- Email: [email protected]
WERNICKE'S ENCEPHALOPATHY IN AIDS PATIENT TREATED WITH ZIDOVUDINE
The Working Group on Services for People with Epilepsy2 has made the modest recommendation that "one or more model epilepsy clinics should be established and evaluated". With this in mind I approached the DHSS’ special medical development fund. After prolonged silence I received a letter discouraging any application ("we were unable to recommend it as a very high priority"). That says it all. Despite the enormous medical, psychological, and social problems of epileptic patients so well described in successive reportsl-3 and your editorialthe DHSS is not willing to back -its own longstanding recommendations for epilepsy clinics. That is why the belatedly published working-party report2 has been sent to regional and district health authorities merely for more "discussion". As you point out, there is no significant public pressure on the DHSS; that Department is responsible for much of the indifference to epilepsy. Department of Neurology, King’s College Hospital,
E. H. REYNOLDS
London SE5 9RS 1. Central Health Services Council
with
(Reid report). People epilepsy. London: HM Stationery Office, 1969. 2. Report of the Working Group on Services for People with Epilepsy: a report to the Department of Health and Social Security, the Department of Education and Science and the Welsh Office. London: HM Stationery Office, 1986. 3. Ministry of Health (Cohen report). Central Health Services Council. Report of the sub-committee on the medical care of epileptics. London: HM Stationery Office,
WERNICKE’S ENCEPHALOPATHY IN AIDS PATIENT TREATED WITH ZIDOVUDINE
SiR,—The neurological manifestations of AIDS include some to direct infection of the brain by human immunodeficiency virus (HIV). We describe a patient with AIDS and Wernicke’s encephalopathy. He had been treated with zidovudine (azidothymidine, AZT). A 46-year-old homosexual man with AIDS was admitted on Dec 25, 1986, with decreased appetite, inability to swallow solid foods, diarrhoea, mild shortness of breath with a dry cough, and weakness. He had lost weight and had oral candidiasis. On Dec 23 he had been started on AZT and had received twelve doses (200 mg every 4 h) ascribable
before admission.
1956.
HEALTH EDUCATION IN UK
SIR,-By attempting to stop the press conference on the Health Education Council publication Health Divide the chairman of the HEC added to the fears many of us had about the ability of the HEC’s successor, the Health Education Authority, to challenge government health policies. The report underlines the growing health divide between the poorer and the more affluent for almost every health indicator. So-called "diseases of affluence" have all but disappeared and what is left is a general health disadvantage of the poor. The growing divide is emphasised by the position of manual workers, who now have twice the death rate for lung cancer of non-manual workers, a divide which has widened over 10 years. There is a similar disadvantage for manual workers for coronary heart disease. Both these diseases are preventable and together they cause about one-third of all male mortality. The Government’s failure to control powerful vested interests in tobacco (and also alcohol) is underlined by the Chancellor of the Exchequer’s budget decision to allow both these substances to become relatively cheaper. The British Medical Association, the medical Royal Colleges, and the medical charities will need to act even more decisively as watchdogs for preventive medicine in future. They can certainly bark and may need to find where best to bite, if the Government fails to respond effectively to this important report. Department of Community Medicine, Middlesex Hospital Medical School, Central Middlesex Hospital, London NW10 7NS
KEITH BALL
POPPER AND KNOWLEDGE
SiR,-One can only envy men such as Jenner, Darwin, and Pasteur in that they spent their time thinking and doing experiments rather than listening to the continuing exegesis of the works of Sir Karl Popper (Feb 14, p 387). Popper has written extensively and clearly about what makes a theory scientific and on how we can choose strategies of acquiring knowledge that are more likely to increase our useful information about the natural world. Nevertheless he must feel like changing his name by deed poll when he reads the beliefs attributed to him-citing Popper has become like citing scripture. Popper’s theories like the scientific theories he discusses are provisional, open to doubt, and ultimately flawed; nobody in the scientific world has absolute knowledge. Dr Davies (March 14, p 630) states "theories can be refuted but confirmed whereas diagnoses can be confirmed but not excluded". I do not think life is quite so straightforward. In a world where the predictions from a theory always come with confidence limits attached, any particular theory may be less or more reasonable not
believe in but absolute refutation is as nonsensical as believing in absolute confirmation. Secondly, new experimental data can be in keeping with the predictions of a certain theory, and in this everyday sense they confirm it, even though they do not prove it correct. I find it worrying that a radiologist doubts whether a diagnosis can ever be excluded, since this will no doubt increase even further the length of X-ray reports. Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne JONATHAN REES to
A computerised tomographic (CT) scan with contrast revealed mild cerebral atrophy and lumbar puncture was unremarkable. On Dec 26 he had two grand mal seizures. There were no focal deficits apart from slight unsteadiness during tests of cerebellar function and hyperreflexia. AZT was discontinued and phenytoin was prescribed. Thereafter the patient was alert, oriented, and had no focal motor or sensory neurological deficits, and no memory deficit apart from inability to recall the seizures. The seizures were attributed to AZT and phenytoin was discontinued. On day 5 the patient had septic shock with gastrointestinal bleeding and disseminated intravascular coagulation. His mental status gradually deteriorated and he died on day 14. The patient had no history of alcohol abuse, had not been treated by dialysis, and had not received intravenous hyperalimentation before death. Necropsy findings (restricted in this letter to those in the brain) included symmetrical bifrontal cortical atrophy and symmetrical petechial haemorrhages in coronal sections occupying most of the cross-sectional area of both mammillary bodies. The haemorrhages were acute, though there was moderate reactive astrocytic gliosis in the region of the mammillary bodies and the deep grey structures adjacent to the third ventricle. There was a focus of anoxicischaemic neuronal change in the thalamus; bilateral necrotic lesions in the pontine tegmentum; reactive gliosis throughout the pons and midbrain tegmentum; and patchy but focally severe reactive gliosis in the subcortical white-matter of the centrum semiovale. The necropsy findings were typical of acute Wernicke’s encephalopathy. The gliosis found in the periventricular and periaqueductal regions suggests that the disease may have been of longer duration, but subcortical gliosis is often found in patients with AIDS and this finding must be interpreted with caution.2 The presence of focally severe subcortical gliosis suggests, but does not prove, that there was primary infection of the central nervous system by HIV.2 This patient had none of the known risk factors for Wemicke’s encephalopathy3 and the diagnosis was not entertained before he died.4 The mammillary body haemorrhage may have been exaggerated by the preterminal coagulopathy.5 Treatment with AZT may have aggravated the tendency for Wernicke’s encephalopathy to develop. This case confirms previous clinical evidence of AZT neurotoxicity:6 grand mal seizures developed soon after AZT treatment began and ended when the drug was discontinued. AZT selectively interferes with the function of DNA polymerase in the synthesis of viral DNA. Cerebral DNA synthesis is significantly impaired in rats fed a diet deficient in thiamine and these animals have a syndrome similar to Wernicke’s encephalopathy.8 Thus a drug that impairs DNA synthesis might increase the likelihood of Wemicke’s encephalopathy in a
susceptible patient.
920 Wernicke’s encephalopathy should be considered in the differential diagnosis of the many AIDS patients who present with
clinically non-specific neurological syndromes. Department of Pathology, UCLA Medical Center, Los Angeles, California 90024, USA
DAVID G. DAVTYAN HARRY V. VINTERS
1. Torvik A. Two types of brain lesions in Wemicke’s encephalopathy. Neuropathol Appl
Neurobiol 1985; 11: 179-90. 2. Navia BA, Cho E-S, Petito CK, Price RW. The AIDS dementia complex II: Neuropathology. Ann Neurol 1986; 19: 525-35. 3. Reuler JB, Girard DE, Cooney TG. Current concepts: Wernicke’s encephalopathy. N Engl J Med 1985; 312: 1035-38. 4. Marx JA. The varied faces of Wernicke’s encephalopathy. J Emerg Med 1985; 3: 411-13. 5. Jagadha V, Deck JHN, Halliday WC, Smyth HS. Wernicke’s encephalopathy in patients on peritoneal dialysis or hemodialysis. Ann Neurol 1987; 21: 78-84. 6. Hagler DN, Frame PT. Azidothymidine neurotoxicity. Lancet 1986; ii: 1392-93. 7. Anon. Azidothymidine for AIDS. Med Letter Drugs Ther 1986; 28: 107-09. 8. Henderson GI, Schenker S. Reversible impairment of cerebral DNA synthesis in thiamine deficiency. J Lab Clin Med 1975; 86: 77-90.
HIV AND HBV INFECTION IN DRUG ABUSERS IN GLASGOW
SIR,-Glasgow has a large drug-abusing population, conservatively estimated at 7000.1 Despite its proximity to Edinburgh, where at least 38% of drug abusers have evidence of human immunodeficiency virus (HIV) infection,2,3 the prevalence of anti-HIV seropositivity in Glasgow-based drug abusers in 1985 was under 1%." In 1986, over 3000 specimens were submitted to our laboratory by clinicians for an HIV antibody test. 960 specimens were from patients who were drug addicts or abusers, and 59 (6-1%) specimens were repeatedly positive in an ELISA test (Wellcome) confirmed by western blot (Dupont) with three specific bands as the criterion of positivity. 31 of these 59 cases were based within the city of Glasgow. The remaining 28 were from Edinburgh or Dundee, and blood samples had been sent to us from prisons or drug rehabilitation centtes in west and central Scotland. Of the 31 HIV antibody-positive drug abusers from within Glasgow 18 were male and the average age was only 21. 27 (87 %) had markers of current or past hepatitis B virus (HBV) infection. Increasing numbers were found within Glasgow as the year , progressed-20 were detected in the last quarter of the year, the proportion in these months reaching over 6 % of those tested (table). Evidence of infection was noted in all areas of Glasgow where drug abuse is a recognised problem. The spread of infection was not uniform, and clustering of cases in certain areas suggested that in these areas the level of positivity was likely to be over 6%. Previous samples taken in 1985 or 1986 were available from 15 of the 31 antibody-positive cases. 2 were positive for HIV antibody but had not been tested because only an HBV status had been requested. The remaining 13 were negative for HIV antibody by the ELISA test. A test for HIV antigen (Abbott) in 8 specimens, which had been taken no more than 6 months before the first positive HIV antibody finding, was positive in 3. This finding indicates that HIV infection in this group follows a course similar to that in homosexuals5 and haemophiliacs;6 and also confirms that even antibody-negative blood from such high-risk individuals is potentially hazardous, and that they and their associates must be dissuaded from donating blood. The number of antibody-positive drug abusers within the city of Glasgow has risen from under 1 0 % in 1985 to over 6 % at the end of 1986. There is evidence that many of the positive cases were infected in 1986 and were not more distant infections undetected until 1986-ie, HIV infection became established within the city’s drug-abusing population in 1986. Compared with HIV antibodypositive drug abusers in Edinburgh,those in Glasgow are much HIV ANTIBODY IN DRUG ABUSERS IN
1986
younger, including 2 aged 16 and 2 aged 17. Exposure to HBV in the positive group is high, which suggests that the group are sharing needles widely and/or are highly promiscuous. A similar high level of exposure to HBV was noted in HIV antibody-positive abusers in
Edinburgh.2z It has been suggested that there is less sharing of needles in Glasgow than in Edinburgh.7 Examination of sera from 290 HIV antibody-negative abusers from Glasgow in the first four months of 1986 for HBV markers indicated exposure to the virus in 200 (69 %). This proportion is almost identical to that in a similar Glasgow group in 19854 and exceeds figures (45 and 51 %) reported in HIV antibody-negative abusers by the two Edinburgh laboratories.2,8 The mechanisms that spread HBV infection in Edinburgh may be operating even more powerfully in Glagow. It was perhaps inevitable that HIV infection should appear in the city’s drug-abusing population but it is nevertheless disappointing. A major effort will be required if further spread of the infection is to be checked. We are particularly concerned at the number of young females with evidence of infection. Several admit to prostitution and hence are a potential source of spread outside the drug-abusing population. In addition, there is considerable risk to such females and their offspring if they become pregnant. Regional Virus Laboratory, Ruchill Hospital, Glasgow G20 9NB
E. A. C. FOLLETT L. A. WALLACE E. A. B. MCCRUDEN
1. HIV infection in Scotland. Report of Scottish committee on HIV infection and intravenous drug misuse. Edinburgh: Scottish Home and Health Department, 1986. 2. Peutherer JF, Edmond E, Simmonds P, Dickson JD, Bath GE. HTLV-III antibody in Edinburgh drug addicts. Lancet 1985; ii: 1129-30. 3. Robertson JR, Bucknall ABV, Welsby PD, et al. Epidemic of AIDS-related virus (HTLV-III/LAV) infection among intravenous drug abusers. Br Med J 1986; 292: 527-29. 4. Follett EAC, McIntyre A, O’Connell B, et al. HTLV-III antibody in drug abusers in the West of Scotland: The Edinburgh connection. Lancet 1986; i: 446-47. 5. Goudsmit J, deWolf F, Paul DA, et al. Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic infection. Lancet 1986; ii: 177-80. 6. Allain J-P, Laurain Y, Paul DA, Senn D. Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs. Lancet 1986; ii: 1233-36. 7. Robertson JR, Bucknall ABV, Wiggins P. Regional variations in HIV antibody seropositivity in British intravenous drug users. Lancet 1986; i: 1435-36. 8. Burns SM, Hargreaves FD, Collacott IA, Inglis JM. Incidence of hepatitis B markers in HIV seropositive and seronegative drug misusers. Comm Dis Scot 1987; 21: 7-8.
SYRINGE EXCHANGE
SIR,-Dr Marks and Mr Parry (March 21,
p 691) report their experience with a needle/syringe exchange programme. Such schemes are now being widely discussed as a means of preventing the spread of human immunodeficiency virus (HIV).1-3 I am concerned lest there be uncritical acceptance of such programmes, whose effect on the prevention of AIDS is unproven and whose influence upon drug misuse is unknown. I accept the potential benefits of needle exchange, as outlined by Marks and Parry- and others1,;! and will comment here only on potentially adverse effects. The supply of needles and syringes may increase the incidence of drug misuse, by detracting attention from its other dangers, by appearing to condone injection of drugs, by making the necessary equipment more available, and by negating the beneficial discouragement provided by the fear of AIDS. Individuals using drugs sporadically or by other routes may find it easier to start injecting. The provision of clean needles does not ensure their proper use. Des Jarlais et a14 have drawn attention to the need for clean needles to be available at the crucial time, immediately after the drug itself has been obtained. Otherwise drug abusers will inject themselves with whatever needles are available (dirty if necessary). What will happen at the "shooting gallery" in Merseyside referred to by Marks and Parry which now has 6 (clean?) needles instead of 197 dirty ones? Use of shared needles has symbolic and other aspects not met by needle exchange programmes.3 Lack of availability is a reason for sharing needles/syringes but it is not the only one. The provision of needles/syringes is likely to promote a maintenance rather than an abstinence approach to treatment, and such an approach is subject to briticism 5
favourably
on
E. H. REYNOLDS
London SE5 9RS 1. Central Health Services Council
with
(Reid report). People epilepsy. London: HM Stationery Office, 1969. 2. Report of the Working Group on Services for People with Epilepsy: a report to the Department of Health and Social Security, the Department of Education and Science and the Welsh Office. London: HM Stationery Office, 1986. 3. Ministry of Health (Cohen report). Central Health Services Council. Report of the sub-committee on the medical care of epileptics. London: HM Stationery Office,
WERNICKE’S ENCEPHALOPATHY IN AIDS PATIENT TREATED WITH ZIDOVUDINE
SiR,—The neurological manifestations of AIDS include some to direct infection of the brain by human immunodeficiency virus (HIV). We describe a patient with AIDS and Wernicke’s encephalopathy. He had been treated with zidovudine (azidothymidine, AZT). A 46-year-old homosexual man with AIDS was admitted on Dec 25, 1986, with decreased appetite, inability to swallow solid foods, diarrhoea, mild shortness of breath with a dry cough, and weakness. He had lost weight and had oral candidiasis. On Dec 23 he had been started on AZT and had received twelve doses (200 mg every 4 h) ascribable
before admission.
1956.
HEALTH EDUCATION IN UK
SIR,-By attempting to stop the press conference on the Health Education Council publication Health Divide the chairman of the HEC added to the fears many of us had about the ability of the HEC’s successor, the Health Education Authority, to challenge government health policies. The report underlines the growing health divide between the poorer and the more affluent for almost every health indicator. So-called "diseases of affluence" have all but disappeared and what is left is a general health disadvantage of the poor. The growing divide is emphasised by the position of manual workers, who now have twice the death rate for lung cancer of non-manual workers, a divide which has widened over 10 years. There is a similar disadvantage for manual workers for coronary heart disease. Both these diseases are preventable and together they cause about one-third of all male mortality. The Government’s failure to control powerful vested interests in tobacco (and also alcohol) is underlined by the Chancellor of the Exchequer’s budget decision to allow both these substances to become relatively cheaper. The British Medical Association, the medical Royal Colleges, and the medical charities will need to act even more decisively as watchdogs for preventive medicine in future. They can certainly bark and may need to find where best to bite, if the Government fails to respond effectively to this important report. Department of Community Medicine, Middlesex Hospital Medical School, Central Middlesex Hospital, London NW10 7NS
KEITH BALL
POPPER AND KNOWLEDGE
SiR,-One can only envy men such as Jenner, Darwin, and Pasteur in that they spent their time thinking and doing experiments rather than listening to the continuing exegesis of the works of Sir Karl Popper (Feb 14, p 387). Popper has written extensively and clearly about what makes a theory scientific and on how we can choose strategies of acquiring knowledge that are more likely to increase our useful information about the natural world. Nevertheless he must feel like changing his name by deed poll when he reads the beliefs attributed to him-citing Popper has become like citing scripture. Popper’s theories like the scientific theories he discusses are provisional, open to doubt, and ultimately flawed; nobody in the scientific world has absolute knowledge. Dr Davies (March 14, p 630) states "theories can be refuted but confirmed whereas diagnoses can be confirmed but not excluded". I do not think life is quite so straightforward. In a world where the predictions from a theory always come with confidence limits attached, any particular theory may be less or more reasonable not
believe in but absolute refutation is as nonsensical as believing in absolute confirmation. Secondly, new experimental data can be in keeping with the predictions of a certain theory, and in this everyday sense they confirm it, even though they do not prove it correct. I find it worrying that a radiologist doubts whether a diagnosis can ever be excluded, since this will no doubt increase even further the length of X-ray reports. Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne JONATHAN REES to
A computerised tomographic (CT) scan with contrast revealed mild cerebral atrophy and lumbar puncture was unremarkable. On Dec 26 he had two grand mal seizures. There were no focal deficits apart from slight unsteadiness during tests of cerebellar function and hyperreflexia. AZT was discontinued and phenytoin was prescribed. Thereafter the patient was alert, oriented, and had no focal motor or sensory neurological deficits, and no memory deficit apart from inability to recall the seizures. The seizures were attributed to AZT and phenytoin was discontinued. On day 5 the patient had septic shock with gastrointestinal bleeding and disseminated intravascular coagulation. His mental status gradually deteriorated and he died on day 14. The patient had no history of alcohol abuse, had not been treated by dialysis, and had not received intravenous hyperalimentation before death. Necropsy findings (restricted in this letter to those in the brain) included symmetrical bifrontal cortical atrophy and symmetrical petechial haemorrhages in coronal sections occupying most of the cross-sectional area of both mammillary bodies. The haemorrhages were acute, though there was moderate reactive astrocytic gliosis in the region of the mammillary bodies and the deep grey structures adjacent to the third ventricle. There was a focus of anoxicischaemic neuronal change in the thalamus; bilateral necrotic lesions in the pontine tegmentum; reactive gliosis throughout the pons and midbrain tegmentum; and patchy but focally severe reactive gliosis in the subcortical white-matter of the centrum semiovale. The necropsy findings were typical of acute Wernicke’s encephalopathy. The gliosis found in the periventricular and periaqueductal regions suggests that the disease may have been of longer duration, but subcortical gliosis is often found in patients with AIDS and this finding must be interpreted with caution.2 The presence of focally severe subcortical gliosis suggests, but does not prove, that there was primary infection of the central nervous system by HIV.2 This patient had none of the known risk factors for Wemicke’s encephalopathy3 and the diagnosis was not entertained before he died.4 The mammillary body haemorrhage may have been exaggerated by the preterminal coagulopathy.5 Treatment with AZT may have aggravated the tendency for Wernicke’s encephalopathy to develop. This case confirms previous clinical evidence of AZT neurotoxicity:6 grand mal seizures developed soon after AZT treatment began and ended when the drug was discontinued. AZT selectively interferes with the function of DNA polymerase in the synthesis of viral DNA. Cerebral DNA synthesis is significantly impaired in rats fed a diet deficient in thiamine and these animals have a syndrome similar to Wernicke’s encephalopathy.8 Thus a drug that impairs DNA synthesis might increase the likelihood of Wemicke’s encephalopathy in a
susceptible patient.
920 Wernicke’s encephalopathy should be considered in the differential diagnosis of the many AIDS patients who present with
clinically non-specific neurological syndromes. Department of Pathology, UCLA Medical Center, Los Angeles, California 90024, USA
DAVID G. DAVTYAN HARRY V. VINTERS
1. Torvik A. Two types of brain lesions in Wemicke’s encephalopathy. Neuropathol Appl
Neurobiol 1985; 11: 179-90. 2. Navia BA, Cho E-S, Petito CK, Price RW. The AIDS dementia complex II: Neuropathology. Ann Neurol 1986; 19: 525-35. 3. Reuler JB, Girard DE, Cooney TG. Current concepts: Wernicke’s encephalopathy. N Engl J Med 1985; 312: 1035-38. 4. Marx JA. The varied faces of Wernicke’s encephalopathy. J Emerg Med 1985; 3: 411-13. 5. Jagadha V, Deck JHN, Halliday WC, Smyth HS. Wernicke’s encephalopathy in patients on peritoneal dialysis or hemodialysis. Ann Neurol 1987; 21: 78-84. 6. Hagler DN, Frame PT. Azidothymidine neurotoxicity. Lancet 1986; ii: 1392-93. 7. Anon. Azidothymidine for AIDS. Med Letter Drugs Ther 1986; 28: 107-09. 8. Henderson GI, Schenker S. Reversible impairment of cerebral DNA synthesis in thiamine deficiency. J Lab Clin Med 1975; 86: 77-90.
HIV AND HBV INFECTION IN DRUG ABUSERS IN GLASGOW
SIR,-Glasgow has a large drug-abusing population, conservatively estimated at 7000.1 Despite its proximity to Edinburgh, where at least 38% of drug abusers have evidence of human immunodeficiency virus (HIV) infection,2,3 the prevalence of anti-HIV seropositivity in Glasgow-based drug abusers in 1985 was under 1%." In 1986, over 3000 specimens were submitted to our laboratory by clinicians for an HIV antibody test. 960 specimens were from patients who were drug addicts or abusers, and 59 (6-1%) specimens were repeatedly positive in an ELISA test (Wellcome) confirmed by western blot (Dupont) with three specific bands as the criterion of positivity. 31 of these 59 cases were based within the city of Glasgow. The remaining 28 were from Edinburgh or Dundee, and blood samples had been sent to us from prisons or drug rehabilitation centtes in west and central Scotland. Of the 31 HIV antibody-positive drug abusers from within Glasgow 18 were male and the average age was only 21. 27 (87 %) had markers of current or past hepatitis B virus (HBV) infection. Increasing numbers were found within Glasgow as the year , progressed-20 were detected in the last quarter of the year, the proportion in these months reaching over 6 % of those tested (table). Evidence of infection was noted in all areas of Glasgow where drug abuse is a recognised problem. The spread of infection was not uniform, and clustering of cases in certain areas suggested that in these areas the level of positivity was likely to be over 6%. Previous samples taken in 1985 or 1986 were available from 15 of the 31 antibody-positive cases. 2 were positive for HIV antibody but had not been tested because only an HBV status had been requested. The remaining 13 were negative for HIV antibody by the ELISA test. A test for HIV antigen (Abbott) in 8 specimens, which had been taken no more than 6 months before the first positive HIV antibody finding, was positive in 3. This finding indicates that HIV infection in this group follows a course similar to that in homosexuals5 and haemophiliacs;6 and also confirms that even antibody-negative blood from such high-risk individuals is potentially hazardous, and that they and their associates must be dissuaded from donating blood. The number of antibody-positive drug abusers within the city of Glasgow has risen from under 1 0 % in 1985 to over 6 % at the end of 1986. There is evidence that many of the positive cases were infected in 1986 and were not more distant infections undetected until 1986-ie, HIV infection became established within the city’s drug-abusing population in 1986. Compared with HIV antibodypositive drug abusers in Edinburgh,those in Glasgow are much HIV ANTIBODY IN DRUG ABUSERS IN
1986
younger, including 2 aged 16 and 2 aged 17. Exposure to HBV in the positive group is high, which suggests that the group are sharing needles widely and/or are highly promiscuous. A similar high level of exposure to HBV was noted in HIV antibody-positive abusers in
Edinburgh.2z It has been suggested that there is less sharing of needles in Glasgow than in Edinburgh.7 Examination of sera from 290 HIV antibody-negative abusers from Glasgow in the first four months of 1986 for HBV markers indicated exposure to the virus in 200 (69 %). This proportion is almost identical to that in a similar Glasgow group in 19854 and exceeds figures (45 and 51 %) reported in HIV antibody-negative abusers by the two Edinburgh laboratories.2,8 The mechanisms that spread HBV infection in Edinburgh may be operating even more powerfully in Glagow. It was perhaps inevitable that HIV infection should appear in the city’s drug-abusing population but it is nevertheless disappointing. A major effort will be required if further spread of the infection is to be checked. We are particularly concerned at the number of young females with evidence of infection. Several admit to prostitution and hence are a potential source of spread outside the drug-abusing population. In addition, there is considerable risk to such females and their offspring if they become pregnant. Regional Virus Laboratory, Ruchill Hospital, Glasgow G20 9NB
E. A. C. FOLLETT L. A. WALLACE E. A. B. MCCRUDEN
1. HIV infection in Scotland. Report of Scottish committee on HIV infection and intravenous drug misuse. Edinburgh: Scottish Home and Health Department, 1986. 2. Peutherer JF, Edmond E, Simmonds P, Dickson JD, Bath GE. HTLV-III antibody in Edinburgh drug addicts. Lancet 1985; ii: 1129-30. 3. Robertson JR, Bucknall ABV, Welsby PD, et al. Epidemic of AIDS-related virus (HTLV-III/LAV) infection among intravenous drug abusers. Br Med J 1986; 292: 527-29. 4. Follett EAC, McIntyre A, O’Connell B, et al. HTLV-III antibody in drug abusers in the West of Scotland: The Edinburgh connection. Lancet 1986; i: 446-47. 5. Goudsmit J, deWolf F, Paul DA, et al. Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic infection. Lancet 1986; ii: 177-80. 6. Allain J-P, Laurain Y, Paul DA, Senn D. Serological markers in early stages of human immunodeficiency virus infection in haemophiliacs. Lancet 1986; ii: 1233-36. 7. Robertson JR, Bucknall ABV, Wiggins P. Regional variations in HIV antibody seropositivity in British intravenous drug users. Lancet 1986; i: 1435-36. 8. Burns SM, Hargreaves FD, Collacott IA, Inglis JM. Incidence of hepatitis B markers in HIV seropositive and seronegative drug misusers. Comm Dis Scot 1987; 21: 7-8.
SYRINGE EXCHANGE
SIR,-Dr Marks and Mr Parry (March 21,
p 691) report their experience with a needle/syringe exchange programme. Such schemes are now being widely discussed as a means of preventing the spread of human immunodeficiency virus (HIV).1-3 I am concerned lest there be uncritical acceptance of such programmes, whose effect on the prevention of AIDS is unproven and whose influence upon drug misuse is unknown. I accept the potential benefits of needle exchange, as outlined by Marks and Parry- and others1,;! and will comment here only on potentially adverse effects. The supply of needles and syringes may increase the incidence of drug misuse, by detracting attention from its other dangers, by appearing to condone injection of drugs, by making the necessary equipment more available, and by negating the beneficial discouragement provided by the fear of AIDS. Individuals using drugs sporadically or by other routes may find it easier to start injecting. The provision of clean needles does not ensure their proper use. Des Jarlais et a14 have drawn attention to the need for clean needles to be available at the crucial time, immediately after the drug itself has been obtained. Otherwise drug abusers will inject themselves with whatever needles are available (dirty if necessary). What will happen at the "shooting gallery" in Merseyside referred to by Marks and Parry which now has 6 (clean?) needles instead of 197 dirty ones? Use of shared needles has symbolic and other aspects not met by needle exchange programmes.3 Lack of availability is a reason for sharing needles/syringes but it is not the only one. The provision of needles/syringes is likely to promote a maintenance rather than an abstinence approach to treatment, and such an approach is subject to briticism 5
favourably
on