HIV screening in pregnancy

HIV screening in pregnancy

1218 LETTERS to the EDITOR HIV screening in pregnancy SIR,-In early 19901 we reported that only 2 of 3760 women who had attended antenatal clinics a...

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HIV screening in pregnancy SIR,-In early 19901 we reported that only 2 of 3760 women who had attended antenatal clinics at St Thomas’ Hospital, London, during 1988 had antibodies to HIV-1, and none to HIV-2. None of 95 requests for named HIV tests was positive. With local ethical approval we have repeated this survey and report a sharp increase in HIV seroprevalence in 1990. In our 1988 study, samples collected for rubella serology were anonymised and tested individually. This approach is expensive and since sera can be efficiently tested in pools2 samples collected during 1990 were tested in pools of 10 by enzyme immunoassay (Abbott Laboratories HIV-1(HIV-2 EIA). Sera from positive pools were then tested individually by the same EIA, positive sera being confirmed by gel particle agglutination (’Serodia-HIV’, Fujirebio) and competitive EIA (Wellcome). All sera were anonymised before pooling except for 4 sera known to be positive as a result of named HIV testing; these were labelled and used as internal controls. The serum from the 1 patient who spontaneously objected to her serum being anonymously tested for HIV antibodies excluded. Of 4106 sera collected during 1990, 18 (0-44%) contained antibodies to HIV-1and none to HIV-2-a nine-fold increase over a similar population attending two years earlier (table). 4 of these sera were already known to be HIV positive (3 from named testing in the genitourinary medicine clinic and 1 from only 52 requests for named HIV tests originating in the antenatal clinics). One of the positive pools contained 2 positive sera, emphasising the necessity to test component sera of pools individually. If all 18 pregnancies had continued to term there would, on average, have been 1 HIVpositive delivery every three weeks at St Thomas’ Hospital last year. This increase in HIV has not been matched by hepatitis B virus infection; the HBsAg prevalence rate has been static, at about 1 %, from 1988 to 1990. This makes it unlikely that the increase in HIV infection is linked to an increase in intravenous drug abuse. An increase in the rate of heterosexual transmission seems more likely. In our previous report we stated that the difference between the low prevalence (0-05%) that we and Peckham et aP had reported in two areas of inner London and the higher prevalence reported in City and Hackney Health District (0-55 %)4 illustrated the importance of testing large numbers of patients in different areas of large cities. The above results also emphasise the need for continuing surveillance. We intend to continue surveying our antenatal clinic population annually. Future studies must try to include such epidemiological data as ethnic origin and HIV risk group, without compromising anonymity or the current very low spontaneous was


*p<0001 t3 other sera identified as HIV positive by named testing clinic t132 sera had insufficient volume for HBsAg testing


genitourinary medicine

Our findings should alert health-care workers who in contact with blood and other body fluids to the importance of infection control measures. They also need to be considered in plans for HIV-related services in the district. It is essential that surveillance is sustained and properly funded. Only with reliable epidemiological data can the future HIV-specific requirements of a community be forecast and provided for. J. E. BANATVALA I. L. CHRYSTIE S. J. PALMER D. SUMNER Departments of Virology and Obstetrics, J. KENNEDY St Thomas’ Hospital, London SE1 7EH, UK A. KENNEY

objection rate. are

1. Banatvala

JE, Chrystie IL, Palmer SJ, Kenney A. Retrospective study of HIV, hepatitis B, and HTLV-I infection at a London antenatal clinic Lancet 1990; 335:

859. 2. Mawson S, Skidmore S, Pandov H, Desselberger U Anonymous testing for HIV infection. Lancet 1990; 335: 858. 3. Peckham CS, Tedder RS, Briggs M, et al. Prevalence of maternal HIV infection based on unlinked anonymous testing of newborn babies. Lancet 1990; 335: 516-19. 4. Heath RB, Grint PCA, Hardiman AE. Anonymous testing of women attending antenatal clinics for evidence of infection with HIV Lancet 1989; i 1394.

SIR,-Dr Barbacci and her colleagues assert (March 23, p 709) that a screening programme directed to pregnant women with risk factors for HIV infection attending their Baltimore clinic would have detected only 57% of HIV-seropositive women and that by offering counselling and HIV testing to all women attending, the detection rate was increased to 87%. These figures overestimate the true detection rates and there is no evidence that the rate was improved by expanding the screening programme. The fallacy arises through the incorrect choice of denominator for the detection rate-namely, women found to be seropositive by voluntary or anonymous testing. An estimate of the number of seropositives among women not tested should also be included. If the women tested anonymously were a random sample of all women not tested voluntarily (this is not clear), this number can be estimated for the first phase of the study (February, 1987, to October, 1988) as (0/31) x 48 + (6/321) x 751 = 14. This gives an estimated detection rate for a screening policy targeted to high-risk women of 20/(29 + 14) = 47% or 29/(29+14)=67% if low-risk women who request testing are all included. Similarly, a policy of offering voluntary testing to all women in the second phase of the study (November, 1988 to May, 1990) gave an estimated detection rate of 46%, although this figure is unreliable because of the small number of women tested anonymously during this phase. A better indicator of the change in detection rate after extension of screening is the number of women identified as seropositive as a proportion of all women enrolled. This was 2-5% (29/1160) during the period of targeted screening and 2-5% (39/1564) during the period of universal screening. On the assumption that the HIV seroprevalence rate among antenatal attenders was not decreasing, the detection rate from targeted screening during the first phase was as successful as that achieved by universal screening during the second phase. The reasons for this seem to be that during the first phase, a high proportion (21 %) of women without acknowledged risk factors nevertheless requested HIV testing, a high proportion (4-5%) of whom were seropositive; and that during the second


high level of seropositivity (6/58) was observed among Anonymous testing of more of the low-risk women in the second phase would have provided valuable information, since confirmation of the high observed seroprevalence rate (12-5%) would have important consequences for the sensitivity of a voluntary screening policy.



women who declined to be HIV tested.

Department of Epidemiology and Population Sciences, London School of Hygiene and Tropical Medicine, London WC1 E 7HT, UK


SIR,-Several UK hospitals are doing epidemiological studies, under the aegis of the Central Public Health Laboratory, Colindale, to find out the incidence of HIV infection in pregnant women. The testing is anonymous, and the only information recorded about the women is their racial origin. At St George’s Hospital, London, we book about 3500 women a year in the antenatal clinic (deliveries in 1990 were 3156). In the past fourteen months, we have tested blood samples from 4070 clinic attenders. 11were seropositive to HIV by the Abbott recombinant HIV-l/HIV-2 enzyme immunoassay. These positive tests were confirmed by the Central Public Health Laboratory. 2 other samples positive in our laboratory have not yet been checked. If they too are confirmed the seroprevalence rate will be 0-32%. We also have a high prevalence of hepatitis B carriage in our women (0-7%) and the data on HIV positivity accord with this. The seroprevalence rates are similar to those published by Heath et al from St Bartholomew’s Hospital in 1988.1 In 1987, we tested some 3000 antenatal women under the same conditions and found not 1 HIV seropositive. Thus, a substantial number of women booking at our clinics are seropositive to HIV. We also offer HIV testing on request and about 60 pregnant women were so tested in 1990, all being counselled before blood was taken. Only 2 were positive: on the assumption that these 2 were in the anonymous testing group, also, that would yield 11 other HIV-seropositive women about whom we did not know. These data have implications for the management of labour and post-partum care of mother and baby. Precautions against accidental infection of staff need to be tightened. We plan to increase the opportunities for women to be tested openly, but that means the provision of more counsellors in the antenatal clinics and increased resources in the virology laboratory. GEOFFREY CHAMBERLAIN

Departments of Obstetrics and Medical Microbiology, St George’s Hospital, London SW17 0RE, UK


1. Heath RB, Grint PC, Hardiman AE. Anonymous testing of women attending antenatal clmics for evidence of infection with HIV. Lancet 1988; i: 1394.

SIR,-Dr Barbacci and colleagues argue in support of HIV antibody testing as a part of routine antenatal care. Such testing is already widespread, though in most areas it is of doubtful cost-benefit. As testing becomes more routine the associated counselling is likely to become truncated or non-existent. In my view Barbacci’s data can be interpreted as showing lack of value in extending HIV antibody testing to all women attending for antenatal care. Barbacci et al report that in Baltimore in the period before November, 1988, HIV antenatal screening, if restricted to women with a history of HIV risk, would have identified only 57% of HIV-seropositive women. Because testing was also made available to women without risk factors who wished to be tested, their programme in fact identified 83% of the HIV-positive women. (The remaining 17% were revealed by anonymous screening.) About one-third of women registering for antenatal care had a voluntary test for HIV. In November, 1988, a system which could be described as routine HIV antenatal testing was introduced; the number of voluntary HIV antibody tests increased to 76% and the proportion of all infected women who were identified in the voluntary programme rose to 87%. This increase in the yield of the voluntary programme (from 83% to 87%) was not significant. From November, 1988, among the women without risk factors

who declined testing a greater proportion were HIV positive than had been so earlier (6 out of 321 declining testing in the earlier period compared with 5 out of 40 in the later one). This decline in acceptance of HIV screening by women denying risk factors is significant (p<0001, X2). Perhaps women at risk in the earlier period had been prepared to accept testing though denying their risk status. The perceived hint of compulsion inherent in the later programme may have made such women more concerned about the consequences of a positive result. Either way in the high-risk Baltimore population, in which 4% of women are HIV positive, a sufficiently large number of HIV-positive women without risk factors will ask for HIV testing when this is not routine, so that the expansion of the programme does not appreciably increase the number of women testing positive. What is most important is the finding that a restriction of a programme to women with an identifiable risk factor, without extending it to other women requesting testing, would seriously underestimate the number of HIV-positive women. Fortunately, it is not the usual practice in which a truly voluntary programme is in place, for HIV testing not to be offered to any woman requesting it. It would be unfortunate ifBarbacci and colleagues’ interpretation that antenatal testing should be routine were to be extended from their high-risk population to low-risk populations such as most women in non-urban United States and women in Australia. Department of Immunology/Allergy, Prince of Wales Children’s Hospital,


Randwick, NSW 2031, Australia

Thrombotic thrombocytopenic purpura and

ticlopidine and

SIR,-Dr Page colleagues report (March 30, p 774) thrombotic thrombocytopenic purpura (TTP) after treatment with ticlopidine. Their finding contrasts with our experience1 and that of others2.3 that ticlopidine is beneficial in the treatment of TTP. We have seen two patients who after reaching complete remission with high-dose ticlopidine (750 mg daily) have been maintained at 250-500 mg daily for 38 and over 39 months, respectively, without relapse. It is difficult to explain the development of TTP after ticlodipine, which is known for its potent and unusual antiaggregating effect. TTP is usually a disease of the young adult, most commonly arising between age 30 and 40; curiously, three of Page and colleagues’ four patients were over 70. Perhaps these patients’ older age associated with impaired vascular conditions may have played a part in the pathophysiology of ticlopidine-associated TTP. We believe that these conflicting data are too few for the conclusion to be drawn that ticlopidine should not be used in patients with TTP.

Institute of Haematology "L. e A. Seràgnoli", Policlinico S Orsola, 40138 Bologna, Italy


L, Mattioli Belmonte M, et al. Ticlopidine in the treatment of thrombotic thrombocytopenic purpura: report of two cases. Haematologica 1990;

1. Vianelli N, Catani

75: 274-77. 2. De Pasquale A, Venturoni LF, Paterlini P, et al. Possible usefulness of ticlopidine in combined treatment of thrombotic thrombocytopenic purpura: report of one case. Haematologica 1986; 71: 53-55. 3. Ishii Y, Ebata H, Satoh K. A case of thrombotic thrombocytopenic purpura, successful treatment by ticlopidine. Clin Hematol 1984; 25: 1097-102.

Ketanserin for hypertension after upper

gastrointestinal surgery SIR,-Dr Mikulic and colleagues (April 20, p 976) demonstrate

efficacy of ketanserin in the treatment of hypertension after gastrointestinal surgery. I disagree with their statement that the hypotensive action of ketanserin is attributable to its ability to act as an antagonist at peripheral postsynaptic serotonin (5-HT2) receptors. Ketanserin is not a specific antagonist at the 5-HTz the