{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,10]],"date-time":"2026-04-10T10:12:30Z","timestamp":1775815950108,"version":"3.50.1"},"reference-count":30,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2017,6,5]],"date-time":"2017-06-05T00:00:00Z","timestamp":1496620800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Scientific and Engineering Research Board (SERB)"},{"name":"Department of Science and Technology, Government of India","award":["SB\/SO\/HS-41\/2013"],"award-info":[{"award-number":["SB\/SO\/HS-41\/2013"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Med Imag Rad Onc"],"published-print":{"date-parts":[[2017,12]]},"abstract":"Abstract<\/jats:title>Introduction<\/jats:title>Although few studies have demonstrated utility of 18<\/jats:sup>F\u2010 fluoro\u20102\u2010deoxy\u2010d<\/jats:sc>\u2010glucose positron emission tomography\/computerised tomography (18<\/jats:sup>F\u2010FDG PET<\/jats:styled-content>\/CT<\/jats:styled-content>) in benign pheochromocytoma\/paragangliomas (PCC<\/jats:styled-content>\/PGL<\/jats:styled-content>s), there limited data on factors predicting the FDG<\/jats:styled-content> uptake in PCC<\/jats:styled-content>\/PGL<\/jats:styled-content>.<\/jats:p><\/jats:sec>Methods<\/jats:title>The study was conducted at a tertiary health care centre. In addition to the routine investigations, all patients (n<\/jats:italic>\u00a0=\u00a096) with PCC<\/jats:styled-content>\/PGL<\/jats:styled-content> were evaluated with 18<\/jats:sup>F\u2010FDGPET<\/jats:styled-content>\/CT<\/jats:styled-content> and majority (n<\/jats:italic>\u00a0=\u00a078) underwent 131<\/jats:sup>I\u2010metaiodobenzyl guanidine (131<\/jats:sup>I\u2010MIBG<\/jats:styled-content>) scintigraphy. Forty\u2010three patients also underwent testing for germline mutations in five PCC<\/jats:styled-content>\/PGL<\/jats:styled-content> susceptibility genes (VHL<\/jats:styled-content>, RET<\/jats:styled-content>, SDHB<\/jats:styled-content>, SDHC<\/jats:styled-content><\/jats:italic> and SDHD<\/jats:styled-content><\/jats:italic>) and all patients were evaluated clinically for neurofibromatosis\u20101.<\/jats:p><\/jats:sec>Results<\/jats:title>The study included 96 patients with PCC<\/jats:styled-content>\/PGL<\/jats:styled-content>(82 benign and 14 malignant). FDGSUV<\/jats:styled-content>max was significantly higher for malignant than benign PCC<\/jats:styled-content>\/PGL<\/jats:styled-content>(P<\/jats:italic>\u00a0=\u00a00.009) and for extra\u2010adrenal PGL<\/jats:styled-content> than adrenal PCC<\/jats:styled-content> (P<\/jats:italic>\u00a0=\u00a00.017). In subgroup analysis, metanephrine\u2010secreting PCC and non\u2010secretory PCC<\/jats:styled-content> had significantly lower FDG SUV<\/jats:styled-content>max than normetanephrine\u2010secreting PCC (P<\/jats:italic>\u00a0=\u00a00.017, P<\/jats:italic>\u00a0=\u00a00.038 respectively), normetanephrine\u2010secreting\u2010sympathetic PGL (P<\/jats:italic>\u00a0=\u00a00.008, P<\/jats:italic>\u00a0=\u00a00.019 respectively) and non\u2010secretory sympathetic PGL (P<\/jats:italic>\u00a0=\u00a00.003, P<\/jats:italic>\u00a0=\u00a00.009 respectively). Patients with mutations in cluster 1 genes (n<\/jats:italic>\u00a0=\u00a014) had significantly higher FDG SUV<\/jats:styled-content>max than those with mutations in cluster 2 genes (n<\/jats:italic>\u00a0=\u00a04) (P<\/jats:italic>\u00a0=\u00a00.04). Sensitivities of 131<\/jats:sup>I\u2010MIBG<\/jats:styled-content> and 18<\/jats:sup>F\u2010FDG PET<\/jats:styled-content>\/CT<\/jats:styled-content>were 77.78% and 100% for cluster 1 genes\u2010related PCC<\/jats:styled-content>\/PGL<\/jats:styled-content> whereas they were 100% and 50% for cluster 2 genes\u2010related PCC<\/jats:styled-content>\/PGL<\/jats:styled-content>, respectively. Multivariate regression analysis of mutation positive patients identified genetic status as the only independent predictor of FDG SUV<\/jats:styled-content>max.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>The study suggests that the underlying genetic status determines FDG<\/jats:styled-content> uptake in PCC<\/jats:styled-content>\/PGL<\/jats:styled-content> and not location, secretory status or malignancy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1754-9485.12620","type":"journal-article","created":{"date-parts":[[2017,6,6]],"date-time":"2017-06-06T05:01:24Z","timestamp":1496725284000},"page":"745-752","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Genetic status determines 18<\/sup>F\u2010FDG<\/scp> uptake in 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