Acute hepatitis B infection in Aboripal Australians Xinan Wan

Bart C u m e Menzies School of Health Research, Darwin

Menzies School of Health Research and Royal Darwin Hospital

Nan Miller D e p a r t m t of Health and Community Services, Daiwin

John D. Mathews Menzies School of Health Research, Darwin

Abstract: The apparent incidence of acute hepatitis B infection in the Top End of the Northern Territory was estimated from notification data and hospital data to be 12 per 100 000 per year, with a marked difference between Aborigines (42 per 100 000) and non-Aborigines (4 per 100 000), and an odds ratio of 9.7 (95 per cent confidence intervals 3 to 33). Sixty percent of Aboriginal cases of acute hepatitis B occurred in children under 10 years of age, whereas non-Aboriginal cases occurred in adults aged 20 to 29, most with behavioural risk factors. These findings confirm the importance of inimunising Aborib.ina1 children to reduce the future incidence of hepatitis B infection and hepatoma. ( A w l ] Public Health 1993; 17: 332-3)

hronic hepatitis B virus infection represents an important public health problem for Abor- c iginal Au~tralians.~-~ However, little is known

about acute hepatitis B infection in Aboriginal Aus- tralians. For example, Hardy reported no clinical evi- dence of infection in his study of the epidemiology and genetics of hepatitis among Australian Aborigines.'j We have used hepatitis B notifications and hospital-based data to estimate the apparent inci- dence rates of acute hepatitis B virus infection by age and ethnic group in the Northern Territoiy.

Subjects and methods This study was based on the population of the Dar- win, Katherine and East Arnhem regions in the Top End of the Northern Territory. The study protocol was approved by the Institutional Ethics Committee of the Royal Darwin Hospital, working to National Health and Medical Research Council guidelines.

During 1988, cases of acute hepatitis B were ident- ified from the Communicable Diseases Centre regis- ter of hepatitis notifications, from hospital discharge diagnosis records of the four regional hospitals (Royal Darwin Hospital, Darwin Private Hospital, Katherine Hospital and Cove Hospital) and from records of the approximately 200 hepatitis :B surface antigen (HBsAg) positive tests from the Royal Darwin Hospital Pathology Laboratory.

Medical records of all putative cases were searched to identify those cases which satisfied the case defi- nition used, a modification of the United States Centers for Disease Control case definition for acute hepatitis B.7 This definition required either: an elev- ated level of serum aspartate aminotransferase (1 00 IU/L or greater) and positive HBsAg, plus at least one of the following clinical symptoms and signs: nausea, vomiting, pain in the right upper quadrant of

Correspondence to Dr Xinan Wan, Menzies School of Health Research, PO Box 41096, Casuarina, NT 081 1 . Fax (089) 27 5 187.

the abdomen, anorexia, jaundice or dark urine; OT the detection of IgM antibodies to hepatitis B core anti- gen with jaundice. In addition, it was required that when performed, the hepatitis A IgM antibody test be negative. Follow-up of all cases was not possible, so that no information is available on clearance rates of HBsAg. Universal hepatitis B vaccination for Aboriginal infants was introduced in 1988, so that past vaccination would have had no significant effect in reducing the risk of acute infection in children born prior to 1988.

Apparent incidence rates were calculated by age, sex and ethnicity using population denominators for the three administrative regions in the Top End obtained from the Northern Territory Department of Health and Community Services. All statistical analyses were performed using the Generalised Lin- ear Interactive Modelling (GLIM) package devel- oped by the Royal Statistical Society, United Kingdom. Odds ratios (OR) and 95 per cent confi- dence intervals (CI) were also estimated using GLIM.

Results There were 14 serologically confirmed acute hepa- titis B cases identified in the Top End of the Northern Territory in 1988 (Table 1). Eight cases were detected from notification records and six cases were verified which had not been notified. The apparent incidence rate was 12 per 100 000 per year, with no significant sex difference. Acute hepatitis B infection was significantly more frequent in Aboriginal people (10 cases), particularly in children (6 cases) (Table 1). The regional incidence was greater for East Arnhem residents, entirely due to Aboriginal cases. All odds ratios had wide confidence intervals because of the small number of cases detected.

Of the four non-Aboriginal cases, two were inject- ing drug users and one was homosexual. None of the 10 Aboriginal cases was identified as homosexual or an injecting drug user. It is assumed that all six Abor-

AUSTRALIAN JOURNAL OF PUBLIC HEALTH 1993 vot. 17 NO. 4 33 1

W A N El At

iginal children acquired hepatitis B through horizon- tal transmission.

Discussion The modified Centers for Disease Control case defi- nition used here for a diagnosis of acute hepatitis B does not absolutely exclude acute hepatitis A in a chronic hepatitis B carrier; five of our cases did not have hepatitis A serology done. However, two of these were hepatitis B core-antibody IgM-positive, and no cases diagnosed as acute hepatitis B were subsequently found to be hepatitis A IgM-positive. Delta virus serology was not available for these cases, but delta virus infection is rare in Australia except in injecting drug usema Hepatitis C has recently been found to be present in Aboriginal communities as well as in other Top End populations (unpublished data). As with hepatitis A, acute hepatitis C in a chronic hepatitis B carrier is not necessarily excluded in our cases. Acute alcoholic hepatitis in a hepatitis B carrier would also fulfd the case definition used, but there was nothing in the case records to suggest that any of the cases had acute alcoholic hepatitis.

The apparent incidence rate of acute hepatitis B was 12 per 100 000 population in the Top End of the Northern Territory, which is similar to 7.7 reported in United K i n g d ~ m , ~ 8 to 12 in France,IO 10.4 in SingaporelI and 11.5 in the United States.'? How-

ever, this figure is much higher than 2.8 per 100 000 in Scotland.IY Racial variation in apparent disease incidence was marked, with 42 per 100 000 in Abor- igines and 4 per 100000 in non-Aborigines; the Aboriginal rate was higher than that in some endemic countries overseas (for example, 20 to 30 per 100 000 in Egypt and Hong Kong).14 Sixty per cent of Aboriginal cases were under 10 years of age, which differs greatly from 2.3 per cent in Melbourne15 and less than 1.0 per cent in the United States.I6

These contrasts are of interest, but must be accepted with caution, because of the potential biases in a retrospective study of this kind. For example, the study would tend to m i s s patients (such as non- Aboriginal children) presenting to urban general practitioners. This might partly explain our failure to detect such cases despite evidence for sero- conversion in non-Aboriginal children in the North- e m Terr i t~ry .~ Thus it is likely that our study has underestimated the incidence of acute hepatitis B infection in the non-Aboriginal population. On the other hand, it is known that there are numerous (asymptomatic) hepatitis B carriers amongst Aborigi- nal children of school age in the Northem Terr i t~ry ,~ and an unknown number of children may have passed through an acute hepatitic phase following horizontal transmission, with or without symptoms. Such cases may have received no medical attention,

Table 1 : Risk factors for acute hepatitis in the Top End, 1988

Acute hepatitis Incidence 95% confidence B cases per 100 000" Odds mtio interval for adds mtio 2 P

Race NonAboriginal Aboriginal Total

Female Male

Non-Aboriginal moles Aboriginol moles NonAboriginal females Aboriginal females

Sex

Race and sex

4 4.1 1 10 42.3 10.4 3.17 to 33.83 . 14 11.51

23.90 <0.001

6 10.4 1 8 12.5 1.2 0.41 to 3.56 0.12 > 0.05

3 5.7 1 5 43.2 7.5 1.74 to 32.49 10.59 <0.01 1 2.2 1 5 41.3 18.9 2.1 1 to 169.00 14.13 <0.001

Age-for Aborigines Under 10 6 91.39 10 to 19 2 34.61 20 to 29 1 21.68 30 to 39 1 34.20

Mean age 12.0 years, medion age 6.5 yeon

Age-for non-Aborigines Under 10 0 0.00 10 to 19 0 0.00 20 to 29 4 20.08 30 to 39 0 0.00

Mean age 24.5 years, median age 25.0 years

3.39 (trend) >0.05

Region of residence Darwin Katherine East Arnhem

8 8.44 3 18.70 3 27.70

Region of residence for Aborigines Darwin 5 38.62 Katherine 2 37.04 East Arnhem 3 56.53

Noh: (a) lnadence mtes are based on the appropriate denominator population. Significance Iewls were deriwd from Poisson models using denominator as OFFSET in GLIM. All analyses presented are univoriate.

332 AUSTRALIAN JOURNAL OF PUBLIC HEALTH 1993 VOL. 17 NO. 4

HEPATITIS B I N ABORIGINAL AUSTRALIANS

and also been missed in the present study. In particu- lar, the observed incidence rate of hepatitis B for Aboriginal children aged nine and under in this study was approximately 90 per 100 000 per year; this inci- dence rate for (symptomatic) infection is possibly an order of magnitude less than the incidence rate for (asymptomatic) infection deduced from sero- prevalence data on Aboriginal ~hi ldren .~ These potential biases are subject to further investigation.

The study is on firmer ground in relation to symp- tomatic cases of hepatitis B in adults. Three of four such cases in non-Aborigines were found to have had behavioural risk factors. Such risk factors were not identified in Aboriginal cases, predominantly chil- dren, who were presumably infected via infected skin soresI7 or other routes of horizontal transmission. Horizontal transmission is recognised as a major mode of spread of hepatitis B virus in developing countries, such as in Africa and India.It’J9 In New Zealand it also appears to be the predominant mode of spread of the virus from Maori to non-Maori children . *O

Although the apparent incidence rates of (sympto- matic) hepatitis B infection (Table 1) will underesti- mate the true rates, our results show that hepatitis B vaccination can be strongly recommended for nonimmune Aboriginal children of three to nine years of age in addition to the current policy of vacci- nating all Aboriginal neonates; this would help to reduce acute hepatitis B infection in the near future, and in the longer term it would also decrease the number of chronic carriers of hepatitis H, and thus decrease the subsequent incidence of cirrhosis and primary hepatocellular carcinoma.

The study also suggests that at least 50 per cent of acute hepatitis cases in the Darwin region were not reported to the Disease Control Centre hy the cur- rent surveillance system. Substantial underreporting of the disease places real constraints on attempts to evaluate the efficacy of the hepatitis B vaccination program introduced in 1988. In the short term the dynamics of hepatitis B infection in the community can be followed only by an accurate reporting system for acute hepatitis B. The long-term value of the vac- cine program will be judged by reduction in the inci- dence of primary hepatocellular carcinoma which is already known to be very high in the Aboriginal population of the Northern Territory (Wan X. and Mathews J.D., unpublished data).

Acknowledgments We thank the Northern Territory Disease Control Centre for access to hepatitis B notifications, and Pathology and Medical Records staff in the Royal

Darwin and Katherine Hospitals for assistance. M r Lindsay Pyne, Dr Bryan Young, Dr Mahomed Patel, Dr Alan Ruben, Dr Jan Bullen and Mrs Yvonne Wood provided valuable advice and assistance.

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