UNLABELLED: The rationale of this study was the evaluation of response to chemotherapy in children with advanced neuroblastoma using currently available diagnostic modalities. METHODS: Iodine-131-metaiodobenzylguanidine (MIBG) imaging and 24-hr urinary vanillylmandelic acid (VMA) measurement were evaluated in 14 patients (7 males, 7 females, age range: 2-68 mo) with advanced neuroblastoma both pre- and postchemotherapy (5.6 +/- 2.8 mo) as well as serum ferritin (FER) and neuron-specific enolase (NSE) levels in 9 and 8 patients, respectively. MIBG images were qualitatively compared in each patient. RESULTS: Prechemotherapy, a total of 39 abnormal foci of MIBG uptake was detected. Postchemotherapy, 15 of these showed unchanged MIBG uptake, 7 had decreased uptake and 17 showed no uptake. In addition, four new abnormal foci of uptake were found. Postchemotherapy, a significant reduction of abnormal MIBG uptake (p < 0.01) was observed using a lesion-by-lesion analysis. When biochemical and MIBG postchemotherapy changes were compared, a significant relationship was found only between MIBG and VMA results (r = 0.84, p < 0.01). CONCLUSIONS: In postchemotherapy follow-up of children with advanced neuroblastoma, laboratory evaluation using VMA, FER and NSE measurements reflect only the global functional status of the disease, and are not helpful in defining the response of individual tumor lesions to treatment. Conversely, qualitative analysis using MIBG imaging may allow lesion-by-lesion evaluation of the heterogeneity of neuroblastoma response to chemotherapy. In this setting, changes in MIBG uptake are mirrored by the changes in catecholamine production, as measured by VMA levels.
UNLABELLED: The rationale of this study was the evaluation of response to chemotherapy in children with advanced neuroblastoma using currently available diagnostic modalities. METHODS:Iodine-131-metaiodobenzylguanidine (MIBG) imaging and 24-hr urinary vanillylmandelic acid (VMA) measurement were evaluated in 14 patients (7 males, 7 females, age range: 2-68 mo) with advanced neuroblastoma both pre- and postchemotherapy (5.6 +/- 2.8 mo) as well as serum ferritin (FER) and neuron-specific enolase (NSE) levels in 9 and 8 patients, respectively. MIBG images were qualitatively compared in each patient. RESULTS: Prechemotherapy, a total of 39 abnormal foci of MIBG uptake was detected. Postchemotherapy, 15 of these showed unchanged MIBG uptake, 7 had decreased uptake and 17 showed no uptake. In addition, four new abnormal foci of uptake were found. Postchemotherapy, a significant reduction of abnormal MIBG uptake (p < 0.01) was observed using a lesion-by-lesion analysis. When biochemical and MIBG postchemotherapy changes were compared, a significant relationship was found only between MIBG and VMA results (r = 0.84, p < 0.01). CONCLUSIONS: In postchemotherapy follow-up of children with advanced neuroblastoma, laboratory evaluation using VMA, FER and NSE measurements reflect only the global functional status of the disease, and are not helpful in defining the response of individual tumor lesions to treatment. Conversely, qualitative analysis using MIBG imaging may allow lesion-by-lesion evaluation of the heterogeneity of neuroblastoma response to chemotherapy. In this setting, changes in MIBG uptake are mirrored by the changes in catecholamine production, as measured by VMA levels.