The diagnostic performance of FDG-PET/CT for N- and M-staging of melanoma patients suggests its use for whole-body tumor staging, especially for detection or exclusion of distant metastases.
Summary:Purpose: Interictal [ 18 F]fluorodeoxyglucose (FDG) positron emission tomography (PET) demonstrates temporal hypometabolism in the epileptogenic zone of 60-90% of patients with temporal lobe epilepsy. The pathophysiology of this finding is still unknown. Several studies failed to show a correlation between hippocampal FDG-PET hypometabolism and neuronal cell loss. Because FDG is metabolized by hexokinase bound to the outer mitochondrial membrane, we correlated the glucose-oxidation capacity of hippocampal subfields obtained after surgical resection with the corresponding hippocampal presurgical FDG-PET activity.Methods: In 16 patients with electrophysiologically confirmed temporal lobe epilepsy, we used high-resolution respirometry to determine the basal and maximal glucose-oxidation rates in 400-m-thick hippocampal subfields obtained after dissection of human hippocampal slices into the CA1 and CA3 pyramidal subfields and the dentate gyrus.Results: We observed a correlation of the FDG-PET activity with the maximal glucose-oxidation rate of the CA3 pyramidal subfields (r p ס 0.7, p ס 0.003) but not for the regions CA1 and dentate gyrus. In accordance with previous studies, no correlation of the FDG-PET to the neuronal cell density of CA1, CA3, and dentate gyrus was found.Conclusions: The interictal hippocampal FDG-PET hypometabolism in patients with temporal lobe epilepsy is correlated to the glucose-oxidation capacity of the CA3 hippocampal subfield as result of impaired oxidative metabolism. Key Words: Temporal lobe epilepsy-FDG-PET-Mitochondrial oxidative phosphorylation.With [ 18 F]fluorodeoxyglucose positron emission tomography (FDG-PET), interictal hypometabolism is found among 60-90% of patients with the clinical syndrome of temporal lobe epilepsy (TLE) (1-3). FDG-PET has become an accepted tool for localization of temporal lobe foci and for prediction of surgical outcome (4-7). FDG-PET hypometabolism is proposed to be associated with the presence of underlying mesial temporal sclerosis (MTS) and seems to correlate with the degree of hippocampal volume loss measured by volumetric magnetic resonance imaging (MRI) (8,9). Conversely, several studies failed to show a clear relation between hippocampal neuronal cell loss, associated atrophy, and interictal hypometabolism (10-12). The pathophysiologic mechanism accounting for the FDG-PET hypometabolism is therefore still under discussion. The purpose of our study was to examine the existence of a relation between regional FDG metabolism in PET scans and intrinsic glucose metabolism in surgical specimens in TLE patients. Because FDG is metabolized in the brain by hexokinase bound to the outer mitochondrial membrane (13), we tried to correlate the glucoseoxidation capacity quantified in resected hippocampal subfield specimens with the corresponding hippocampal FDG-PET in patients with TLE.
FDG PET/CT is useful for the assessment of pulmonary metastases. The frequency of lesion detection is similar for AC and NAC PET images. A reduced sensitivity of FDG PET has to be considered for lesions smaller than 11 mm in diameter.
Indium- 111 labelled DTPA-D-Phe1-octreotide (DTPA-OC, OctreoScan) has been introduced into clinical routine for the detection of somatostatin receptor (SSTR)-positive tumours, which are predominantly of neuroendocrine origin. Potential further applications in other SSTR-positive cancers (e.g. small cell lung cancer, breast cancer, melanoma) have been limited mainly by the restricted availability and the high radionuclide costs. Previous attempts to introduce technetium-99m labelled analogues of octreotide have not been very successful in terms of the labelling procedure, in vivo biodistribution and/or tumour detection capabilities. The aim of this study was to assess the performance of the new 99mTc-labelled analogue HYNIC-D-Phe1-Tyr3-octreotide (HYNIC-TOC), using tricine as co-ligand, for the detection of SSTR-positive tumours in patients in comparison with 111In-DTPA-OC. Overall, 13 patients were examined using 99mTc-tricine-HYNIC-TOC. Twelve patients had proven SSTR-positive tumours, while one patient presented with an SSTR-negative tumour. In 9 of the 13 patients both tracers (99mTc-tricine-HYNIC-TOC and 111In-DTPA-OC) were used. Serial whole-body scans, spot views and/or single-photon emission tomography studies were performed. Images were qualitatively and semi-quantitatively (ROI analyses) evaluated. The biodistribution of 99mTc-tricine-HYNIC-TOC in patients showed high physiological uptake in kidneys, moderate uptake in liver and spleen and little uptake in the gut. The tracer showed predominantly renal and negligible hepatobiliary excretion. Known SSTR-positive tumour sites showed rapid and intense tracer accumulation. 99mTc-tricine-HYNIC-TOC demonstrated rapid tissue uptake within the first hour after injection and had basically no significant clearance (<20%) from normal or tumour tissue thereafter. In contrast, 111In-DTPA-OC showed continuous clearance from normal tissues as well as renal and very little hepatobiliary excretion. Nevertheless, the patterns of accumulation of 99mTc-tricine-HYNIC-TOC in tumours and normal organs were comparable to those of 111In-DTPA-OC. A lesion-by-lesion comparison showed comparable tumour detection capabilities in intrahepatic tumour sites and superior capabilities of 99mTc-tricine-HYNIC-TOC in respect of extrahepatic lesions. In conclusion, 99mTc-tricine-HYNIC-TOC shows promise as a tracer for SSTR imaging, given its favourable clinical characteristics (specific and high receptor affinity, good biodistribution, renal excretion, low radiation exposure, high imaging quality, on-demand availability) and cost-effectiveness. 99mTc-tricine-HYNIC-TOC allows earlier diagnosis (10 min-4 h) compared with 111In-DTPA-OC (4-24 h).
This retrospective study compared the effects of single and multiple administrations of 186 Re-HEDP) on palliation and survival of prostate cancer patients presenting with more than 5 skeletal metastases. Methods: A total of 60 patients were divided into 3 groups. Group A (n 5 19) consisted of patients who had received a single injection; group B (n 5 19), patients who had 2 injections; and group C (n 5 22), patients who had 3 or more successive injections. The 188 Re-HEDP was prepared using non-carrieradded 188 Re obtained from an in-house 188 W/ 188 Re generator after dilution with carrier perrhenate. Patients' data available from the referring physicians-including prostate-specific antigen levels-were entered into a Windows-based matrix and analyzed using a statistical program. The Gleason scores were similar for all 3 groups. Results: Mean survival from the start of treatment was 4.50 6 0.81 mo (95% confidence interval [CI], 2.92-6.08) for group A, 9.98 6 2.21 mo (95% CI, 5.65-14.31) for group B, and 15.66 6 3.23 (95% CI, 9.33-22.0) for group C. Although the 3 groups did not differ in Gleason score, the number of lost life-years was significantly lower in group C than in groups A and B. Pain palliation was achieved in 89.5% of group A, 94.7% of group B, and 90.9% of group C. Conclusion: Posttreatment overall survival could be improved from 4.50 to 15.66 mo by multiple-injection bone-targeted therapy with 188 Re-HEDP, when compared with a single injection. Significant pain palliation was common and independent of administration frequency. Bone metastases are frequent and encountered by all physicians treating oncologic patients (1). About 50% of prostate cancer patients will develop bone metastases, which are predominantly osteoblastic. The osteolytic type has the tendency to develop fractures resulting in serious morbidity. Chronic pain syndrome is the most important complication of bone metastases and has a negative impact on quality of life. Many of these patients are candidates for radionuclide therapy, since as many as 50% of patients are reported to receive only inadequate pain treatment by alternative methods (2).Radionuclide therapy of bone metastases was first used decades ago by administration of 32 P (3), which is incorporated in the DNA of rapidly proliferating bone marrow cells as well as in the trabecular and cortical bone structures. A relatively low 1:2 ratio of normal bone to metastatic tissue has been estimated (4). More recently, a variety of b-emitting radioisotopes has been investigated for therapy of bone metastases. The maximal b-energy of these radioisotopes is in the range of 0.8-2.3 MeV, with an average b-energy between 0.27 and 0.8 MeV (Table 1). 89 Sr-chloride and ionic 90 Y are both calcium analogs that are sequestered as cations by bone in relation to the intensity of osseous metabolism (5-9). 89 Sr is excreted renally to 70%-90% and is eliminated from the vascular compartment within the first few hours (10). Except for bone uptake and excretion via the urinary system, there i...
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