Session: MON 758-775-Beta Cells, Glucose Control & Complications
Poster Board MON-763
Method: Two groups of childhood ALL survivors were studied: Group 1) Treated with(n=21,11M) and Group 2) without(n=31,13M) BMT/TBI. BMT/TBI survivors received 10-14.4Gy TBI at mean age 9.3(1.0-10.8) yr. A control Group 3) was selected of obese subjects (n=30,10M). All were age 16-26yr at time of study and had assessment of: pancreatic volume by abdominal MRI; IR by insulin composite insulin sensitivity index(ISIcomp) from oral glucose tolerance test(OGTT); and b-cell function by acute-insulin-response(AIR) from Arginine intravenous glucose tolerance test(AIRarg). Data were logarithmically transformed if positively skewed and analysed by ANOVA with post-hoc Scheffé’s multiple comparison tests, multiple regression and Pearson's correlations at 5% significance. Results are reported as mean(SD) or geometric means(range) as appropriate.
Results: Abnormal OGTT were reported in Groups 1(DM=2,IGT=7) and 3(IGT=1). ISIcomp was lower in Groups 1[1.7(0.35-44.7) p<0.001] and 3[4.8(0.75-9.6) p=0.001] compared with Group 2[2.2(0.76-7.5)]. b-cell function assessed in the context of IR was significantly lower in Group 1 [60.0(CI:43.8-76.7)] than in Groups 2[105.4(CI:79.8-138.4) p=0.003] and 3[83.8(CI:69.7-100.9) p=0.034]. Absolute pancreatic volume(cm3) (PV) was lower in Group 1[52.0(14.2)] than in Groups 2[72.8(23.5),p=0.003] and 3[72.8(19.7),p=0.006] and correlated with AIR (r=0.3,p=0.01). As PV correlated positively with height (r=0.45,p<0.001) and as Group1 were shorter (p<0.001) than Groups 2 or 3 (height SDS: -1.4(1.5); 0.2(0.9) and 0.5(1.0) respectively), PV was corrected for height(cm3/m2) but remained less in Group 1[19.9(5.5)] than in Group 2[24.9(8.0) p=0.048] or 3[25.6(6.6) p=0.03]. PV did not differ between Groups 2 and 3(p=1.0) and did not correlate with age at ALL diagnosis(p=0.9), time from treatment(p=0.3), age at BMT(p=0.7), time from BMT(p=0.3) or TBI dose(p=0.8).
Conclusions: This study suggests that reduction in pancreatic size, and loss of b-cell compensation contribute, with increased IR, to the mechanism of abnormal glucose homeostasis in survivors of BMT/TBI in childhood.
Nothing to Disclose: CW, MT, LPH, KJB, RE, MCS, ECC
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