Guenther Schneider1, Paul Raczeck1, Arno Buecker1, and Jonas Stroeder1
1Saarland University Medical Center, Homburg, Germany
Synopsis
The possibility of Gd deposition in the pediatric brain following exposure to GBCAs is a potentially serious issue. Our study of 34 pediatric patients that received between 5 and 15 administrations of low dose (0.05 mmol/kg bodyweight) gadobenate dimeglumine (MultiHance; Bracco) revealed no differences in T1-signal in the DN, GP, pons and thalamus relative to measurements made in 24 age- and weight-matched control subjects that had never been exposed to any GBCA. Likewise no meaningful differences were seen in DN–pons and GP–thalamus SI ratios. We consider low dose gadobenate to be safe and effective for diagnosis and routine follow-up of pediatric oncologic patients.
Introduction:
Recent years have seen a plethora of reports detailing high signal intensity (SI) in certain brain areas (primarily the dentate nucleus [DN] and globus pallidus [GP]) on unenhanced T1-weighted images following multiple exposures to gadolinium-based contrast agents (GBCAs). With this background we wanted to determine if T1-signal changes potentially indicative of Gd-deposition occur in pediatric brain structures after multiple exposures to gadobenate dimeglumine (MultiHance; Bracco).Method and Materials:
34 mainly oncologic patients (Group 1; 17M/17F; mean age: 7.18 years; range: 9 months-17 years) that received between 5 and 15 injections (mean: 7.8 injections; each at 0.05 mmol/kg bw) of gadobenate over a mean of 2.24 years (range: 9 months-7 years) were compared with 24 control patients (Group 2; 16M/8F; mean age: 8.78 years; range: 7 months-17 years) that had never been exposed to any GBCA. Exposure to gadobenate was for diagnosis and for therapy monitoring. Five blinded readers independently determined the signal intensity (SI) at regions-of-interest placed in the dentate nucleus (DN), globus pallidus (GP), pons, and thalamus on unenhanced T1-weighted spin echo images from both groups. Unpaired t-tests were used to compare SI values and DN–pons and GP–thalamus SI ratios between Groups 1 and 2.Results:
Mean SI values in the DN, GP, pons and thalamus of patients exposed to gadobenate ranged from 366.4–389.2, 360.5–392.9, 370.5–374.9, and 356.9–371.0, respectively across readers 1 to 5. Corresponding values in GBCA-naïve control subjects were not significantly different (p>0.05), ranging from 368.3–374.3, 377.0–383.4, 364.4–385.4, 363.2–376.8, respectively. Similarly, no significant differences were noted by any reader for comparisons of DN–pons SI ratio. One reader noted a difference in GP–thalamus SI ratio (1.06±0.006 vs. 1.02±0.009; p=0.002) but this reflected non-significantly higher T1-signal in the thalamus of control subjects. The number of exposures and the time between first and last exposures did not influence SI values among patients in group 1.Conclusion:
Injection of 0.05 mmol/kg bodyweight of gadobenate dimeglumine in pediatric patients undergoing MRI seems to be a safe procedure, since no signs of Gd-deposition in the brain could be demonstrated. SI increases in the DN, GP, pons and thalamus that are potentially indicative of Gd-deposition were not detected in pediatric patients after multiple exposures to gadobenate dimeglumine, even in patients with 15 injections over a time interval of 6 years.Acknowledgements
No acknowledgement found.References
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