primary hepatocellular carcinoma in aboriginal australians

Primary hepatocellular carcinoma in Aboriginal Australians Xinan Wan and John D. Mathews Menzies School of Health Research, Darwin

Abstract: We identified incident cases of primary hepatocellular carcinoma (PHC) in the Northern Territory from 1980 to 1989: there were 18 Aboriginal and six non-Aboriginal cases, yielding incidence rates of 5.2 per 100 000 (Aboriginal) and 0.5 per 100 000 (non-Aboriginal) with a relative risk of 10.4 (95 per cent confidence interval (CI) 4.0 to 26.6). The carcinoma was more Frequent in males (2.3 per 100 000) than in Females (0.7 per 100 000), with a relative risk of3.4 (GI 1.3 to 9.3). Incidence increased with age; the trend was statistically significant in Aborigines (f, = 4.7, P < 0.05) but not in non- Aborigines (Xy1 = 3.4, P > 0.05). Hepatitis B virus (HBV) serology was available For 11 Aboriginal and four non-Abonginal cases; seven of the Aboriginal cases and two of the non-Aboriginal cases were positive For hepatitis B surface antigen (HBsAg). The prevalence of HBsAg in Aboriginal patients with the carcinoma (63.6 per cent) was much higher than that (13.1 per cent) in Aborigines surveyed from communities in the Northern Territory k2, = 21.7, P < 0.001). Our results show that the age-specific incidence of PHC in Aborigines in the Northern Territory (30.9 For ages 40 and over) is comparable to that in high-incidence countries such as China (36.9 For ages 40 and over), and that hepatitis B is of major aetiological importance in the Aboriginal population. This underlines the importance of universal immunisation for prevention of HBV infection and for long-term prevention of PHC. (AustJ Public Health 1994; 18: 286-90)

ince hepatitis B antigen in serum from an Abor- iginal Australian was first described by S Blumberg and colleagues in 1965,' the

increased prevalence of hepatitis B virus (HBV) infection in Aborigines has been well documented.'.Y Camage rates of hepatitis B surface antigen (HBsAg) for Aborigines can be as high as 26 per cent,Y which is much higher than the 0.05 per cent in blood don01-s.~

The HBV carrier state is a predictor of liver cirrhosis and primary hepatocellular carcinoma (PHC).5.6 The prospective study of Beasley et al. in Taiwan showed that the death rate from PHC was over 200 times higher in HBsAg carriers than in HBsAg noncarriers, suggesting a strong causal association between HBV infection and PHC6

Although PHC is rare in Australia (less than five incident cases per 100 000 per annum)' it would be expected to be an important cause of premature death in minority groups with high HBsAg camer rates. However, for Aboriginal Australians, there is little information on PHC and on the role of HBV infection in its aetiology.' This study was designed to examine the incidence of PHC and the relationship of HBV to PHC in the Aboriginal Australians in the Northern Territory.

Data and methods Ethical approval This study was considered and approved by the Joint Institutional Ethics Committee of the Royal Darwin Hospital and the Menzies School of Health Research and the Alice Springs Institutional Ethics Com- mittee; these committees have Aboriginal represen- tation and work to the National Health and Medical Research Council guidelines.

Comspondence to Dr Xinan Wan. Menzies School of Health Research. PO Box 41096, Casuarina, NT 0811. Fax (089) 27 5187.

Ascertainment Death certificates and hospital discharge diagnoses were used to identify incident cases of PHC in the Northern Territory diagnosed in the period from January 1980 to December 1989. Registration numbers for deaths due to PHC for the whole Northern Territory were abstracted from the Australian Bureau of Statistics and sent to the Department of Births, Deaths and Mamages of the Northern Terri- tory. With permission from the Deputy Registrar, copies of death certificates were obtamed where the underlying cause of death was classified as PHC (ICD9 1 55.08).

To ensure that no case was missed, we examined a list of all cases where PHC was the discharge diagnosis in the five Northern Territory hospitals. This list was checked with death registers obtained from the Department to identify all PHC cases and dupli- cate ascertainments.

All available medical records of subjects with a diagnosis of PHC in the 1980s were examined to assess hepatitis B serology, diagnostic criteria and demographic information.

Case definition For this study, a confirmed PHC case was defined as an individual with PHC proven by at least one of the following: autopsy, liver biopsy, laparotomy, com- puted tomography scan, ultrasound or alpha- fetoprotein higher than 20 pg/L (adult reference range < 12 pg/L).

Copies of death registration for 20 putative PHC cases were obtained from the Department of Births, Deaths and Marriages; 24 cases were identified from hospital discharge diagnoses. Of these 44, 11 cases were common to both lists. Of the 33 possible PHC cases, medical records were found for 30 cases, of which nine were excluded for the following reasons: one was a resident of South Australia; one had cholangiocarcinoma and seven had metastatic carcinoma of the liver.

286 AUSTRALIAN JOURNAL OF PUBLIC HEALTH 1994 v a . 18 NO. 3

ABORIGINAL HEPATOCELLULAR CARCINOMA

Thus, 2 1 cases satisfied the ascertainment criteria. Of the 18 cases identified from the Department for whom medical records could be found, all were confirmed as PHC cases. In contrast, only fifteen of 23 cases (65.2 per cent) ascertained through hospital discharge diagnoses were confirmed as PHC cases by medical record review (records were missing for one case).

On the basis of these probabilities, the three ascertained cases for whom medical records could not be found were also regarded as confirmed cases for the calculation of incidence rates. Two of these cases (one Aborigine and one non-Aborigine) were identified from Departmental notification, and one case (Aborigine) from a hospital discharge diagnosis.

Ethnic classifcation For this study, we defined three ethnic groupings based on previous reports of PHC occurrence in different population^:?.^ 1. Expected low incidence: persons with ethnic ori-

gins in the United Kingdom, Ireland or northern Europe;

2. Aboriginal Australians; 3. High-risk population: persons with origins in Asia,

the Pacific, the Middle East and southern Europe. Ethnicity is not recorded on death certificates.

Nevertheless, Aboriginal descent was defined on the basis of tribal marriage, place of usual residence and an Aboriginal name, and by reference to hospital medical records. For non-Aboriginal patients, ethnicity was decided by reference to the country or place of birth and the names of the patient and relatives.

Calculation of incidence rates f i pn'mav hepatocellular carcirunna The Northern Territory population estimates from the 1986 census were used to calculate race-, sex- and age-specific incidence rates.g Population denominators according to birthplace obtained from the Australia Bureau of Statistics were used to estimate the incidence for low- and high-risk groups. All incidence rates were expressed per 100 000 population for Aborigines and non-Aborigines.

Relative risk was estimated as the ratio of the incidence rates. l o All statistical analyses were performed using the GLIM packages developed by Royal Stat- istical Society, United Kingdom." Interactive effects of disease and age were analysed by log-linear models; binomial models were used to evaluate effects of race and gender on the incidence and to calculate confidence intervals.

Hepatitis B carriage rates Since 1971, there have been several studies of HBV infection in Northern Territory Aboriginal c~rnmunities;"-'~ these results were used to calculate reference camer rates of HBsAg in the adult Abor- iginal population for comparison with carriage rates in Aboriginal patients with PHC.

Comparative rates from Victoria and the People's Republic of China The incidence rates for PHC (ICD9 155.0) for 1983 to 1989, stratified by country of birth, age and sex, were obtained from the Victorian Cancer Registry for comparative purposes (H. Farrugia, personal communication); these data were used as a standard

Table 1 : Risk foctors for primary hepatocellular carcinoma (PHC) in the Northern Territory, 1980 to 1989

Number of cases Incidence per 95% confidence intend of PHC 100 000 a Relative risk for relative risk 21 P

Race Non-Aboriginal 6 0.5 1 .o Aboriginal 18 5.2 10.4 4.0 to 26.6 37.7 < 0.001 Total 24 1.6 sew Female Male

5 0.7 1 .o 19 2.3 3.3 1.3 to 9.3 6.8 <0.01

Race and sex NonAboriginal men 5 0.8 1 .o Aboriginal men 14 8.3 10.4 3.8 to 30.3 32.4 <0.001 NonAboriginal women 1 0.2 1 .o Aboriginal women 4 2.2 11.0 1.3 to 116.6 8.4 co.01 &+for nondborigines 40 to 49 1 0.7 1 .o 50 to 59 1 1.2 1.7 0.1 to 28.9 60 to 69 3 5.1 7.3 0.7 to 74.9 2 70 1 4.0 5.7 0.3 to 98.9 3.4 (trend) > 0.05 &+for Aborigines 40 to 49 3 11.5 1 .o 50 to 59 6 36.8 3.2 0.8 to 13.3 60 to 69 7 67.4 5.9 1.5 to 23.6 t 70 2 37.7 3.3 0.5 to 20.6 4.7 (trend) c 0.05 Mean age 59 Median age 59 N o h (a) lnddenos mter am bared on appropriate denominator populafion. Significance I d s am d o r i d from Poiuon d s using denominators as OFFSET in GLIM. All analym prsrented am uniwrida

AUSTRALIAN JOURNAL OF PUBLIC HEALTH 1994 v a . 18 NO. 3 287

WAN ET AI

to calculate the age-standardised incidence ratios of PHC for Aboriginal males and females in the North- ern Territory, using the indirect method. Standard- ised incidence ratios were calculated as the ratio of the observed number of PHC cases to the expected number. Ninety-five percent confidence intervals for the ratios were calculated, assuming a Poisson distribution.

Rates of PHC for the Aboriginal population in the Northern Territory were also compared with PHC incidence rates for the People's Republic of China for the year 1979.16

Results With 24 confirmed PHC cases, the overall incidence was 1.6 per 100 000 population in the Northern Ter- ritory; however, 18 cases were Aboriginal and there was great variation by race, with a rate of 5.2 per 100 000 for Aborigines and 0.5 per 100 000 for non- Aborigines, yielding a relative risk of 10.4 (95 per cent confidence interval (CI) 4.0 to 26.6) (Table 1). Table 1 also shows the variation in PHC incidences by sex and age.

Because of the relatively late age of onset (Table 1) and the relatively young age of the Northern Terri- tory population, the incidence rates of PHC were much greater when calculated on the basis of the at-risk population over the age of 40 (Figure 1). The rate of 30.9 per 100 000 in Aborigines exceeded that (18.9) in high-risk populations. and was 76-fold the rate (0.4 per 100000) in low-risk populations. Although the latter rate was based on only one case, the Aboriginal excess was clearly significant (f, = 51.0, P < 0.001; CI for relative risk 9.4 to 568.5). When the Aboriginal incidence of PHC (30.9 per 100 000) was compared with that from China (36.9 per 100 000), a high-incidence country, it was not statistically different w', = 0.6, P > 0.05).

Because of the very small numbers of cases of PHC in low-risk ethnic groups in the Northern Territory, we compared local incidence rates with those from the larger population of Victoria. As shown in Tables 2 and 3, PHC occurred at a higher rate in Northern

70

60

L a g 4 0

30

n" 20 e - 10

0 Total 40-49 50-59 60-69 >69

Aae (years) Figure 1 : Incidence (in populations over the oge of 401 of prlmory hepotocellular carcinoma for different rlsk groups In the Northern Ter- ritory, Australia ond China

Territory Aborigines than in different ethnic groups in Victoria; the standardised incidence ratio for Aboriginal males ranged from 1.4 (compared to Vic- torian men born in Asia) to 18.7 (compared to Vic- torians born in United Kingdom, Ireland or northern Europe); the ratio for Aboriginal females ranged from 4.3 (Asian-born comparison population) to 18.9 (United Kingdom, Ireland or northern Europe comparison).

Eleven Aboriginal and four non-Aboriginal PHC cases had results for HBV serological tests; 63.6 per cent (7 of 11) of Aboriginal cases and 50.0 per cent (2 of 4) of non-Aboriginal cases of PHC were HBsAg carriers. Serological markers (HBsAg or antibody to HBsAg) of HBV infection occurred in 72.7 per cent of Aborigines and 75.0 per cent of non-Aborigines, respectively. The HBsAg carriage rate of 63.6 per cent in Aboriginal cases of PHC was much higher than the 13.1 per cent obtained from community- based surveys among Aboriginal adults aged 40 and over in the Northern Territory; the odds ratio was 1 1.2 and the difference was highly statistically significant w2, = 21.7, P < 0.001).

Discussion Primary hepatocellular carcinoma is the most fre- quently occurring cancer in many developing

Table 2: Standardised incidence mtios (SIR) a of primary hepatocellular carcinoma (PHC) in Aboriginal males in the Northern Territory

~ ~~ ~~ ~

Observed Aboriginal Australia Britain

40 to 49 3 33.0 6.8 to 96.3 40.1 8.3 to 117.3 50 to 59 4 11.6 3.2 to 29.6 - - 60 to 69 5 11.1 3.6 to 25.8 9.1 3.0 to 21.2 2 70 2 6.0 0.7 to 21.5 16.5 2.0 to 59.5 Total 14 11.4 6.3 to 19.2 18.7 10.2 to 31.4

Age (pan) PHC cases (n) SIR CI SIR Clb

~~

Asia SIR Clb

1.3 0.3 to 3.8 1.6 0.4 to 4.0 1.8 0.6 to 4.3 0.9 0.1 to 3.4 1.4 0.8 to 2.4

~

Southern Europe SIR CI

72.4 14.9 to 21 1.4 6.2 1.7 to 15.8 8.2 2.7 to 19.1 3.4 0.4 to 12.4 7.4 4.1 to 12.5

N o h : (a) Estimated from Wdorian male mtes by country of birth. (b) CI -95% confidence interwls

Table 3: Standardised incidence mtios (SIR) a of primary hepatocellular carcinoma (PHC) in Aboriginal females in the Northern Territory

SouthemEuro e r Age (years) PHC cases (n) SIR Clb SIR CI SIR Clb SIR CI 40 to 49 0 - - - - - - 50 to 59 2 41.4 5.0 to 149.5 24.5 3.0 to 88.5 - - 15.2 1.8 to 54.8 60 to 69 2 15.6 1.9 to 56.4 25.1 3.0 to 90.7 3.4 0.4 to 12.4 5.9 0.7t021.5 2 70 0 - - - - Total 4 13.1 3.6 to 33.6 18.9 5.2 to 48.4 4.3 1.2 to 10.9 4.4 1.2t011.3

Observed Aboriginal Australia Britain Asia

- -

- - - - ~~~ ~

Ndar: (a) Estimated from Victorian female mter by country of birth. (b) CI -95% confidence intemlr


ABORIGINAL HEPATOCELLULAR CARCINOMA

countries7 and in countries such as China." Despite the small numbers in absolute terms, our study shows that the age-specific incidence of PHC in Aboriginal Australians in the Northern Territory is comparable to that in China (Figure l).16 Furthermore, incidences of PHC for Aborigines are comparable to rates for immigrants from Asian and Mediterranean countries where PHC is relatively comrn~n. '~ '~

Incidence rates of PHC in Aboriginal males and females of 8.3 per 100000 and 2.2 per 100000 (Table 1) are similar to rates of 7.9 and 1.4 per 100 000 for Alaskan males and females and rates of 13.1 and 2.2 per 100 000 for Eskimo males and females in the United States,ls but much higher than rates in low-incidence populations such as in the United Kingdomyo and Victoria (Tables 2 and 3).

The mean age of PHC patients, 58.7 years for Aboriginal Australians, was similar to 58.0 years in Britain,'O 53.0 years for American blacks and 61.0 years for American whites;" this age of onset is nearly 10 years later than the 49 years in Maori in New Zealand.'2

Our results suggest that HBV infection is a significant risk factor for PHC in Aborigines. The HBsAg detection rate (63.6 per cent) in Aboriginal patients was much higher than that (1 3.1 per cent) in the general Aboriginal population and was similar to rates (59.5 per cent to 80 per cent) in PHC patients in Asia and Afri~a.'~:!~

Internationally, liver cirrhosis is considered an important contributor to PHC risk in many Euro- pean population^^^'^ and hepatitis B infection is also a possible risk factor for cirrhosis.28:2s However, mortality data in the Northern Territory over ten years (1 980 to 1989) showed that the mortality rate for cirrhosis of the liver in Aborigines (1.2 per 100 000) was similar to that in non-Aborigines (1.1 per cent 100 000). This suggests either that cirrhosis of the liver is not important in explaining racial differentials in the development of PHC in the Northern Terri- tory or that there is considerable underreporting of cirrhosis in Aborigines.

Is there any possibility of bias in the PHC incidence rates reported here? It is possible that a few Aborigi- nal cases of PHC would have been missed entirely in this study, as some Aboriginal death certificates are still completed and attributed to causes 'not other- wise specified' when an elderly person dies in a community without a hospital admission or an autopsy. A bias in the opposite direction could have been intro- duced when three cases with no medical records for confirmation were used to calculate the incidence. However, any such bias must be small, as all other PHC death certificates (1 8 of 18) were confirmed by medical records when available.

This study shows that PHC is of public health importance in Aboriginal Australians and that HBV infection is of aetiological importance. Known carriers of HBsAg can benefit from screening for the early detection of PHC; for example, adults aged 40 years and over have been followed with serum a- fetoprotein and imaging of the liver at intervals of six months to detect small asymptomatic carcinomas, which are potentially curable by surgical resection.$* Five-year survival rates of PHC patients have increased to 68 per cent in South Africa.3o For younger HBsAg camers, interferon has been intro-

duced as an experimental treatment to terminate viral carriage,$' but it would be premature to con- sider its use in the Northern Territory.

From a public health perspective, the introduction of hepatitis B immunisation for Northern Territory infants and children will provide the long-term sol- ution by reducing the reservoir of carriers, thus reducing transmission rates of HBV. The efficacy of infant immunisation will be improved by screening to detect carriers during pregnancy and by use of immune globulin with vaccine to protect the new- born infants of carriers.3' Improved hygiene and living conditions and changing social practices will also help to reduce the transmission rates of HBV and thus reduce the risk of PHC in later life.

Acknowledgments Sincere thanks are due to Ms G. Fleay, Dr Dan Black, Dr Helen Farrugia and Dr Graham Giles for providing data, to staff of the Medical Records Depart- ments in Northern Territory hospitals for assistance and Dr David Scrimgeour for reviewing medical records in Alice Springs. We thank Dr Aileen Plant, Mr Lindsay Pyne and Dr Bryan Young for institutional approvals and support and Dr Tarun Weeramanthri, Dr Sam Heard and Dr Bart Cume for checking causes of death and for providing valu- able advice.

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Participation in breast cancer screening: randomised controlled trials of doctors' letters and of telephone reminders Ann Richardson, Sheila Williams, Mark Elwood and Margaret Bahr

Tim Medlicott

Department of Preventive and Social Medicine, University of Otago, Dunedin

Mornington Health Centre, Dunedin

Abstract: The study used a randomised controlled trial to find out whether supporting letters from general practitioners accompanying the invitations from a screening centre affected participation in a population-based breast cancer screening program for women aged 50 to 64. A further randomised controlled trial compared the effect o f postal reminders with telephone reminders for women who did not respond t o an initial invitation t o participate in the program. There were 482 women in the first trial and 641 in the second. Excluding women who were ineligible or could not be contacted, participation in screening was 71 per cent in the group which received letters from their general practitioners compared with 62 per cent in the group which did not receive letters (P = 0.059). In the group that received letters, 56 per cent were screened without a reminder compared with 43 per cent of the group that did not receive letters (P= 0.01). Fewer women who received letters from their general practitioners declined the invitation to be screened (P = 0.048). In the second trial, there was n o difference in participation between the group receiving telephone reminders and the group receiving postal reminders. As in breast cancer screening programs in other countries, general practitioner endorsement of invitations increased participation in breast cancer screening. Postal reminders were as effective as telephone reminders in encouraging women who did not respond to an initial invitation t o participate in screening. (AustJ Public Heulfh 1994; 18: 290-2)

omen living in Otago and Southland, New Zealand, and aged 50 to 64 are eligible to W participate in a pilot breast cancer

screening program which offers free two-yearly screening using two-view mammography. This pilot program will provide information about the accept- ability, effectiveness and efficiency of breast cancer screening in New Zealand.'.!

Correspondence to Professor J.M. Elwood, Director, Hugh Adam Cancer Epidemiology Unit, Otago Medical School, PO BOX 93, Dunedin, New Zealand. Fax 64 3 479 7298.

One of the most important determinants of the effectiveness and efficiency of a screening program is the participation of the target group. If participation is high, the benefits of screening are available t o a greater proportion of the target group, and the program will also have greater cost-effectiveness. Eli- gible women are identified using general practice age-sex registers, supplemented with information from the electoral roll. Registration on the electoral roll is compulsory in New Zealand, but the proportion of the population on general practitioner


primary hepatocellular carcinoma in aboriginal australians

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