550
tract, disseminated intravascular coagulationand fatal shock. Hantavirus infection in Europe can easily be confused with various other infectious diseases, including septicaemia. I agree that hantavirus serology should be done in cases with acute renal failure but in endemic regions this investigation should also be done liberally for acute febrile illnesses of unknown aetiology with only slightly or moderately impaired renal function and/or thrombocytopenia and raised serum transferase or lactate dehydrogenase activities. Department of Infectious Diseases, University of Umeå, Regionsjukhuset, S-901 85 Umeå, Sweden
poisoning are being reported world wide,2 especially associated with imported ceramic pottery, should we not follow Food and Drug Administration recommendations3 and give high inspection priority to ceramics and make suppliers more accountable for their products? Finally, urinary delta-amino laevulinic acid, measured spectrophotometrically,4 may serve as a simple screening test if techniques to measure blood lead concentration are not readily available. Department of Medical Microbiology, Royal London Hospital London E1 2AD, UK
M. A. ZUCKERMAN
BO SETTERGREN Zuckerman MA, Savory D, Rayman G. Lead encephalopathy from an imported Toby mug Postgrad MedJ 1989, 65: 307-09. 2. Anonymous. Lead poisoning from ceramics. Lancet 1988; ii: 1358 3. US Department of Health, Education and Welfare. FDA consumer memo "glazes and decals on dinnerware". Washington, DC: Food and Drug Administration, 1979. 4. Tomokmi K, Ogata M. Simple method for the rapid determination of lead in blood by atomic absorption spectrophotometry. Analyst 1970; 18: 1534-36. 1.
J. Nephropathia epidemica in Finland: a clinical, histological and epidemiological study. Ann Clin Res 1971; 3 (suppl 8): 1-154. 2. Settergren B, Juto P, Trollfors B, Wadell G, Norrby SR. Hemorrhagic complications and other clinical findings m nephropathia epidemica in Sweden: a study of 355 serologically venfied cases. J Infect Dis 1988; 157: 380-82. 3. Launes J, Hautanen A. Nephropathia epidemica encephalitis. Acta Neurol Scand 1988; 78: 234-35. 4. Settergren B, Juto P, Trollfors B, Wadell G, Norrby SR. Clinical characteristics of nephropathia epidemica in Sweden: prospective study of 74 cases. Rev Infect Dis 1989; 11: 921-27. 1. Lahdevirta
Anticardiolipin antibody cofactor SIR,-In
Lancet paper last year! we did not adequately the work of Dr Steven Krilis and colleagues in
our
acknowledge
Australia. Before the 4th International Meeting on Antiphospholipid Antibodies, held in Sirmione, Italy, from April 9 to 11,1990, we had considered the possibility that ACA-cofactor was identical to &bgr;2-glycoprotein I, but important discrepancies made us decide that we might be dealing with two different proteins. Discussions with Krilis at Sirmione prompted me to re-evaluate some of our earlier data and do some new experiments. After my return from Sirmione my group did find support for ACA-cofactor being identical to &bgr;2-g1ycoprotein I, but two uncertainties on the anticoagulant properties of both proteins and on the binding of affinity-purified ACA to cofactor in the absence of lipid remained. When we amended our Lancet paper at proof stage we stated that ACAcofactor has properties "very similar" to those of &bgr;2-glycoprotein I, leaving room for alternatives. The Sirmione meeting and discussions there with Krilis thus stimulated a change in our opinion on the protein’s identity. I very much regret that I did not take the opportunity, when altering our paper, to give credit to Krilis and his team. In our letter of Oct 13 (p 952) we indicated that the Australian group were the first to establish the identity of ACA-cofactor; we now wish to state this explicitly. Biochemistry Department, Rijksuniversiteit Limburg, Maastricht, The Netherlands
E. M. BEVERS
1. Galli
M, Comfurius P, Maassen C, Hemker HC, de Baets MH, van Breda-Vriesman PJC, Barbui T, Zwaal RFA, Bevers EM. Anneardiolipin antibodies (ACA) directed not to cardiolipm but to a plasma protein cofactor. Lancet 1990, 335: 1544-47.
Lead exposure from lead
crystal
SIR,-Dr Graziano and Dr Blum describe the elution of lead from crystal decanters and glasses (Jan 19, p 141) and highlight the potential health hazard associated with lead compounds in glassware and ceramics. With my colleagues, I reported a 33-year-old woman who was admitted with lead encephalopathy after drinking cider over a 4 month period from a partly lead glazed mug made in Italy in 1976.1 A lead concentration of 130 pg/1 was recorded after leaving cider in the mug for 12 h (the European Community maximum is 50 Lg/1). In the UK the Pottery (Health) Special Regulations 1942 apply to both the manufacture and importation of pottery, but there are no guidelines about personal use. In addition, the Consumer Protection Act 1987 and General Safety Requirements include lead glaze recommendations but the onus is on the supplier to ensure that goods are safe. Since an increasing number of cases of lead
Spread of HIV-2 in India SIR,-in 1987, the year when HIV-1 was isolated for the first time in India, the reported number of HIV-1 infections was 145, and only 1 case of AIDS was seen. However, the detection of HIV antibodies in samples of anti-rhesus(Rh) immunoglobulin and other products derived from donated blood in 1989 indicated that HIV infection was a severe problem for the Asian subcontinent.’ Blood samples and blood products of Indian origin were screened and as a result all locally made blood products were withdrawn and destroyed. The prevalence of HIV infection in the population of India appears very low according to some reports,2,3 but the number of HIV infections in the big cities has been increasing sharply.’ So far, HIV-2 has not been observed. In December, 1990, and January, 1991, 22 serum samples from patients at the G.T. Hospital and STD Clinic (Municipal), Bombay, which had been prescreened for HIV-1 by ELISA and found to be HIV positive were analysed further at the GeorgSpeyer-Haus, Frankfurt. 1 sample could not be confirmed by western blot or immunofluorescence and must be regarded as a false positive. 16 samples were confirmed as HIV-1 positive by immunofluorescence and western blot. 4 sera (A, CE in table) showed a double reaction to HIV-1 and HIV-2 in all tests andI other sample (not shown) demonstrated clear reaction to HIV-1 but only a weak reaction to HIV-2. Further study is need to reveal whether these results are due to double infections or to doubly reactive virus types. 1 sample (B) was HIV-2 positive, this being confirmed by western blot and immunofluorescence. The patient, a 25-year-old pregnant prostitute, had inguinal lymphadenopathy, fever, jaundice, and vulvaloedema, but no neurological symptoms. All 21 HIV-positive patients were born and raised in India. Only 1 man had been abroad (Uganda), so all others must have acquired the infection locally. 1 was a 3-year-old girl, probably infected through her mother. Of the 20 adults 7 were male (18-43 years old, average 26) 13 were female (20-50 years old, average 33). 12 of the females were prostitutes; the other woman had had a blood transfusion. Only 1 of the men was homosexual; the others were heterosexual. The finding of sera doubly reactive to HIV-1 and HIV-2 and the 1 case of HIV-2 infection in this small sample is reminiscent of the situation in the Ivory Coast and AngolaS.6 and indicates that HIV-2 has probably existed for some time in India. One explanation could be the old connections between India and Africa. A high degree of variation can be expected between Indian strains and strains from other parts of the world, and possibly even among Indian strains. More HIV-2 infections are probably present than have so far been identified. That the spread of HIV-2 in India is substantial is indicated by other data. Out of 46 additional sera from the same STD clinic in Bombay not prescreened with ELISA we found 15 HIV-1 positive, 3 HIV-2 positive, and 7 doubly reactive (confirmed by western blot and immunofluorescence). Also, A. Shanmugasundararaj and colleagues have recorded HIV-2 ELISA positivity in Madurai, Tamil Nadu, though without confirmatory tests (Virus Information Exchange Newsletter, vol 5 [no 4], p 132).
tract, disseminated intravascular coagulationand fatal shock. Hantavirus infection in Europe can easily be confused with various other infectious diseases, including septicaemia. I agree that hantavirus serology should be done in cases with acute renal failure but in endemic regions this investigation should also be done liberally for acute febrile illnesses of unknown aetiology with only slightly or moderately impaired renal function and/or thrombocytopenia and raised serum transferase or lactate dehydrogenase activities. Department of Infectious Diseases, University of Umeå, Regionsjukhuset, S-901 85 Umeå, Sweden
poisoning are being reported world wide,2 especially associated with imported ceramic pottery, should we not follow Food and Drug Administration recommendations3 and give high inspection priority to ceramics and make suppliers more accountable for their products? Finally, urinary delta-amino laevulinic acid, measured spectrophotometrically,4 may serve as a simple screening test if techniques to measure blood lead concentration are not readily available. Department of Medical Microbiology, Royal London Hospital London E1 2AD, UK
M. A. ZUCKERMAN
BO SETTERGREN Zuckerman MA, Savory D, Rayman G. Lead encephalopathy from an imported Toby mug Postgrad MedJ 1989, 65: 307-09. 2. Anonymous. Lead poisoning from ceramics. Lancet 1988; ii: 1358 3. US Department of Health, Education and Welfare. FDA consumer memo "glazes and decals on dinnerware". Washington, DC: Food and Drug Administration, 1979. 4. Tomokmi K, Ogata M. Simple method for the rapid determination of lead in blood by atomic absorption spectrophotometry. Analyst 1970; 18: 1534-36. 1.
J. Nephropathia epidemica in Finland: a clinical, histological and epidemiological study. Ann Clin Res 1971; 3 (suppl 8): 1-154. 2. Settergren B, Juto P, Trollfors B, Wadell G, Norrby SR. Hemorrhagic complications and other clinical findings m nephropathia epidemica in Sweden: a study of 355 serologically venfied cases. J Infect Dis 1988; 157: 380-82. 3. Launes J, Hautanen A. Nephropathia epidemica encephalitis. Acta Neurol Scand 1988; 78: 234-35. 4. Settergren B, Juto P, Trollfors B, Wadell G, Norrby SR. Clinical characteristics of nephropathia epidemica in Sweden: prospective study of 74 cases. Rev Infect Dis 1989; 11: 921-27. 1. Lahdevirta
Anticardiolipin antibody cofactor SIR,-In
Lancet paper last year! we did not adequately the work of Dr Steven Krilis and colleagues in
our
acknowledge
Australia. Before the 4th International Meeting on Antiphospholipid Antibodies, held in Sirmione, Italy, from April 9 to 11,1990, we had considered the possibility that ACA-cofactor was identical to &bgr;2-glycoprotein I, but important discrepancies made us decide that we might be dealing with two different proteins. Discussions with Krilis at Sirmione prompted me to re-evaluate some of our earlier data and do some new experiments. After my return from Sirmione my group did find support for ACA-cofactor being identical to &bgr;2-g1ycoprotein I, but two uncertainties on the anticoagulant properties of both proteins and on the binding of affinity-purified ACA to cofactor in the absence of lipid remained. When we amended our Lancet paper at proof stage we stated that ACAcofactor has properties "very similar" to those of &bgr;2-glycoprotein I, leaving room for alternatives. The Sirmione meeting and discussions there with Krilis thus stimulated a change in our opinion on the protein’s identity. I very much regret that I did not take the opportunity, when altering our paper, to give credit to Krilis and his team. In our letter of Oct 13 (p 952) we indicated that the Australian group were the first to establish the identity of ACA-cofactor; we now wish to state this explicitly. Biochemistry Department, Rijksuniversiteit Limburg, Maastricht, The Netherlands
E. M. BEVERS
1. Galli
M, Comfurius P, Maassen C, Hemker HC, de Baets MH, van Breda-Vriesman PJC, Barbui T, Zwaal RFA, Bevers EM. Anneardiolipin antibodies (ACA) directed not to cardiolipm but to a plasma protein cofactor. Lancet 1990, 335: 1544-47.
Lead exposure from lead
crystal
SIR,-Dr Graziano and Dr Blum describe the elution of lead from crystal decanters and glasses (Jan 19, p 141) and highlight the potential health hazard associated with lead compounds in glassware and ceramics. With my colleagues, I reported a 33-year-old woman who was admitted with lead encephalopathy after drinking cider over a 4 month period from a partly lead glazed mug made in Italy in 1976.1 A lead concentration of 130 pg/1 was recorded after leaving cider in the mug for 12 h (the European Community maximum is 50 Lg/1). In the UK the Pottery (Health) Special Regulations 1942 apply to both the manufacture and importation of pottery, but there are no guidelines about personal use. In addition, the Consumer Protection Act 1987 and General Safety Requirements include lead glaze recommendations but the onus is on the supplier to ensure that goods are safe. Since an increasing number of cases of lead
Spread of HIV-2 in India SIR,-in 1987, the year when HIV-1 was isolated for the first time in India, the reported number of HIV-1 infections was 145, and only 1 case of AIDS was seen. However, the detection of HIV antibodies in samples of anti-rhesus(Rh) immunoglobulin and other products derived from donated blood in 1989 indicated that HIV infection was a severe problem for the Asian subcontinent.’ Blood samples and blood products of Indian origin were screened and as a result all locally made blood products were withdrawn and destroyed. The prevalence of HIV infection in the population of India appears very low according to some reports,2,3 but the number of HIV infections in the big cities has been increasing sharply.’ So far, HIV-2 has not been observed. In December, 1990, and January, 1991, 22 serum samples from patients at the G.T. Hospital and STD Clinic (Municipal), Bombay, which had been prescreened for HIV-1 by ELISA and found to be HIV positive were analysed further at the GeorgSpeyer-Haus, Frankfurt. 1 sample could not be confirmed by western blot or immunofluorescence and must be regarded as a false positive. 16 samples were confirmed as HIV-1 positive by immunofluorescence and western blot. 4 sera (A, CE in table) showed a double reaction to HIV-1 and HIV-2 in all tests andI other sample (not shown) demonstrated clear reaction to HIV-1 but only a weak reaction to HIV-2. Further study is need to reveal whether these results are due to double infections or to doubly reactive virus types. 1 sample (B) was HIV-2 positive, this being confirmed by western blot and immunofluorescence. The patient, a 25-year-old pregnant prostitute, had inguinal lymphadenopathy, fever, jaundice, and vulvaloedema, but no neurological symptoms. All 21 HIV-positive patients were born and raised in India. Only 1 man had been abroad (Uganda), so all others must have acquired the infection locally. 1 was a 3-year-old girl, probably infected through her mother. Of the 20 adults 7 were male (18-43 years old, average 26) 13 were female (20-50 years old, average 33). 12 of the females were prostitutes; the other woman had had a blood transfusion. Only 1 of the men was homosexual; the others were heterosexual. The finding of sera doubly reactive to HIV-1 and HIV-2 and the 1 case of HIV-2 infection in this small sample is reminiscent of the situation in the Ivory Coast and AngolaS.6 and indicates that HIV-2 has probably existed for some time in India. One explanation could be the old connections between India and Africa. A high degree of variation can be expected between Indian strains and strains from other parts of the world, and possibly even among Indian strains. More HIV-2 infections are probably present than have so far been identified. That the spread of HIV-2 in India is substantial is indicated by other data. Out of 46 additional sera from the same STD clinic in Bombay not prescreened with ELISA we found 15 HIV-1 positive, 3 HIV-2 positive, and 7 doubly reactive (confirmed by western blot and immunofluorescence). Also, A. Shanmugasundararaj and colleagues have recorded HIV-2 ELISA positivity in Madurai, Tamil Nadu, though without confirmatory tests (Virus Information Exchange Newsletter, vol 5 [no 4], p 132).
