Several new observations with important implications for clinical practice and for understanding the pathogenesis of SDB in children emerged from this study. We report for the first time the longitudinal outcome of adenotonsillectomy in healthy children, the important influence of BMI gain velocity and African-American race on recurrence of SDB, and the longitudinal changes in BP associated with the recurrence of SDB.
An important observation made in this study relates to the timing of the assessment of SDB after adenotonsillectomy. To date, most postadenotonsillectomy outcome studies have focused on the assessment of SDB 6 to 16 weeks after surgery (24
). Resolution of SDB during this window of time was usually interpreted as a cure for the disorder. However, the high rate of recurrence of SDB that we observed 1 year after surgery in both obese and nonobese children indicates that SDB is a chronic condition. In fact, the absence of a significant correlation between the 6-week postoperative AHI and AHI measured at any earlier or later time speaks to the limited predictive value of the 6-week evaluation. Furthermore, large BP increases in children who had recurrence of SDB and the independent association of AHI with both 1-year systolic and diastolic BP point to the potential morbidity of unrecognized residual SDB after adenotonsillectomy. In view of our findings, it would be clinically prudent to extend the traditional 6-week follow-up, commonly used in clinical practice, to at least a 1-year follow-up.
In our study population, adenotonsillectomy was associated with partial to complete resolution of SDB in both obese and nonobese children. Although in obese children the 1-year AHI decreased significantly from that measured preoperatively, the number of obese children with an AHI greater than 3 increased from 67 to 79%. On one hand, these findings appear to indicate the beneficial effect of adenotonsillectomy in all children with SDB independent of BMI. On the other hand, they suggest the presence of a subset of children who are refractory to a long-term benefit, and in fact susceptible to progression of SDB despite adenotonsillectomy. Although children who were obese at baseline were more likely to be refractory to the benefit of adenotonsillectomy, there was an additional and independent risk of SDB reoccurrence due to the rate of BMI gain during the duration of the study. These results highlight the differential disease mechanisms between those due to obesity and those due to the rapid change in body composition associated with accelerated BMI gain.
Different obesity-related conditions and parameters, as distinct mediators of disease morbidity, have emerged from studies of pathways linking obesity to abnormal glucose homeostasis and cardiovascular diseases. Among these conditions is adiposity rebound, defined by the age after infancy at which BMI starts to rise and measured as BMI gain from birth to childhood. The role of BMI gain from infancy to childhood in obesity-related morbidity was highlighted by Bhargava and colleagues (27
). In their study of 1,492 young adults, they examined the relation of serial changes in childhood BMI to impaired glucose tolerance in young adulthood. Children, in whom impaired glucose tolerance or diabetes later developed, were characterized by a low BMI between birth and 2 years of age, a young age at adiposity rebound, and a sustained accelerated gain in BMI until adulthood. A similar association between rate of weight gain and the risk of cardiovascular disease in children and adults has been recently described (18
Our study, together with those noted above, regarding the independent role of BMI gain in disease development, clearly support the concept of BMI gain trajectory as an independent risk factor for SDB, diabetes, and cardiovascular disease. The association of BMI gain with abnormal glucose homeostasis and markers of early atherosclerosis in children (15
) is similar to the trend we observed between BMI gain and risk for SDB after adenotonsillectomy. The similarity in these trends raises the important question of whether SDB is one link between a high rate of BMI gain during childhood and abnormal glucose homeostasis and cardiovascular disease in adulthood.
In all regression models examined in our study, being African American increased the risk of recurrence of SDB after adenotonsillectomy. This observation identifies the racial differences in conferring the risk of developing SDB in children.
A limitation of this study design is that it did not address the reproducibility of AHI in untreated children with SDB over a 1-year period. Because measuring the reproducibility of AHI over a period of 1 year in children with varying degrees of severity of SDB would require withholding therapy, and is not ethically acceptable, we included a healthy control group, which was followed for the same duration as children with SDB. Although the findings derived from the comparison group do not necessarily reflect the reproducibility of AHI in children with SDB, they nevertheless demonstrate the small variation of this index over a period of 1 year.
There is a high risk of recurrence of SDB in children 1 year after adenotonsillectomy that was associated with increasing BP. Gain velocity in BMI, being obese, and being African American increased the risk of recurrence of SDB 1 year after adenotonsillectomy. We advocate long-term follow-up of children with SDB, monitoring of BMI gain, and reevaluation of children who demonstrate rapid BMI gain, especially those who are African American.