma of hepatitis B, hepatitis C and non-B non-C patients. Hepatogastroenterology. 2003;50(54):2022–2027. [PubMed] [Google Scholar]
  • 25.Chen CH, Huang GT, Yang PM, et al. Hepatitis B- and C-related hepatocellular carcinomas yield different clinical features and prognosis. Eur J Cancer. 2006;42(15):2524–2529. doi: 10.1016/j.ejca.2006.06.007. [DOI] [PubMed] [Google Scholar]
  • 26.Jiang Y, Han Q, Zhao H, Zhang J. The mechanisms of HBV-induced hepatocellular carcinoma. J Hepatocell Carcinoma. 2021;8:435–450. doi: 10.2147/JHC.S307962. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Heredia-Torres TG, Rincón-Sánchez AR, Lozano-Sepúlveda SA, et al. Unraveling the molecular mechanisms involved in HCV-induced carcinogenesis. Viruses. 2022;14(12):2762. doi: 10.3390/v14122762. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Axley P, Ahmed Z, Ravi S, Singal AK. Hepatitis C virus and hepatocellular carcinoma: a narrative review. J Clin Transl Hepatol. 2018;6(1):79–84. doi: 10.14218/JCTH.2017.00067. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Health Care Services; Committee on Health Care Utilization and Adults with Disabilities . Health-Care Utilization as a Proxy in Disability Determination. National Academies Press; 2018. Accessed April 8, 2023. https://www.ncbi.nlm.nih.gov/books/NBK500102/ [PubMed] [Google Scholar]
  • 30.Floyd A, Sakellariou D. Healthcare access for refugee women with limited literacy: layers of disadvantage. Int J Equity Health. 2017;16(1):195. doi: 10.1186/s12939-017-0694-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Morisako AK, Tauali’i M, Ambrose AJH, Withy K. Beyond the ability to pay: The health status of Native Hawaiians and Other Pacific Islanders in relationship to health insurance. Hawaii J Med Public Health. 2017;76(3 Suppl 1):36–41. [PMC free article] [PubMed] [Google Scholar]

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