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Læknablaðið - 01.12.1978, Page 69

Læknablaðið - 01.12.1978, Page 69
LÆKNABLAÐIÐ 203 was much increased. All histologic sub- types were seen throughout the whole period. Menwhile, Correa and O’Conor,4 utilising data from Volume I of „Cancer in Five Continents" had shown that there were at least three distinct types of epidemiologic patterns of H.D., the differences lying principally in the proportion of cases in childhood. They showed that there was a reciprocal difference between the child- hocd peak and the young adult peak. They showed that socio-economic factors ac- counted for this and clearly with increasing affluence, the impact of H.D. shifts from childhood to young adult life; intermediate patterns exist as might be expected. This change with affluence seems very im- portant because it is shared by no other childhood cancer. But there are close parallels in the field of infectious disease and this made it work considering the school situations in more detail. Vianna and Polan had much basic in- formation to hand from Nassau-Suffolk where we only had to update and extend our records of persons under 40 years, considering only the public but not the parochial and private schools."’152 Two methods were used, firstly two sequential quinquennial periods were compared for schools with and without H.D. cases. We found that schools that had cases in the previous quinquennium almost always had cases in the second quinquennium, while only a few cases occurred in school with no cases in the first quinquennium. In subsequent criticism of these findings, it was suggested because we found an annual incidence rate of only 1.9 per 100.000 per annum we must have missed cases of H.D. and that this might explain these find- ings.:i0 We do not believe cases were missed to any great extent but that if they were, that this might negate this finding is ad- mitted. But it is impossible to believe that missing cases could affect the other find- ings using the index-secondary case ap- proach. Follow up for a decade of all students in the schools after the index case had been recognised enabled the person/years at risk of the school popu- lation to be calculated and applying the New York State rates for age we could obtain rates or alternatively observed to expected ratios for students; for teachers an overall rate rather than a specific age rate had to be applied. The rates and the ratios both for students and teachers were remarkably and significantly high and any missing cases would only raise these rates far higher. Though indeed we know that in one school at least there have subse- quently been cases which would increase both rates and ratios.54 These findings have essentially been confirmed in Connecticut schools.59 Other interesting aspects of this study were the infrequency of cases in ele- mentary schools and that the incidence rates varied significantly with school size. Thus in schools with less than 1500 students in toto the rates were 5.3/100.000 per annum while with schools of greater size the rates were 23.8/100.000 per annum. Moreover, the mean interval in diagnosis between cases in those school with an index and at least one secondary case was 3.8 years with a median of 3 years, figures very close to those found in the Albany epidemic. This also was very close to thaí found in our survey of familial cases of H.D. in New York State.53 These included family members living in the same house and those who lived apart. In the latter, the diagnostic interval was 3.4 years (Mean 4.1, Range 08—8.7 years) whereas for those living in the same house the interval was 1 year (Mean 1.2, Range 0.2—2 years), surely a significant finding. We also found some other interesting things in this survey in which familial cases were selected via the New York State Cancer Bureau to avoid bias. We found 23 familial pairs, 46 cases in all. Following the suggestion of MacMahon of Harvard30 that if with sib pairs, of which we had 7, that if the diagnostic interval was significantly shorter than the differences between the ages at diagnosis, this pointed to the likelihood that it was an environmentally determined disease rather than a genetic one. Criticism31 was directed to this suggestion of MacMahons

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