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Pain relieving medicines such as aspirin or ibuprofen are used forheadache, pain, and arthritis. Prolonged use of these medicines isknown to harm the gastric mucosa. If used by a person withpre-existing ulcer, the damage can be serious and cause severebleeding. Doctors warn patients and take necessary precautions. Ihave noticed a preparation, Vendana Nigraha Rasa, which isrecommended for pain relief by several lay people. These words areSanskrit (ancient Indian language), and vendana means pain,nigraha determination, and Rasa juice. The Sanskrit words give afalse sense of the product being Ayurvedic and hence herbal andsafe. Actually, its main ingredients are aspirin (530 mg) andparacetamol (100 mg). Like other Ayurvedic preparations the drugis effective, which is not surprising since it contains almost doublethe quantity of aspirin used in normal aspirin tablets. I am aware ofone educated patient, with known duodenal ulcer, who had startedtaking this medicine for headache, believing it to be Ayurvedic anddespite the facts that it is labelled as containing 530 mg aspirin and100 mg paracetamol and that he had been instructed by his doctor torefrain from all pain-relieving medications like aspirin.

In a survey of pharmacies, I have not come across any other suchmisbranded medications. Doctors, patients, and law-enforcingauthorities should take a note of this warning and patients shouldascertain that the Ayurvedic medicines they are taking do notcontain anything other than Ayurvedic medicine.

Clinical Pharmacology,Seth G. S. Medical College,K. E. M. Hospital,Parel, Bombay 400 012, India N. A. KSHIRSAGAR

1. Dandekar UP, Chandra RS, Dalvi SS, et al. Analysis of a clinically importantinteraction between phenytoin and Shankhapushpi, an Ayurvedic preparation.J Ethnopharmacol 1992; 35: 285-88.

Lack of association between myelin basicprotein gene microsatellite and multiple

sclerosis

SIR,-Dr Rose and colleagues (May 8, p 1179) report that atetranucleotide repeat polymorphism, 5’ to the myelin basic protein(MBP) gene, is not genetically linked with familial multiple sclerosis(MS). This finding is in contrast to previous population-basedstudies by Boylan et al and Tienari et al2 and their co-workers, inwhich this locus was shown to be associated with MS. The Finnish

study2 also demonstrated linkage in families said to have clinicalMS. However, both these studies used a low resolution technique totype a complex tetranucleotide repeat polymorphism, and thusalleles assigned the same fragment length may be geneticallyheterogeneous. This difficulty was recognised by Boylan et al.3 Amuch improved method for typing this polymorphism has since

ALLELE FREQUENCIES FOR A AND B LOCI OF MBP GENE INHEALTHY CONTROLS AND PATIENTS WITH MULTIPLE

SCLEROSIS

bp=base-pairs. xZ-test. locus A, p=060, locus B, p=0-34.

been reported.4 This procedure enables accurate discrimination ofallele sizes for a pair of tetranucleotide repeats at the 5’ end of thiscomplex repeat, and is the method used by Rose and colleagues.We have also used this refined method to type alleles of the A and

B loci of this MBP marker in 122 unrelated patients with clinicallydefinite MS from neurology clinics in Belfast and Coleraine and 106blood donor controls.5 The table shows the allele frequencies forboth the A and B loci in the healthy and MS populations. Thefrequencies for all the alleles of both markers are very similar in thetwo populations and there is no allelic association with MS. Analysisof genotype frequencies in both groups also failed to reveal anygenotypic association with MS.Thus this study, in the Northern Ireland MS population,

confirms the work of Rose and colleagues, and infers that the myelinbasic protein gene is not a candidate for conferring susceptibility toMS.

This work is supported by the Multiple Sclerosis Society of Great Britainand Northern Ireland.

Regional Genetics Service,Belfast City Hospital,Belfast BT9 7AB, UK

C. A. GRAHAMC. W. KIRKN. C. NEVIN

Department of Neurology,Royal Victoria Hospital,Belfast

A. G. DROOGANS. A. HAWKINS

Department of Immunology,Belfast City Hospital

S. A. MCMILLANT. A. MCNEILL

1. Boylan KB, Takahashi N, Paty DW, et al. DNA length polymorphism 5’to the myelinbasic protein gene is associated with multiple sclerosis. Ann Neurol 1990; 27:291-97.

2. Tienan PJ, Wikstrom J, Sajantila A, et al. Genetic susceptibility to multiple scelrosislinked to myelin basic peotein gene. Lancet 1992; 340: 987-91.

3.Boylan KB, Ayres TM, Popko B, et al. Repetitive DNA (TGGA)n 5’ to the humanmyelin basic protein gene: a new form of oligonucleotide repetitive sequenceshowing length polymorphism. Genomics 1990; 6: 16-22.

4. Polymeropoulos MH, Xiao H, Merril CR. Tetranucleotide repeat polymorphism atthe human myelin basic protein gene (MBP). Hum Mol Genet 1992; 1: 658.

5. Hughes AE. Optimization of microsatellite analysis for genetic mapping. Genomics1993; 15: 433-34.

AIDS predictions in the UK

SIR,-In his table (April 3, p 898) Professor Stewart gives hisown predictions for new AIDS cases for 1991 and 1992, implyingthat he made them in 1989 and citing his article CommunicableDiseases (Scotland) Weekly Report 1991/24. This article contains nosuch prediction. Stewart now indicates (May 15, p 1287) that thereference in his table should have been to a PHLS working group’sreport published in 1990 and that he should have cited anotherpaper of his Commun Dis (Scotland) Wkly Rep 1990/33. Thesereferences do not contain Stewart’s 1989 predictions either. In hissecond letter Stewart tells us to whom he had circulated hiscalculations but are they published or not?

Communicable Diseases (Scotland) Unit,Ruchill Hospital,Glasgow G20 9NB, UK DAVID GOLDBERG

Department of Infection and Tropical Medicine,Ruchill Hospital, Glasgow STEPHEN T. GREEN

Author’s replySIR,—In Communicable Diseases (Scotland) Weekly Report

1990/33, wrote: "These findings support the view that AIDS iscontinuing its spread in Scotland as in the remainder of the UKfrom 1982 in accordance with simple linear projections... The datado not support predictions that there is an extensive spread of AIDSby heterosexual transmission, or that an epidemic with this patternof transmission is imminent in the UK" It should be obvious to Dr

Goldberg and Dr Green, as epidemiologists, that projections of theincidence of AIDS made by linear regression early in 1990 dependon data for 1982-89. The (largely erroneous) predictions by thesymposium of the Royal Societyl were printed in 1990 and it is amatter of available record that my comments and suggestedcorrections were submitted to that society and others soon after.

It is strange that Goldberg and Green are so interested in mydates rather than my data. However, later in that 1990 paper, they

1597THE LANCET

will read: "Prediction and strategy for control are impeded by lackof some essential data". This is why there is widespread andcontinuing confusion as to whether or not AIDS is extendingbeyond risk groups to the general population. Data from officialsurveillance units, including theirs, are being presented in a mannerwhich suggests that it is. If so, we should by now be seeing typicalcases of AIDS in at least a few women and girls who are not engagedin risky behaviour, and in infants born to them.

Glenavon,Clifton Down,Bristol BS8 3HT, UK GORDON T. STEWART

1. Cox DR, Anderson RM, Hillier HC, eds. Epidemiological and statistical aspects of theAIDS epidemic. Phil Trans R Soc Lond (B) 1989; 325: 37-187.

SiR,—In not accepting our explanation (May 15, p 1286) for thedifference between the November, 1988, and January, 1990,forecasts for AIDS incidence in England and Wales-namely, aslowing down in the rate of transmission ofHIV among homosexualmen-Professor Stewart (p 1287) states that we are not reading thedata correctly. The data he cites are misleading or irrelevant and hisline of argument is contradictory.

Stewart uses quarterly surveillance datal to suggest that newreports of AIDS in homosexual men increased by 62% (from 785 to1268) in late 1987 to early 1988, and that there was subsequently afurther rise of 50%. He arrived at these numbers by comparingreported AIDS cases in homosexual/bisexual males for the UK in1986 and 1987 (785) with reports for 1988 and 1989 (1268) and for1990 and 1991 (1907). Grouping data in this way obscures theunderlying trend. The figure summarises data for England andWales (excluding visitors). Locally weighted scatter plotsmoothingz illustrates the slowing of the rate of increase in AIDSincidence in homosexual/bisexual males, beginning in 1987 andbecoming more striking in 1988. The trend in total AIDS incidencereflects this change.

Stewart also implies that our statement could be based upon the"impressive 30% drop in the number of homosexual men

serotesting positively for HIV in late 1987 to early 1988". This dropis largely irrelevant because the long incubation period of 10 years ormore between HIV-1 infection and AIDS onset results in a

complex relation between the time of HI V-1 infection diagnosis andAIDS incubation period. In a symptom-free person diagnosis ofHIV-1 infection depends on factors such as risk recognition,willingness to have an HIV-1 test, and test accessibility, all of whichchanged during the 1980s. The amount of HIV-1 testing, theproportion found infected when first having an HIV-1 test, and thenumbers of HIV-1 infections diagnosed among homosexual/bisexual men between 1985 and 1989, are a poor guide to theunderlying incidence of HIV-1 infections and should not be used tointerpret the AIDS incidence curve directly.

Incidence of AIDS cases in England and Wales by quarter ofdiagnosis.

*See text. Homo/bi = homosexual/bisexual.

We find a contradiction in Stewart’s statement that the sharp risein (AIDS) reports in 1987-88 was statistically merely a blip. Theeffect of the introduction of the 1987 expanded AIDS casedefinition was much less in England and Wales than elsewhere anddid not result in a sharp rise in incidence among homosexual/bisexual men (figure). Stewart does not successfully refute thestatement that the principal reason for the difference between the19883 and 19904 forecasts was the reduction in HIV transmission

among homosexual/bisexual men in the mid-1980s, the extent ofwhich only became apparent between the reports.

Public Health Laboratory Service AIDS Centre,Communicable Disease Surveillance Centre,London NW9 5EQ, UK

O. NOEL GILLK. PORTERDANIELA DE ANGELISC. L. R. BARTLETT

MRC Biostatistics Unit,Institute of Public Health,Cambridge N. E. DAY

1. AIDS-HIV Quarterly Surveillance Tables, no 18, data to end December 1992.London: Public Health Laboratory Service, AIDS Centre, and the CommunicableDiseases (Scotland) Unit, 1993.

2. Chambers JM, Cleveland WS, Kleiner B, Tukey PA. Graphical methods for dataanalysis. Boston: Wadsworth International and Duxbury Press, 1983.

3. Department of Health and the Welsh Office. Short-term prediction of HIV infectionand AIDS: report of a working group (Chairman, Sir David Cox). London: HMStationery Office, 1988.

4. Acquired immune deficiency syndrome (AIDS) in England and Wales to the end of1993. Report of a working group convened by the Director of the Public HealthLaboratory Service (Chairman, Professor N. E. Day). London: Public HealthLaboratory Service, 1990.

Opportunistic infections and CD4lymphocytopenia with interferon treatment

in HIV-1 infected patientsSIR,-Dr Vento and colleagues (April 10, p 958) reported a

decline of CD4 cells after interferon (IFN) treatment in HIV-1infection. We recently observed two cases of such cytopeniacomplicated by opportunistic infections.

Case 1 was a female intravenous drug user, 32, and seropositivesince 1987. IFN treatment (IFN<x-2a, Roferon, Roche) was startedin August, 1992, for chronic viral hepatitis C. Alanineaminotransferase (ALT) was 69 IU/L, CD4 cells 310/L, andserum p24 antigen was negative. Three months later, the patienthad fever and headache which led to the diagnosis of cerebraltoxoplasmosis with multiple cerebral abscesses. CD4 cells were130/L, and serum p24 antigen was strongly positive (242 pg/ml).ALT was normal. IFN treatment was stopped. The patient ispresently well and taking zidovudine, with a CD4 cell count of90/mm3.

Case 2 was a male intravenous drug user, 32, and seropositivesince 1986. IFN was started in February, 1993, for chronic viralhepatitis C. ALT was 180 IU/L, CD4 cells 600/uL, and serum p24antigen was negative. Six weeks later, the patient was febrile, withperineal pain and oral candidosis. Biopsy and culture of anal ulcersshowed anorectal tuberculosis. CD4 cells were 134/L and serump24 antigen was negative. ALT was 72 IU/L. The patient is nowwell and taking four antituberculous antibiotics and zidovudine.None of Vento’s three patients developed AIDS during IFN

therapy. We report here 2 cases of opportunistic infections

occurring after 3 months and 6 weeks, respectively, of IFN given forchronic viral hepatitis C in intravenous drug using seropositivepatients. Most HIV-positive intravenous drug users are alsoinfected by hepatitis C virus. IFN treatment in these patients musttake into consideration the CD4 cell count and HLA haplotypes.1,2

Departments of Internal Medicineand Haematology,

H&ocirc;pital Cimiez,University of Nice-Sofia Antipolis,06003 Nice, France

A. PESCEE. ROSENTHALH. VINTI

B. TAILLANG. GARNIERP. DUJARDIN

J. P. CASSUTO

1. Kaslow RA, Duquesnoy R, VanRaden M, et al. A1CW7B8DR3HLA antigencombination associated with rapid decline of T-helper lymphocytes in HIV-1infection. Lancet 1990; 335: 927-30.

2. Mallal S, Cameron PU, French MAH, Dawkins RL. MHC genes and HIV infections.Lancet 1990; 335: 1591-92.