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The Australian Study of HIV and Injecting Drug Use. Part I: Prevalence for HIV, hepatitis B and hepatitis C among injecting drug users in four Australian cities
Author(s) -
LOXLEY WENDY M.,
PHILLIPS MIKE,
CARRUTHERS SUSAN J.,
BEVAN JUDE S.
Publication year - 1997
Publication title -
drug and alcohol review
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.018
H-Index - 74
eISSN - 1465-3362
pISSN - 0959-5236
DOI - 10.1080/09595239800187381
Subject(s) - medicine , seroprevalence , hepatitis c , demography , hepatitis b , hepatitis , viral hepatitis , hepatitis a , human immunodeficiency virus (hiv) , drug , cohort , needle sharing , drug injection , environmental health , immunology , syphilis , serology , psychiatry , antibody , condom , sociology
The objective of this study was to assess differences in HIV, hepatitis B and hepatitis C seroprevalence among injecting drug users (IDU) in four Australian cities. Eight hundred and seventh‐two current IDU were recruited in approximately equal numbers from each of Adelaide, Melbourne, Perth and Sydney, and interviewed individually using a structured questionnaire. Fingerprick blood samples were taken from the majority of respondents, and tested for past exposure to the three viruses. HIV and hepatitis B and C raw seroprevalences were compared across cities, and comparisons were made of age‐standardized seroprevalences for hepatitis B and C. Three percent of all respondents were HIV seropositive; 19% (23% age‐standardized) were hepatitis B seropositive and 55% (60% age‐standarized) were hepatitis C seropositive. There were general city differences and gender, sexual preference and treatment status group differences between the cities. Sydney respondents had the highest risk of infection for all three viruses in all comparisons. This was particularly striking for HIV among non‐heterosexual men. Various explanations for the findings were considered, including city differences in demographic and drug use variables, underlying patterns of risk behaviour, and period/cohort effects. It was concluded that none of these explanations appeared to fit the pattern of findings, and that these probably represented true underlying differences in size of pools of infection. The reasons for this, however, cannot be ascertained from this study.