Archives of Disease in Childhood, 1977, 52, 512-517

Paediatric Pathology Society and DevelopmentalPathology SocietyProceedings of the Twenty-second Annual Meeting

The Twenty-second Annual Meeting of the Pae-diatric Pathology Society was held jointly with theDevelopmental Pathology Society on 22-24 Septem-ber 1976 at the Birmingham Maternity Hospital,Queen Elizabeth Medical Centre, Birmingham.

Scientific communications.Lymphoreticular aggregates in the pancreas of infants.W. Naughten. Children's Hospital, Sheffield.Sections from 1700 pancreases were studied.Lymphoreticular aggregates were found in 24% ofcases, varying from 28% at birth to 2 *0% at 4 years.No relationship with disease or cause of death couldbe found, but aggregates were seen most commonly atbirth and declined in incidence with age. The aggre-gates were composed of large and small lymphocytes,reticulum cells, thin-walled blood vessels withprominent endothelial lining cells and sometimesgerminal centres. The relationship to gut-associatedlymphoid tissue is an inverse one according to age.In the pancreas the lymphoreticular aggregates occurin the septa between lobules and in lobules, replacingthem and apparently causing destruction or dysplasiaof acini and islet tissue. It is postulated that theaggregates are induced by degenerating A or B isletcells leaking their contents into the interstitium andprovoking a reaction.

Pancreatic islet-cell hyperplasia and sudden infantdeath syndrome. G. Guelpa and J. N. Cox. InstitutUniversitaire de Pathologie, 1211 Geneve 4, Switzer-land.During a 6-year period necropsies were performed on36 cases clinically diagnosed as sudden unexpecteddeath in infants and children. 11 of these presentedpathological lesions which explained the cause ofdeath. Of the remaining 25 cases, 9 showed variousdegrees of pancreatic islet-cell hyperplasia (nesi-dioblastosis) with an adenomatous appearance ininstances. Special histochemical and immunocyto-chemical techniques showed extensive endocrinecell proliferation with diffuse infiltration of theexocrine tissue in all cases. The liver in these casespresented cellular swelling with disorganization ofthe cell columns and in some, slight to moderatefatty infiltration. From these findings one can assume

that there might have been an acute episode ofhypoglycaemia in these 9 cases due to pancreaticislet-cell hyperplasia with hyperinsulinism andsevere metabolic disturbances leading to death.

Pulmonary vascular changes in sudden infant deathsyndrome. S. R. Kendeel and J. A. J. Ferris. Ministryof the Solicitor General, 26 Grenville Street, Toronto,Canada M7A 1Y6.Pulmonary arterioles and small arteries werestudied and their musculature and its nuclei quanti-fied in 90 infants and young children who hadsuffered from a variety of clinical and hypoxicconditions before death. Among the 90 casesstudied, 30 were of sudden infant death syndrome(SIDS). No evidence was found to support the viewthat cases of SIDS are subjected to chronic hypoxiabefore death. Significantly more muscle tissue wasfound in the pulmonary arterioles and small arteriesin the chronic hypoxic group compared to the SIDS,the non-hypoxic, and the acute hypoxic groups.Furthermore, there was no statistically significantdifference in the amount of medial muscle tissueof the pulmonary vessels as between the SIDS, thenon-hypoxic, and the acute hypoxic groups. Withother signs of acute hypoxia found at the necropsyof SIDS, the results of this study could be consideredto support the view that SIDS results from an acuteepisode of hypoxia, or possibly repeated shortduration episodes of acute hypoxia which do notproduce pulmonary vascular changes.

Breakdown of causes of postperinatal death inSheffield during 1974-76. 1. Forrest-Hay and J. L.Emery. Children's Hospital, Sheffield.

Quantitative study of carotid body in children. F.Dinsdale, J. L. Emery, and D. Gadsdon. TheChildren's Hospital, Sheffield.The carotid body from 100 children ranging in agefrom 36 weeks' gestation to 9i years was studied.34 of the children presented as 'unexpected death ininfancy'. Blocks of the carotid bifurcation were takenand serially sectioned at 6 ,um and stained withhaematoxylin and eosin. Every tenth section wasprojected on to white card, drawn, cut out, and

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weiglhed. Using Simpson's rule, the total volumeof each carotid body was calculated. The meanvalues showed gradual increase with age from 0*3mm3 at birth to 1 -2 mm3 at 4 5 years. The volumeof glomic tissue was then measured using a pointcounting technique on sections at one-tenth intervalsthroughout each carotid. The mean values againshowed a progressive increase in volume from 0 *0824mm3 at birth to 0 4677 mm3 at 4 5 years. Thehistories of all cases were then examined, particularattention being paid to any indication of hypoxia.While individual cases, notably a child with sicklecell disease, showed a very great increase in glomictissue, our results show no general increase in thevolume of the carotid body in children dyingunexpectedly.

Teeth as markers of some growth disturbances. B.Garton, E. P. Turner, R. S. Levine, J. Dobbing, andA. J. Barson. Dental School, University of Manches-ter, Manchester 15.Unlike bone, teeth grow by incremental depositionof calcified matrix without resorption and remodell-ing to form permanent structures. Since there isevidence that the developing tooth is sensitive tosome systemic disturbances, its value as a record ofdevelopmental disturbance is being studied. Thisrecord extends from the fourth month in utero, whenthe first dental tissue begins to calcify, until aboutthe 17th year, when the wisdom teeth are completed.The chronology of any recorded disturbance canbe fixed with the aid of the neonatal incrementalline to an accuracy of ± 3 weeks. Material isobtained from two sources, developing teeth frompost-mortem examinations and shed deciduous teethfrom children having a history of the condition understudy. The teeth are sectioned and examined bypolarized light microscopy and bymicroradiography.Observed disturbances are then correlated with themedical history. Initial results confirm that majorin utero systemic disturbances are recorded andsuggest that even some minor changes are detectable.

Further studies on oedema of the umbilical cord. J. M.Scott and R. Wilkinson. Glasgow Royal MaternityHospital, Glasgow G4 ONA.

The pathogenesis of encapsulated subdural haema-toma and hygroma of the dura. S. Ranstrom.Department of Pathology, Sahlgrenska Hospital,Gothenberg.A histological study has shown great similaritiesbetween free subdural bleeds of different causesand ages and of encapsulated subdural haematomas.The pathogenesis of the encapsulated chronic sub-dural haematoma is as follows. A free subduralbleed is resorbed by an organization membrane

developed from the inner surface of the dura. Withinthe basal layer of this membrane the thin walledcapillaries become dilated and the tissue becomes thesite of a spongy oedema. Because of these changesthere may occur a new bleed within the membranewith formation of a haematoma encapsulated bymembranes which are the inner, superficial andouter, basal parts of the original organizationmembrane. This encapsulated haematoma mayincrease in volume until clinical symptoms appeargradually or suddenly. The histology of the mem-branes encapsulating a hygroma of the dura is thesame as for the haematoma. The hygroma may beinterpreted as a further development of the spongy,microcysticoedema of the basal part of the organi-zation membrane to macrocysts.

Examination of cerebellums of infants using theQuantimet 720. D. R. Gadsdon and J. L. Emery.Children's Hospital, Sheffield.

Focal pituitary calcification in the newborn. A. J.Barson and J. Symonds. Department of Pathology,Medical School, University of Manchester, M139PT.A high proportion of fetal and newborn pituitaryglands contain round lamellated bodies measuringbetween 10 ,4m and 70 jAm in diameter. The majorityare strongly basophilic with affinity for the von Kossastain for phosphates. A study of the anteriorpituitary glands from 200 fetuses and infants rangingin age from 22 weeks' gestation to one year of lifeshowed a declining incidence in these calified fociafter birth. They were rarely seen after the sixthmonth of life. It is thought that these bodies representa degenerative change in cells subject to the vigoroussecreting activity that is part of the normal physiologyof the anterior lobe of the pituitary from mid-gestation.

Reaction to subependymal plate haemorrhage in thehuman neonate. A. Sherwood, A. Hopp, and J. F.Smith. Department of Morbid Anatomy, UniversityCollege Hospital Medical School, London WC1E6JJ.In the past decade subependymal plate haemorrhage(SPH) has become the leading cause of death in termbabies and is now comparable to that produced byischaemic heart disease in adults. Thus between 1970and 1975 inclusive, 83 of the 150 babies of birthweight below 2000 g on whom necropsies wereperformed at UCH had SPH, and in 63 of theseextension into the ventricle had occurred. (6 of the72 babies over 2000 g had SPH, these were between2000 g and 2250 g. Most cases died in the first fewdays of life but we were able to examine materialfrom 20 of the 29 who lived for 4 days or more.

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In 15 of these, whose ages ranged from 4 to 59 dayswe were able to see a definite tissue reaction to thehaemorrhage. This consisted of an initial mononu-clear phagocytic respose and a variable but limitedastrocytic reaction within the plate.

Some problems in diagnosis and pathogenesis ofLeigh's encephalomyelopathy. A. Green. Departmentof Chemical Pathology, Children's Hospital, SheffieldS10 2TH.Diagnosis of Leigh's disease cannot be madeclinically due to the nonspecific nature of the pre-senting symptoms and relies essentially upon thenecropsy finding of characteristic necrotizing lesionswithin the brain stem. Pathogenesis of the diseaseis poorly understood though there has been a gooddeal of speculation centred around pyruvate metabo-lism and the role of thiamine. Impaired metabolismof pyruvic acid, due to a deficiency of eitherpyruvate carboxylase or pyruvate dehydrogenase,has been shown in some patients with Leigh's diseasethough it is not known whether these are primaryenzyme deficiencies or secondary effects of an asyet unknown primary defect. The role of thiaminein Leigh's disease is not clear. Identification of anenzyme inhibitor which prevents production ofthiamine triphosphate in the brain has been shown inbody fluids and recently evidence of a possible defectof thiamine pyrophosphate function has beensuggested by measurements of the red cellenzyme transketolase. Comprehensive biochemicalinvestigations of possible cases of Leigh's diseasemight enable precise diagnosis of this disorder in thefuture-this being of utmost importance for thebasis of treatment.

Appearance of astrocytes in reaction to injury indeveloping brain. J. F. Smith. Department of Patho-logy, University College Hospital Medical SThool,London.

Neuroblastoma in Turkish children. S. Gogus andK. Tinaztepe. Hacettepe, Ankara, Turkey.Histopathological and clinical studies of 56 childrenwith primary neuroblastoma seen at HacettepeChildren's Hospital during the last 6 years werecarried out to evaluate their relationship to age, site,histology, clinical staging, and survival of more than4 years. Overall survival rate was 8 %. This is lowerthan in various centres in developed countries. Allsurviving patients were younger than 3 years and theearlier the age the better the survival noted. In 88 %of the cases the primary tumours were below thediaphragm, but in 4 out of 5 surviving patients thetumours were above the diaphragm. Survivors werein histological grades I and II.

Recent increase in limb reduction deformities in northLondon. P. Jaffe, M. M. Lieberman, I. McFadyen,H. B. Valman, D. R. Harvey and S. N. Wallace.Department of Paediatrics and Obstetrics, NorthwickPark Hospital, Harrow, Middlesex, and QueenCharlotte's Maternity Hospital, London, W6 OXG.There was an apparent increase in limb reductiondeformities in North London in 1974, figures from 4hospitals showing a significant difference from theyears preceding and following (0 025 > P > 0 01).Data from West London shows a peak in 1975. Noaetiological agents have been identified but the datesof last menstrual periods show clustering in springand early winter. Unlike previous surveys, all 6infants born after hormonal exposure were female.

Effect of vitamin D deficient diet on pregnancy in therat. R. G. Lendon. Department of Anatomy,Medical School, University of Manchester.Groups of Wistar-derived rats were kept on a dietdevoid of vitamin D for 3 to 4 months. The animalswere then mated and the outcome of the pregnancies,as judged initially by overt inspection of embryostaken by caesarean section, was noted and comparedwith the outcome from animals fed a normal diet.No difference was noted apart from a slight dropin litter size on a deficient diet.As congenital malformations may normally be

attributable to a combination of environmentaleffects, we next studied the influence of a vitamin Ddeficient diet on the teratogenic action of trypanblue. A base line dose of aqueous 1% trypan bluewas established for the stock which produced aminimal manifestation of one of the commonestmalformations-exencephaly. The effect of the samedose/kg body weight on litters from a group fed avitamin D deficient diet was to increase significantlythe numbers of embryos with exencephaly. A signi-ficant enhancement of the action of trypan blue wasalso noted for the incidence of a second overtlyrecognizable malformation-microphthalmia. Herethe deficient diet doubled the incidence of the mal-formation.

Achondroplasia in sheep. S. J. Duffel. Fisheries andFood Veterinary Investigation Centre, Block C,Government Buildings, Whittington Road. Worces-ter WR5 2LQ.

Some unusual neuromuscular disorders of rectumand colon. R. 0. C. Kaschula. Department ofHistopathology, Red Cross War Memorial Child-ren's Hospital, Cape Town, South Africa.Over a 6-year period during which approximately200 children had rectal biopsies performed forpossible Hirschsprung's disease, cases of delayed

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maturation of rectal ganglia (1), neurologicaldysplasia (5), and Bantu pseudohirschsprung'sdisease (8) were encountered. In the case of thechild with delayed maturation it was possible tomonitor maturation by means of repeated submu-cosal biopsy. The cases with neurological dysplasiashowed the presence of abnormal peripheral nerveswith variable numbers of nerve cells both in thesubmucosa and at the site of Auerbach's plexus toa significant distance above the anorectal margin.In one of these cases the ganglia contained bothmature and immature nerve cells. The 8 childrenwith pseudohirschsprung's disease were all Bantuchildren ranging in age from 4 to 12 years. Theygradually acquired marked abdominal distensionafter undergoing apparent normal neonatal andinfantile growth and development. Histologicallythere was hypertrophy, fibrosis, and oedema of themuscularis of the rectum and colon. Radiographicstudies showed depressed bowel motility but normalanorectal reflexes were found.

Pathology of Pig Bel. R. Cooke and A. Shepherd.Department of Pathology, Royal Brisbane Hospital,Australia, and Department of Public Health, Papua,New Guinea.Surgical specimens from 88 cases of pig bel operatedupon in the Eastern Highlands of New Guineabetween 1971 and 1974 were examined. This in-vestigation showed that the pathology of pig belwas constant and almost certainly unique. The smallintestine was affected in all cases. On the mucosalsurface of the bowel the earliest changewas gross sub-mucosal oedema producing thickening of the mucosalfolds. Ultimately, large portions of the mucosa wereconverted into a green coloured membrane. Histologi-cally this was infarcted mucosa which then separatedoff leaving tiny islands of surviving mucosa simu-lating multiple small pseudopolyps. In cases oflonger standing, healing occurred, producing sub-mucosal fibrosis going on to stricture formation insome cases. The veins in the submucosa, particularlyat the junction between viable and necrotic mucosashowed gross endothelial proliferation. The vesselsdistal to this became thrombosed, causing infarctionof the mucosa. It is postulated that the processof veno-occlusion plays an important part in thepathogenesis of this disease. It may be akin to veno-occlusive disease of the liver and perhaps it is dueto ingestion of some food toxin rather than toinfection with Clostridium welchii as was previouslythought.

Effects of aerosolized fat sprays on mammalian lung.D. G. Fagan. Department of Pathology, Hospitalfor Sick Children, Toronto, Canada M5G 1X8.

Renal histopathology of 27 children with lupusnephritis. J. Huber and E. M. Scent Gyorgi. Depart-ment of Pathology, Hospital for Sick Children,Toronto, Canada, M5G 1X8.33 renal biopsies from 27 patients with systemiclupus erythematosus were classified into the followingcategories: minimal change (MIN), mesangial lupusnephritis (MESLN), focal proliferative lupus nephri-tis (FPLN), and diffuse proliferative lupus nephritis,mild, moderate, and severe (DPLN). Membranouslupus nephritis (MLN) was not observed in ourseries. There were 19 females (age at biopsy 9-17years) and 8 males (6-14 years). 21 patients had onebiopsy with the following diagnoses MIN 6, MESLN5, FPLN 3, DPLN mild 1, mod 2, severe 4. 6patients had two biopsies with diagnosis at firstbiopsy MIN 1, MESLN 1, FPLN 2, DPLN mild 2.The diagnosis at second biopsy had to be changedin 2 patients: one from MIN to MESLN, one frommild to moderate DPLN. All patients combinedwere finally classified as follows: MIN 6 (4 females,2 males) MESLN 7 (6 females, 1 male) FPLN 5(4 females, 1 male) DPLN 9 (5 females, 4 males).Survival was better than is generally assumed with 2deaths in our series, one from other than renalcauses, one from severe DPLN.

Complement-fixing anti-DNA in systemic lupuserythematosus: sensitive indicator of disease activity.0. Huber. Department of Pathology, Hospital forSick Children, Toronto, Canada M5G 1X8.The immunofluorescence Crithidia method fordetecting antibodies to native (n) DNA, differentiatedaccording to immunoglobin class and complement-fixing (CF) properties, showed high specificity ofanti-nDNA for systemic lupus erythematosus (SLE)and high sensitivity for activity of the disease. Inserial sera from 32 patients with SLE, CF anti-nDNA was detected in 13 of 15 patients with activedisease and in none with inactive disease. In 7patients followed during active disease and remission,the CF antibodies disappeared from the blood asearly as 2 weeks after the start of high-dose steroidtherapy; 3 patients had positive test results for 1-2months during low-dose steroid therapy of activedisease; and 7 with clinically inactive disease hadanti-nDNA but not CF anti-nDNA. CF anti-nDNAcorrelated closely with low serum complement levelsin patients with and without renal involvement. CFanti-nDNA as measured by the Crithidia methodappears to be a sensitive marker of disease activity inSLE. Weekly performance of the test while the diseaseis active is recommended, as a guide to therapy: earlyattainment of adequate steroid dosage may preventorgan damage, and early reduction in dosage will

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lessen side effects, improving both the prognosisand the quality of life.

Comparative study of sickle-cell anaemia in childrenin London and in Lagos. L. R. Davis, F. E. A. Lesi,and J. M. White. Department of Paediatric Patho-logy, King's College Hospital, London SE5 9RS.The growth and blood picture of children withsickle-cell anaemia attending sickle-cell clinics inLondon and Lagos was compared. The children,aged 1-11 years, were free from symptoms of thedisease and infections and had not received bloodtransfusions within the preceeding 3 months. TheLondon children were, on average, taller and heavierthan those in Lagos. The degree of anaemia and thepercentage of haemoglobin F was similar in the twocountries and fell with age in a similar manner.Differences were noted in the percentages of reti-culocytes, irreversibly sickled cells, and target cellsin the two countries, but this could in part have beendue to differences in techniques. In both centres theirreversibly sickled cells rose with age, and thereticulocytes were unaffected by age. Target cellsfell with age in London but not in Lagos, and noexplanation for this difference could be offered. Itwas concluded that differences in growth might havebeen due to differences in environment but thatthis was not reflected in gross changes in the bloodpicture. It was emphasized that selected groups ofchildren in each country had been studied and theresults might not apply to children in other areas.

Serum uracil levels in acute leukaemia-preliminaryfindings. T. E. Parry. Llandough Hospital, PenarthCF6 lXX.Uracil has been measured in the sera of 18 cases ofacute childhood leukaemia (13 males, 5 females;age range 10 months to 14 years; 14 with acutelymphoblastic leukaemia (ALL), 4 with acutemyelocytic leukaemia (AML)) and compared with97 normal subjects (including paired controls).The mean control level was 15 a 7 ,umol/l (range 5 7-40 5 ,tmol/l, SD 5 26). In the leukaemic cases themean was 22*27 ,umol/l (range 7 2-66*9 ,umol/l, SD19-14). The difference was due to levels of 58 2,62 * 7 and 66 * 9 /tmol/l-all more than 8 SDs above thenormal mean-in 3 cases, 2 with ALL and 1 withAML, the remainder being normal. The 3 deviantcases had extremely high blast cell counts (38-4,131 *0, and 123 *0 x 109/l, respectively). Serum uricacid was raised (0 * 54 mmol/l) in 1 and normal in theother 2 (0 06 and 0 19 mmol/l). This suggests thatthe raised uracil is related to the leukaemic cell butis not the consequence of cell necrosis. The resultsare consistent with impaired conversion of uracil tocytosine, at least in some cases of acute leukaemia.

Diagnosis of inherited metabolic disease using acomputer-operated matrix matching system. D. N.Raine. Department of Clinical Chemistry, Children'sHospital, Birmingham B16 8ET.A system has been devised in which 157 disordersinherited by a recessive or X-linked mechanism aredescribed in a standardized manner using 22 para-meters which are recorded as being either present orabsent. The resulting 22 x 157 matrix is scanned,using a small computer, for matches against the 22parameters for a given patient and two factorsdetermined: the number of positive features in thepatient coinciding with positive features in thetypical description of each disease, and the propor-tion of the former to the latter expressed as a per-centage. The diseases are then listed for the patientwhose diagnosis is required in descending order ofthenumber of matches and within a given number ofmatches, the descending order of percentage match.This preferred order of diagnosis has been testedagainst 36 patients with one of 21 diseases and theposition of the correct diagnosis in the list deter-mined. Two-thirds of the diagnoses occurred withinthe top five diseases listed. The system is consideredto be a feasible approach to diagnosis of these raredisorders and is now being improved in a number ofrespects.

Epicardial aneurysm as a late sequel of cardiaccatheterization. J. D. Elema and J. W. Oosterhuis.Department of Pathology, University Hospital,Groningen, The Netherlands.The introduction of catheters into the cardiovascularsystem carries a number of risks which includeperforation of the vascular wall. These perforationsmay lead to serious acute blood loss, but also canpass unnoticed, especially when they involve thecardiac muscle. The unexpected finding of anepicardial aneurysm at necropsy is reported in 2children with congenital heart disease. A link be-tween this finding and cardiac catheterization isproposed on the basis of experience in childrendying shortly after undergoing catheterization.Subepicardial bleeding ranging from petechiae tofrank haematomas can be found which are alwaysconnected to the ventricular lumen by one or morefine fibrin-coated channels. Localization of the les-ions in the region of the pulmonary outflow tract isprobably related to the fact that this area often givestechnical difficulties during the catheterizationprocedure. An iatrogenic aetiology should be kept inmind when an epicardial aneurysm is found inchildren with congenital heart disease.

Organization of a regional diagnostic amniocentesisservice. D. I. Rushton. Department of Pathology,

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Birmingham Maternity Hospital, Birmingham B152TG.

Development of germinal centres in the spleen ininfants, related to birth and unexpected death. A. J.Barzanji. Children's Hospital, Sheffield.The spleens of 266 children dying in hospital and 205children presenting as unexpected deaths betweenthe ages of 1 and 90 weeks were examined. Thepercentage of malpighian bodies with germinalcentres in the spleen was greater in children dyingunexpectedly at home when these were comparedwith hospital deaths. It was concluded that childrenpresenting as unexpected deaths in infancy show noevidence of any deficiency in cellular immunolo-logical response, as indicated by the production ofgerminal centres. Spleens from 230 sequentialstillbirths between 28 and 42 weeks' gestation andfrom 220 term babies who died between 1 and 28days postnatally were also examined. No splenicgerminal centres were found in any of the stillbirthsor in 150 babies aged 1 and 14 days. All the neonatal

deaths showed definite signs of infection at nec-ropsy. Out of six 15-day-old babies, one showed agerminal centre with mild reaction and one of thefour 16-day-old babies showed germinal centres.The number of cases showing germinal centresincreased progressively after 14 days.

A Symposium was held on 'Transplacental Carcino-genesis and Neoplasia in the Newborn' with thefollowing contributions.

Introduction and theoretical considerations. C. L.Berry (London).Ethylnitrosourea carcinogenesis. E. L. Jones(Birmingham).Effect of maternally administered stilboestrol onthe genital tract of the fetus. J. A. Jordan (Birming-ham).Incidence and pattern of tumours in the newborn.A. J. Barson (Manchester).The Society's experience. A summary of casessubmitted by members. D. I. Rushton (Birming-ham).

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