328

HeLa cells. However, the two isolates produced a-haemolysin onoxoid CM-55 agar containing 7% defibrinated sheep blood’ andexpressed Gal-Gal binding adhesin, as assessed by agglutination ofhuman OPl erythrocytes in 4% D-mannose. A gene probe for theGal-Gal binding adhesin’ hybridised with the DNA of the twostrains, confirming the Gal-Gal binding phenotype.

This is the first report of pyelonephritic E coli strains beingpathogenic in the intestine and of a bacterium being responsible forbenign rectal bleeding associated with ecchymotic lesions of

rectosigmoid mucosa in the neonatal period. We hypothesise thatboth x-haemolysin and Gal-Gal binding adhesin are involved in thepathogenesis. ot-Haemolysin damages several cell types in vitro andcauses tissue injury.s Moreover enteritis in swine and otherdomestic animals is associated with an a-haemolysin producing Ecoli in the gut.6 On the other hand E coli strains possessing Gal-Galbinding adhesins have been shown to colonise enterocytic cells.7 Weare studying whether the expression in the distal colon and therectum of cell receptors for Gal-Gal binding adhesin, especially thehuman blood group antigens Pi’ Pz, and Pk, are restricted to theneonatal period, as described for other blood group substances.8

We thank Jean-Luc Beretti for technical assistance, Agnes Labigne-Roussel and Pascale Courcoux for testing for Gal-Gal binding adhesin gene,Marylene Bohnert for testing for Sta-P and Sta-H gene, and Marie-LaurenceFoumeaux for typing.

Microbiology Laboratory,Department of Paediatrics,

and Pathology Laboratory,Hôpital Necker-Enfants Malades,75015 Paris, France

J. L. GAILLARDG. CHERONJ. F. MOUGENOTJ. P. DESLYSC. NEZELOFM. VERONJ. SCHMITZ

1. O’Hanley P, Low D, Romero I, et al. Gal-Gal binding and hemolysin phenotypes andgenotypes associated with uropathogenic E coli. N Engl J Med 1985; 313: 414-20.

2. Dupont C, Badoual J, Le Luyer B, et al. Rectosigmoidoscopic findings during isolatedrectal bleeding in the neonate J Pediatr Gastroenterol Nutr 1987; 6: 257-64.

3. Bohnert M, d’Hauteville H. Sansonetti P. Detection of enteric pathotypes byhybridisation using six DNA probes. Ann Inst Pasteur (Microbiol) 1988; 139:189-202.

4. Archambaud M, Courcoux P, Labigne-Roussel A. Detection by molecular

hybridisation of PAP, AFA and SFA adherence systems in Escherichia coli strainsassociated with urinary and enteral infections Ann Inst Pasteur (Microbiol) 1988;149: 575-88.

5. Cavalieri SJ, Bohach GA, Snyder I S. Eschenchia coli &agr;-hemolysin: characteristics andprobable role in pathogenicity. Microbiol Rev 1984; 48: 326-43.

6. Gregory DW. Role of the &bgr;-hemolytic coliform organisms in edema disease of swine.Vet Med 1955; 50: 609-10.

7. Wold AE, Thorssen M, Hull S, Svanborg Eden C. Attachment of Escherichia coli viamannose- or Gal &agr; 1 → 4 Gal &bgr;-containing receptors to human colonic epithelialcells Infect Immun 1988; 56: 2531-37.

8. Wiley EL, Murphy P, Mendelsohn G, Eggleston JC. Distribution of blood groupsubstances in normal human colons: use of the unlabeled antibody (PAP)immunoperoxidase technic to identify A and B blood group substances. Am J ClinPathol 1981; 76: 806-09.

GENDER AND SURVIVAL IN NEUROBLASTOMA

SIR,-In published series of patients with neuroblastomasurvival tends to be better in females than in mates," and in UK’and Germans studies this superiority was significant. We would liketo suggest an explanation.

Since January, 1982, details of all newly diagnosed cases ofneuroblastoma presenting at the twenty-three hospitals in theEuropean Neuroblastoma Study Group (ENSG) have been

collated in a central registry. Treatment for boys and girls isidentical. By June, 1988, 757 cases had been registered. 5-yearactuarial survival has been 50% for girls and 44% for boys.However, boys were less likely than girls to have good prognosisdisease6 (stages ivs, I, and 11). When stages were ordered as lvs,1,11,III, iv a statistical test for ordered categorical data confirmed atendency for males to be at a more advanced disease stage thanfemales (p < 0-05):

Gender IVs I 11 III IVMale 47 49 49 54 58Female 53 51 51 46 42

The outcome for boys and girls within each individual stage is verysimilar. Analysis by age at diagnosis (less than or greater than oneyear), which is, apart from stage, the only established independent

prognostic criterion in neuroblastoma, also revealed no differencebetween the genders. The median age at diagnosis was similar forboys and girls.

Little is known about what influences the aggressiveness oftumours. In neuroblastoma the association between amplificationof the oncogene N-myc and advanced stage is well known Perhapsthere are gender-associated differences in N-myc amplification (orother natural biological response modifiers) in children withneuroblastoma.

We thank colleagues in the ENSG for supplying data and Dr G. Draper forhelpful advice. The Cancer Research Campaign and Neuroblastoma Society(a parents’ charity) provided financial support.

Department of Haematologyand Oncology,

Hospital for Sick Children,London WC1N 3JH,

and UK Children’s Cancer Study Group,University of Leicester

JON PRITCHARDJ. M. BARNESS. M. GERMONDK. R. WALLENDSZUS,For the EuropeanNeuroblastoma Study Group

1. Thomas PRM, Lee JY, Fineberg BB, et al. An analysis of neuroblastoma at a singleinstitution. Cancer 1984; 53: 2079-82.

2. Carlsen NLT. Epidemiological investigations on neuroblastomas in Denmark1943-80. Br J Cancer 1986; 54: 977-88.

3. Evans AE, S’Angio GJ, Propert K, et al. Prognostic factors in neuroblastoma. Cancer1987; 59: 1853-59.

4. Kinnear Wilson LM, Draper GJ. Neuroblastoma, its natural history and prognosis.Br Med J 1984; 289: 301-07.

5. Berthold F, Brandeis WE, Lampert F. Neuroblastoma: diagnostic advances andtherapeutic results in 370 patients. Monogr Paediatr 1986; 18: 206-23.

6. Pritchard J, Kemshead J. Neuroblastoma: recent developments in assessment andmanagement. Rec Results Cancer Res 1983; 88: 69-78.

7. Schwab M, Ellison J, Busch M et al. Enhanced expression of the human gene N-mycconsequent to amplification of DNA may contribute to malignant progression ofneuroblastoma. Proc Natl Acad Sci (USA) 1984; 81: 4940-44.

TREATMENT OF HYPONATRAEMIA SECONDARYTO WATER OVERLOAD

SiR,&mdash;Dr Tanneau and colleagues (Oct 29, p 1031) report a caseof fatal central pontine myelinolysis in a polydipsic, hyponatraemicschizophrenic patient after spontaneous correction of

hyponatraemia. The patient, who also had chronic alcoholism andinadequate nutrition, had water intoxication after further reducingfood intake and ingesting large quantities of beer. 3 days later, afterfluid restriction alone had led to a rise in serum sodium from 110 to135 mmol/l, the patient had spastic quadriparesis and pseudobulbarpalsy. Tanneau et al recommend that vasopressin be administeredduring fluid restriction in such patients to slow the rate of rise inserum sodium.

In agreement with Dr Seckl (Nov 26, p 1254), we caution againstadministering vasopressin in these patients since they may have aprimary disorder in thirst! and are notoriously resourceful in

finding fluids to ingest. Furthermore we" and others3,4 have foundthat water restriction is not only safe in hyponatraemicschizophrenic inpatients (many of whom, as did Tanneau andcolleagues’ patient, have a history of alcohol abuse),5 but also, wheninstituted after precipitous drops in serum sodium, preventsepisodes of water intoxication.We weigh inpatients with a history of water intoxication three

times weekly and when staff observe prodromal signs of severehyponatraemia (ataxia, confusion, tremors, nausea, vomiting).When weight increases above a predetermined level, serum sodiumis measured and if below 125 mmol/1 (or lower, depending on thepatient’s basal sodium level), we eliminate all fluids for 16 hours,except for those on the meal tray. We measured serum sodiumbefore and after 16 hours of fluid restriction in 5 patients during sixof these hyponatraemic episodes. Serum sodium rose from an initialmean level of 119 [SD 3] mmol/1 to a final level of 138 [3] mmol/1 (arise of 14-21 mmot/1), for a mean rate of increase of 1 1 [0-2] mmol/1per hour. Weight fell on average 7-0 kg. We have instituted thisintervention over fifty times in more than 20 patients with episodicwater intoxication who had initial sodium levels between 110 and125 mmol/1. All showed similar degrees of spontaneous diuresis,and none had delayed neurological symptoms.We believe that the concurrent alcohol abuse and associated

malnutrition in the patient reported by Tanneau et al were likely