HIV and hepatitis C among injecting drug usersBMJ 1998; 317 doi: http://dx.doi.org/10.1136/bmj.317.7156.424 (Published 15 August 1998) Cite this as: BMJ 1998;317:424
Success in preventing HIV has not been mirrored for hepatitis C
- R A Coutinho, Director and professor of epidemiology and control of infectious diseases
Papers p 433
Injecting drug users have been capable of reducing their risky behaviour in the face of the HIV-AIDS epidemic.1 To many this risk reduction, shown in numerous studies from different parts of the world, was unexpected as drug users are often regarded as self destructive. Nevertheless, because of the decrease in risky behaviour, the incidence of HIV infection among drug users in most industrialised countries has declined over the years. Thus, in this issue, van Beek et al report that among young injecting drug users in Sydney the incidence of HIV infection in 1992-5 was only 0.2 per 100 person years (p 433).2 Not so good is their finding that the incidence of infection with hepatitis C virus (HCV) was extremely high: 21 per 100 person years; among those aged under 20 the rate was 76 per 100 person years. Other groups from different countries have also reported a continuing high prevalence and incidence of hepatitis C virus among injecting drug users,3 though not as high as in this study; this may be to do with the young age of the Australian group.
The low incidence (and prevalence) of HIV among injecting drug users in Australia may be ascribed to that country's public health approach, with wide implementation of preventive measures including needle and syringe exchange programmes. But how can we explain the discrepancy between the low incidence of HIV infection and the high incidence of hepatitis C? One reason is the difference in prevalence between the two viral infections. The prevalence of HIV in the Australian group was 2.5% while that of hepatitis C virus was 45%. So, if in that environment an injecting drug user shares injecting equipment with someone else the chance that this equipment is infected with hepatitis C virus is considerably greater than for HIV.
But this is not the only explanation. Hepatitis C virus is much more efficiently transmitted through blood than HIV infection—for sexual transmission it is the other way around. The rate of hepatitis C virus antibody seroconversion among healthcare workers in Japan who had been exposed through needlestick injuries to blood from patients positive for hepatitis C virus was 3-9%.3 This is more than 10 times higher than the 0.3% HIV seroconversion rate after needlestick incidents with HIV positive patients.4 The high transmission efficiency of hepatitis C virus may also explain its transmission in drug users in the Australian study who did not report a history of sharing equipment. This could have been due to indirect sharing—that is, sharing of injecting accessories such as spoons and cotton —or to front and back loading—dividing drugs by sticking the needle of one syringe into another (used) syringe—which is often not seen as sharing by drug users.
The clinical consequences of hepatitis C virus infection are serious, especially in the long term.5 Although most acute hepatitis C infections are subclinical, in 80-85% of cases the infection persists and usually leads to chronic hepatitis, which can result in cirrhosis and rarely hepatocellular carcinoma. The mean period between infection with the virus and its consequences is long: about 20 years for cirrhosis and 29 years for hepatocellular carcinoma. There is no convincing evidence that the progression to cirrhosis is influenced by drug use itself, but other risk factors like coinfection with hepatitis B and HIV and hepatotoxic agents like alcohol enhance progression. As these risk factors are common among injecting drug users, their incubation period between infection and its sequelae may be shorter. On the other hand, mortality among injecting drug users is high: a study among injecting drug users in the Netherlands showed 1.8 deaths per 100 person years in those who were HIV negative and 6.4 per 100 person years in those who were HIV positive.6 Therefore, some drug users with hepatitis C virus will not survive long enough to develop cirrhosis or carcinoma.
Because of its long term consequences hepatitis C virus infection should be treated, although the sustained response rate after treatment (currently with interferon, preferably in combination with ribavirin) is only 20-30%.7 Other drugs for treating the infection are being developed and may have better results.
What can we do about the hepatitis C virus epidemic in injecting drug users? It is clearly an extra reason to strengthen programmes aimed at reducing sharing of injecting equipment by drug users. However, many industrialised countries have, like Australia, already implemented such programmes and there seems to be only limited room for improvement. More attention could be paid to preventing indirect sharing, as this may be an important transmission route for hepatitis C virus. And peer education—which has been shown to be very effective among homosexual men—is an option that has not been sufficiently explored among injecting drug users. But we have to remain realistic. The residual risk among injecting drug users will be hard to prevent, especially as part of this behaviour appears to be deliberate (unpublished data). In the Netherlands stopping injecting (“the switch”) was recently the topic of a national campaign implemented by an organisation with close links to injecting drug users. Another approach is to try to prevent drug users from starting injecting. And, of course, the best option is not to use drugs at all.
We have been reasonably successful in stemming (but not stopping) the HIV epidemic among injection drug users. The Australian data show that we have not been at all successful in stemming the spread of hepatitis C virus.