567

CALCULATED EFFECT OF IMPLEMENTING PROPOSED SCREENING

TEST FOR PREGNANCIES IN WOMEN AGED 20-49

*Number of non-DS pregnancies subjected to amniocentesis was calculated from thenumber of non-DS births that were test-positive corrected by the fetal loss rate of 3 2%after 16 weeks’ gestation.’

due to amniocentesis (1 %, the estimate of the Copenhagen group;"and 0,5%, that reported in five major studies from the USA andWestern Europe6). The number of D S births detected in

. midtrimester is greater than the number of non-DS fetuses

spontaneously aborted when the 0-5% risk figure is used, but thisorder is reversed for the 1 % fetal loss rate. Thus the decision aboutwhether to introduce mass screening for D S based on maternal ageand MSAFP depends upon what risk from amniocentesis is used inthe calculations. Unfortunately, there is considerable variation inreported fetal loss rates due to amniocentesis.6 It is not yet possibleto give unqualified approval to a mass screening programme.However, this does not mean that published risk tablesl-3 may not beused to counsel individual women whose MSAFP has beenmeasured.

Biological Materials AnalysisResearch Unit,

Department of Biological Sciences,University of Salford,Salford M5 4WT

R. P. AGERR. W. A. OLIVER

1 Palomaki GE, Haddow JE. Maternal serum &agr;-fetoprotein, age, and Down syndromerisk. Am J Obstet Gynecol 1987; 156: 460-63.

2. Cuckle HS, Wald NJ, Thompson SG. Estimating a woman’s risk of having apregnancy associated with Down’s syndrome using her age and serum alpha-fetoprotein level. Br J Obstet Gynaecol 1987; 94: 387-402.

3 Tabor A, Larsen SO, Nielsen J, et al. Screening for Down syndrome using an iso-riskcurve based on maternal age and serum alpha-fetoprotein level. Br J ObstetGynaecol 1987; 94: 636-42.

4. Houlsby WT Maternal serum AFP as screening test for Down syndrome. Lancet1984; i: 1127.

5 Cuckle HS, Wald NJ, Lindenbaum RH. Maternal serum alpha-fetoproteinmeasurement: a screening test for Down syndrome. Lancet 1984; i: 926-29.

6. Ager RP, Oliver RWA. The risks of midtrimester amniocentesis. Bramhall: HarboroPublications, 1986.

7. Hook EB, Chambers GM. Estimated rates of Down syndrome in live births by oneyear maternal age intervals for mothers aged 20-49 in a New York State study:Implications of the nsk figures for genetic counselling and cost-benefit analysis ofprenatal diagnosis programs. In: Bergsma D, Lowry RB, Trimble BK, FeingoldM, eds. Numerical taxonomy of birth defects and polygenic disorders. New York:Alan R. Liss, 1977.

8. Office of Population Censuses and Surveys. Birth statistics, England and Wales, 1985(series FM1, no 12). London: HM Stationery Office, 1986.

9. Harlap S, Shiono PH, Ramcharan S. A life table of spontaneous abortions and theeffects of age, panty, and other variables. In: Porter IH, Hook EB, eds. Humanembryonic and fetal death. New York Academic Press, 1980.

10. Tabor A, Philip J, Madsen M, Bang J, Obel EB, Nørgaard-Pedersen B. Randomisedcontrolled trial of genetic amniocentesis in 4606 low-risk women. Lancet 1986; i:1287-93.

CEREBRAL INFARCTION ASSOCIATED WITHMYCOPLASMA PNEUMONIAE INFECTION

SIR, Mycoplasma pneumoni{U] infection is usually confmed tothe respiratory tract but it can cause a variety of extrapulmonarymanifestations such as rashes, haemolytic anaemia, myalgia,meningoencephalitis, and transverse myelitis. Most of these

conditions, although varying in severity, produce reversible

damage. Here we report an extrapulinonary manifestation ofMpnewnoniae infection that resulted in severe and persistentdisability arising from cerebral infarction.A previously healthy 31-year-old man became ill with general

malaise, anorexia, and myalgia, followed over a 3 week period bydyspnoea and a productive cough. He then became confused and

drowsy and in transit to hospital weakness of the left arm and legdeveloped. On admission he had fever (38’5°C), signs ofconsolidation over the- right lung, confusion, and a dense left

hemiparesis. After investigations M pneumoniae infection was

diagnosed (antibody titres rising to greater than 320).A computerised tomographic scan demonstrated a large recent

infarct in the right middle cerebral artery territory. Further

investigations excluded, as far as possible, recognised causes ofcerebral infarction; there was no evidence on echocardiography ofa clot or of valve disease, the major cerebral vessels seemed normalon angiography, and an autoantibody screen did not indicatecollagen vascular disease.The patient was treated with intravenous erythromycin and his

pneumonia resolved. However, recovery from the hemiparesis wasslow and he has a residual deficit.

Cerebral infarction has been reported in a child withM pneumoniae infection, with full recovery. In our case, in a youngman with M pneumoniae infection, a cerebral infarct resulted inpersistent and significant neurological dysfunction. Another

interesting facet of this was the presence of cold agglutinins.Haemagglutination would not be expected to cause vascularocclusion at body temperature and our patient was not exposed tohypothermia. Although we cannot prove that the mycoplasmainfection caused the cerebral infarction, the timing and the fact thatsuch profound neurological damage ensued in a previously healthyyoung man are strong indicators that it did. An autoimmunevasculitis with superadded thrombosis affecting the middle cerebralartery could have been responsible for the neurological defect.

Hope Hospital,Salford M6 8HD

A. B. DOWDR. GRACEW. D. W. REES

1 Parker P, Puck J, Fernandez L. Cerebral infarction associated with Mycoplasmapneumomae. Pediatrics 1981; 67: 373-75.

TUBERCULIN AND ’MULTI-TEST’ SKIN-TESTS INDRUG ABUSERS

SIR,-From 1981 to 1984 in the USA the average annualdecrease in tuberculosis cases was 6-7%. In 1985, there was a dropof 1-1% in the case rate.! The rate of tuberculin prevalence andtuberculosis disease has increased more than 50% in areas with a

large population of drug users in New York City.z3 Concomitantly10% of AIDS patients have been found with tuberculosis. IIn Amsterdam the number of cases of tuberculosis has increased

among drug users. Because of this we have used intradermalskin-testing in drug users in Amsterdam with the Mantoux test andthe ’Multitest’ (Institut Merieux), which consists of seven recallantigens. Our study population was 350 drug users, of whom 166had used drugs intravenously in the past five years. All were clientsof a methadone maintenance programme. The age distribution was:32% aged 25-29, 29% aged 30-34, and 22% over 35. Thedistribution according to land of birth was: 47 % Dutch, 26 % fromSurinam and the Netherlands Antilles, 16% from other Europeancountries and North America, and 11 % from elsewhere.

Significant tuberculin reactions (induration over 10 mm) wereseen in 98 cases (Dutch and foreign born), an overall prevalence of28-0%. However, of the 75 non-Dutch reactors more than half hadhad BCG vaccinations, which makes clinical interpretationdifficult. The tuberculin prevalence of the native-born Dutch whohad not had BCG vaccinations was 13-7% (23/168). This is higherthan the 5% national prevalence of the 25-35 age-group.’With the multitest 11 cases showed anergy (ie, negative to all

seven antigens); all were intravenous drug users. There were 40cases who were hypoergic (less than three positive antigen responsesor under 10 mm total induration score); 37 were intravenous drugusers. Therefore, of the 252 negative tuberculin reactors, 51 had adiminished delayed-type hypersensitivity response. This suggeststhat the number of true tuberculin positives may be greater.

Abnormalities in the cellular and humoral immune systemdemonstrated by anergy and hypoergy may be due to drugmisuse. S,6 Infection with HIV may be another cause. We did not testfor HIV antibodies in this particular group. However, a study of 310