How We Read Oncologic FDG PET/CT | Cancer Imaging | Full Text - 0 views
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In early PET literature focusing on analysis of solitary pulmonary nodules, some researchers defined malignancy based on a SUVmax threshold of greater than 2.5
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We contend that SUV analysis has virtually no role in this setting.
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tumours grow as spheres, whereas inflammatory processes are typically linear
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Far more important than the SUVmax is the pattern rather than intensity of metabolic abnormality and the correlative CT findings
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Descriptively, we define SUV < 5 as “low intensity”, 5–10 as “moderate”, 10–15 as “intense” and >15 as “very intense”
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Evolving literature suggests that intensity of uptake is an independent prognostic factor and in some tumour subtypes superior to histopathologic characterisation.
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aerobic glycolysis
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Our practice of thresholding the grey and colour scale to liver as detailed above results in similar image intensity to a fixed upper SUV threshold of 8 to 10
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The advantage of using the liver as a reference tissue is also aided by this organ having rather low variability in metabolic activity
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When the liver is abnormal and cannot be used as a reference organ, we use the default SUV setting of an upper SUV threshold of 8
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One of the most challenging aspects of oncologic FDG PET/CT review, however, is to recognise all the patterns of metabolic activity that are not malignant and which consequently confound interpretation
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Many benign and inflammatory processes are also associated with high glycolytic activity
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Future articles in the “How I Read” series will address the specific details of reading PET/CT in various cancers
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The intensity of uptake in metastases usually parallels that in the primary site of disease
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For example, discordant low-grade activity in an enlarged lymph node in the setting of intense uptake in the primary tumour suggests it is unlikely malignant and more likely inflammatory or reactive
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By CT criteria the enlarged node is ‘pathologic’ but the discordantly low metabolic signature further characterises this is as non-malignant since such a node is not subject to partial volume effects and therefore the intensity of uptake should be similar to the primary site
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The exception is when the lymph node is centrally necrotic as a small rim of viable tumour is subject to partial volume effects with expectant lower intensity of uptake; integrating the CT morphology is therefore critical to reaching an accurate interpretation
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Small nodes that are visualised on PET are conversely much more likely to be metastatic as such nodes are subject to partial volume effects.
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The exception to this rule is tumours with a propensity for tumour heterogeneity at different sites
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The combination of FDG and a more specific tracer, which visualises the well-differentiated disease can be very useful to characterise this phenomenon
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“metabolic signature”
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For the majority of malignant processes, the intensity of metabolic abnormality correlates with degree of aggressiveness or proliferative rate.
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a negative PET/CT study in a patient with biopsy proven malignancy would be considered false-negative
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Warburg effect
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There, however, are a significant minority of tumours that utilise substrates other glucose such as glutamine or fatty acids as a source of the carbon atoms required for growth and proliferation
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This includes a subset of diffuse gastric adenocarcinomas, signet cell colonic adenocarcinomas and some sarcomas, particularly liposarcoma
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There may be a role for other radiotracers such as fluorothymidine (FLT) or amino acid substrates in this setting.
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Some tumours harbour mutations that result in defective aerobic mitochondrial energy metabolism, effectively simulating the Warburg effect
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patients with hereditary paraganglioma and pheochromocytoma highlight this phenomenon
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These have intense uptake on FDG PET/CT despite often having low proliferative rate.
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Uterine fibroids, hepatic adenomas, fibroadenomas of the breast and desmoid tumours are benign or relatively benign lesions that can have quite high FDG-avidity.
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Metabolic activity switches off rapidly following initiation of therapy
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Common examples where patients have commenced active therapy but the referrer is requesting “staging” includes hormonal therapy (eg. tamoxifen) in breast cancer, oral capecitabine in colorectal cancer or high dose steroids in Hodgkin’s lymphoma
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It is therefore critical to perform PET staging before commencement of anti-tumour therapy
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The potential advantage of routine diagnostic CT is improved anatomic localisation and definition
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Without intravenous contrast, additional identification of typical oncologic complications such as pulmonary embolism or venous thrombosis cannot be identified
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If the study is performed as an “interim” restaging study after commencement of therapy but before completion, in order to reach a valid or clinically useful conclusion findings must be interpreted in the context of known changes that occur at a specific timing and type of therapy
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The most well studied use of interim PET is in Hodgkin’s lymphoma where repeat PET after two cycles of ABVD-chemotherapy provides powerful prognostic information and may improve outcomes by enabling early change of management
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good read on the PET/CT scan reading. They mention that tumors are spheres and inflammation is linear, yet inflammation coexists with cancer; hard to simply delineate these on simple terms. I do agree aon the metabolic signature of the PET/CT scan
