Treatment of neuroendocrine tumours in adults with I-131-MIBG therapy
ABSTRACT This is a retrospective review of 131I-MIBG therapy for metastatic neuroendocrine tumours in 25 adult patients. The tumours comprised 17 carcinoids, six paragangliomas, one somatostatinoma and one intestinal smooth muscle sarcoma. All patients (age range 28-84 years) had stage IV disease and a positive diagnostic 123I-MIBG scan. Patients received 11.1 GBq (300 mCi) of 131I-MIBG given in three cycles at 3-monthly intervals. The mean cumulative dose was 27.7 GBq (751 mCi). Symptomatic response was observed in 80%, hormonal response in 55% and tumour response in 48% (WHO criteria). Of the 25 patients, 40% are still under follow-up. Death was due to disease progression in all except one. The median survival time was 48 months from diagnosis of metastatic disease, and 17 months from the last 131I-MIBG therapy. The 5-year survival rate was 59% (95% confidence interval, 34%-78%). There was no statistical difference in survival between previously treated (chemo/radiotherapy) and treatment-naive patients. Side-effects were minimal and commonly include nausea (in the first 24 h) and a transient fall in platelet count. 131I-MIBG provides a good therapeutic response in patients with metastatic neuro-endocrine tumours.
SourceAvailable from: Jesús Oria-Hernández[Show abstract] [Hide abstract]
ABSTRACT: Summary Background: Paragangliomas are neoplasms of the chromaffin tissue characterized by the synthesis and/or secretion of catecholamines. Their treatment depends on the extension and functional characteristics of the tumor. In this pathology, the anatomic and functional diagnostic evaluations provided by nuclear medicine imaging studies have significant usefulness. Clinical case: A 34-year-old male was diagnosed with a paraganglioma at the aortic bifurcation level by means of laboratory tests, imaging studies and nuclear medicine studies. Nuclear medicine was carried out with a scintigraphy with a norepinephrine analog, radioactive metaiodobenzylguanidine ( 131 I-MIBG), which demonstrates functionally and specifically the presence of neoplastic adrenergic tissue and extratumoral extension. In addition, a positron emission tomography coupled with computed tomography with a radioactive analog of glucose locates the extratumoral activity at bone level. Nuclear medicine studies allow the diagnosis of a malignant paraganglioma with presence of bone metastasis. The therapy includes surgical removal of the tumor and ablation of residual malignant tissue and metastatic lesions by radiotherapy with 131 I-MIBG. Radiotherapeutic treatment was possible due to the capacity of the tumor to uptake and concentrate the radioactive hormonal analog. Conclusions: In cases of paraganglioma, in addition to the localization of the tumor and the evaluation of biochemical alterations, it is indispensable to obtain anatomic and functional evaluation provided by nuclear medicine studies in order to achieve appropriate diagnoses and treatment.
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ABSTRACT: The growing interest in neuroendocrine tumours is due to the dynamic growth of detection of this type of cancer. Neuroendocrine tumours (neuroendocrine neoplasms - NENs / neuroendocrine tumours - NETs) derive from glands, groups of endocrine cells and diffuse neuroendocrine system cells. Mainly they derive from the gastrointestinal tract (gastroenteropancreatic-neuroendocrine tumours - GEP-NETs). Currently the modified WHO classification from 2010 is widely used. An important element in the choice of treatment is histological maturity based on mitotic activity and on assessment of proliferation activity (Ki-67). The treatment of choice is surgery. In most cases, complete surgical removal is impossible because of the advanced staging at the time of diagnosis. In well-differentiated neoplasms where the expression of somatostatin receptors is expected, patients are qualified for somatostatin analogues therapy. Poorly differentiated lesions are qualified for chemotherapy. In the guidelines of ENETS (European Neuroendocrine Tumor Society) from 2007 the rules concerning monitoring depending on the WHO classification were specified.Contemporary Oncology / Wspólczesna Onkologia 11/2012; 16(5):371-375. DOI:10.5114/wo.2012.31764 · 0.22 Impact Factor
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ABSTRACT: (131) I-MIBG therapy can be used for palliative treatment of malignant paraganglioma and pheochromocytoma. The main objective of the present study was to perform a systematic review and meta-analysis assessing the effect of (131) I-MIBG therapy on tumor volume in patients with malignant paraganglioma/pheochromocytoma. A literature search was performed in December 2012 to identify potentially relevant studies. Main outcomes were the pooled proportions of complete response, partial response and stable disease after radionuclide therapy. A meta-analysis was performed with an exact likelihood approach using a logistic regression with a random effect at the study level. Pooled proportions with 95% confidence intervals (CI) were reported. Seventeen studies concerning a total of 243 patients with malignant paraganglioma/pheochromocytoma were treated with (131) I-MIBG therapy. The mean follow-up ranged from 24 to 62 months. A meta-analysis of the effect of (131) I-MIBG therapy on tumor volume showed pooled proportions of complete response, partial response and stable disease of respectively 0.03 (95% CI 0.06-0.15), 0.27 (95% CI 0.19-0.37) and 0.52 (95% CI 0.41-0.62) and for hormonal response 0.11 (95% CI 0.05-0.22), 0.40 (95% CI 0.28-0.53) and 0.21 (95% CI 0.10-0.40), respectively.Separate analyses resulted in better results in hormonal response for paraganglioma patients than for pheochromocytoma patients. Data on the effects of (131) I-MIBG therapy on malignant paraganglioma/pheochromocytoma suggest that stable disease concerning tumor volume and a partial hormonal response can be achieved in over 50% and 40% of patients respectively, treated with (131) I-MIBG therapy. It cannot be ruled out that stable disease reflects not only the effect of MIBG-therapy, but also(partly) the natural course of the disease. This article is protected by copyright. All rights reserved.Clinical Endocrinology 10/2013; 80(4). DOI:10.1111/cen.12341 · 3.35 Impact Factor