Pheochromocytomas that do not accumulate metaiodobenzylguanidine: localization with PET and administration of FDG.

Shulkin, Barry L.; Koeppe, Robert A.; Francis, I R; Deeb, G. Michael; Lloyd, R V; Thompson, Norman W.

doi:10.1148/radiology.186.3.8430179

Cited by 89 publications

(37 citation statements)

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“…One report has concerned the detection of medullary phaeochromocytoma while another has evaluated the role of PET in differentiating indeterminate adrenal mass in patients with cancer [121,283]. No report has as yet dealt with the diagnosis of hyperfunctioning cortical tumours.…”

Section: Adrenalsmentioning

confidence: 99%

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Oncological applications of positron emission tomography with fluorine-18 fluorodeoxyglucose

Rigo¹,

Paulus²,

et al. 1996

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Abstract. Positron emission tomography (PET) is now primarily used in oncological indication owing to the successful application of fluorine-18 fluorodeoxyglucose (FDG) in an increasing number of clinical indications at different stages of diagnosis, and for staging and followup. This review first considers the biological characteristics of FDG and then discusses methodological considerations regarding its use. Clinical indications are considered, and the results achieved in respect of various organs and tumour types are reviewed in depth. The review concludes with a brief consideration of the ways in which clinical PET might be improved.

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Section: Adrenalsmentioning

confidence: 99%

“…Shulkin et al have reported on two patients in whom metaiodobenzylguanidine failed to demonstrate the tumour [283,284]. FDG PET enabled correct localization of the tumour in both cases with high contrast and should be useful in turnouts that do not accumulate MIBG.…”

Section: Adrenalsmentioning

confidence: 99%

Oncological applications of positron emission tomography with fluorine-18 fluorodeoxyglucose

Rigo¹,

Paulus²,

et al. 1996

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“…Shulkin et al [95] was the first to report the advantages of 18F-FDG imaging in PCCs/PGLs that do not accumulate MIBG. The uptake of 18F-FDG is not related to tumor secretory status; its superiority in malignant PCCs that do not accumulate I 131 or I 123 MIBG has been confirmed [87,96].…”

Section: Positron Emission Tomographymentioning

confidence: 99%

Molecular and Therapeutic Advances in the Diagnosis and Management of Malignant Pheochromocytomas and Paragangliomas

et al. 2013

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Pheochromocytomas (PCCs) and paragangliomas (PGLs) are rare catecholamine-secreting tumors derived from chromaffin cells originating in the neural crest. These tumors represent a significant diagnostic and therapeutic challenge because the diagnosis of malignancy is frequently made in retrospect by the development of metastatic or recurrent disease. Complete surgical resection offers the only potential for cure; however, recurrence can occur even after apparently successful resection of the primary tumor. The prognosis for malignant disease is poor because traditional treatment modalities have been limited. The last decade has witnessed exciting discoveries in the study of PCCs and PGLs; advances in molecular genetics have uncovered hereditary and germline mutations of at least 10 genes that contribute to the development of these tumors, and increasing knowledge of genotype-phenotype interactions has facilitated more accurate determination of malignant potential. Elucidating the molecular mechanisms responsible for malignant transformation in these tumors has opened avenues of investigation into targeted therapeutics that show promising results. There have also been significant advances in functional and radiological imaging and in the surgical approach to adrenalectomy, which remains the mainstay of treatment for PCC. In this review, we discuss the currently available diagnostic and therapeutic options for patients with malignant PCCs and PGLs and detail the molecular rationale and clinical evidence for novel and emerging diagnostic and therapeutic strategies. TheOncologist2013; 18:391-407 Implications for Practice: Malignant pheochromocytoma and paraganglioma represent a significant management challenge.The diagnosis of malignancy is frequently made in retrospect and traditional treatment modalities have been limited. Recent exciting advances in molecular genetics have uncovered hereditary and germline mutations of at least 10 genes that contribute to the development of these tumors. Increasing knowledge of genotype-phenotype interactions facilitates more accurate determination of malignant potential and has prompted investigation into targeted therapeutics with promising results. There have also been significant advances in functional and radiological imaging and in the surgical approach to adrenalectomy, which remains the mainstay of treatment for pheochromocytoma. Due to the rarity of this tumor, large-scale clinical studies that would progress clinical practice are rare, and the requirement for international collaboration is crucial. The need for large-scale international multicenter studies to effectively exploit the molecular and genetic knowledge gained in this area is highlighted in this review.

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“…Esse método pode localizar feocromocitomas extra-adrenais não localizados com 131 I MIBG. Entretanto, mais estudos são necessários para a determinação de sua real eficácia 27 . Maurea et al compararam a captação com 131 I MIBG, tomografia computadorizada e ressonância magnética, evidenciando, em pacientes ainda não submetidos à cirurgia do feocromocitoma, sensibilidade de 82% no 131 I MIBG, e de 100% nos dois outros métodos.…”

Section: ) Diagnóstico Anatômicounclassified

“…Os principais riscos na cateterização seletiva são: infarto da glândula adrenal e liberação de catecolaminas pela manipulação do tumor. A localização precisa dos pontos de coleta sanguínea é obtida por meio da flebografia e dosagem de cortisol plasmático 6,9,27,28 . A arteriografia pode ser realizada quando há suspeita de feocromocitoma extra-adrenal ou quando a tomografia não localiza o tumor, mas é um método invasivo pouco utilizado, freqüen-temente precipitando crises hipertensivas 2,29 .…”

Section: ) Diagnóstico Anatômicounclassified

Feocromocitoma: atualização diagnóstica e terapêutica

Faiçal¹,

Shiota²

1997

Rev. Assoc. Med. Bras.

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Feocromocitomas são tumores originários das células cromafins do eixo simpático adrenomedular, caracterizados pela autonomia na produção de catecolaminas, mais freqüentemente adrenalina e/ou noradrenalina 1 . A localização medular é a mais freqüente (90% dos casos), podendo, entretanto, ter origem em paragânglios da base do crânio até a bifurcação das artérias ilíacas, ou no órgão de Zuckerkandl, localizando-se mais raramente em tórax, bexiga ou cérebro, sendo assim denominados feocromocitomas extra-adrenais ou paragangliomas 2-5 . A incidência destes tumores situa-se em torno de 0,1% nos hipertensos diastólicos, sendo mais freqüentes entre a 3 a e 5 a décadas de vida, e com incidência ligeiramente maior em mulheres que em homens. Dentre eles, mais de 90% são benignos e únicos, e na maioria dos casos a ressecção tumoral leva à cura. Por outro lado, quando malignos, estes tumores apresentam metástases freqüentemente em ossos, linfonodos regionais, fíga-do, pulmões, cérebro e cordão espinhal 2-7 . Em estudo de Deal et al., 32% dos feocromocitomas são tumores múltiplos ou bilaterais, apresentando maior incidência em crianças e nos casos de caráter familiar (cerca de 10% a 15%). Essas características ocorrem mais freqüentemente na neoplasia endócrina múltipla -NEM -tipo 2a e 2b. A NEM tipo 2a é caracterizada pela presença de feocromocitoma, carcinoma medular de tiróide e hiperparatiroidismo. O feocromocitoma e o carcinoma medular de tiróide são diagnosticados simultaneamente em 73% dos casos, mas o intervalo de diagnóstico dos dois pode ser prolongado. Já a NEM tipo 2b consiste em feocromocitoma, carcinoma medular de tiróide, neuromas de mucosas, ganglioneuromatose e hábito marfanóide [2][3][4]8 . FISIOPATOLOGIAA hipertensão arterial é a manifestação clínica mais comum do feocromocitoma, acometendo mais de 90% dos pacientes, geralmente resistente ao tratamento anti-hipertensivo convencional, mas podendo responder a bloqueadores alfa-adrenér-gicos, bloqueadores dos canais de cálcio e nitroprussiato de sódio. A hipertensão arterial é sustentada em 50% das vezes, e o restante dos quadros hipertensivos, associando-se a paroxismos, com duração de minutos até horas, com intervalos variáveis, enquanto, por outro lado, cerca de 25% a 40% dos feocromocitomas manifestam-se isoladamente na forma de paroxismos hipertensivos. Ocasionalmente, a hipertensão arterial evolui com caráter maligno, acompanhado de proteinúria e/ ou retinopatia hipertensiva e, às vezes, complicando com encefalopatia hipertensiva 2,3,5,7 . A tríade clássica do feocromocitoma, associado à hipertensão arterial, é composta por cefaléia, sudorese profusa e palpitações. Entretanto, muitos pacientes não apresentam taquicardia, e durante os paroxismos raramente pode ser observada bradicardia. Outros sintomas são ansiedade, rubor facial, palidez cutânea, náuseas, vômitos, dispnéia e dor precordial, provavelmente provenientes das alterações vasomotoras 2-5,9 . Comprometimento cardiovascular no feocromocitoma pode caracterizar-se por angina do peito e infarto agudo...

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Pheochromocytomas that do not accumulate metaiodobenzylguanidine: localization with PET and administration of FDG.

Cited by 89 publications

References 0 publications

Oncological applications of positron emission tomography with fluorine-18 fluorodeoxyglucose

Oncological applications of positron emission tomography with fluorine-18 fluorodeoxyglucose

Molecular and Therapeutic Advances in the Diagnosis and Management of Malignant Pheochromocytomas and Paragangliomas

Feocromocitoma: atualização diagnóstica e terapêutica

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