Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours

Ramage, John

doi:10.1136/gut.2004.053314

Cited by 326 publications

(352 citation statements)

References 171 publications

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“…Based on several secretory activities of neuroendocrine differentiated cells, there are many potential markers. The most important and commonly used markers of neuroendocrine differentiation are Chromogranin A (CgA) and NSE (Ramage et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

For Which Cancer Types can Neuron-Specific Enolase be Clinically Helpful in Turkish Patients?

Bilgin

Dizdar²,

Serilmez³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

For Which Cancer Types can Neuron-Specific Enolase be Clinically Helpful in Turkish Patients?

Bilgin

Dizdar²,

Serilmez³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Many tumours grow slowly, although some can grow very rapidly (Modlin et al, 2003(Modlin et al, , 2005. They express neuroendocrine differentiation markers, have secretory characteristics and may present with hypersecretory syndromes (Plockinger et al, 2004;Ramage et al, 2005). Unlike patients with adenocarcinomas at the same sites, patients with NETs tend to experience a longer indolent duration of their condition.…”

mentioning

confidence: 99%

“…Unlike patients with adenocarcinomas at the same sites, patients with NETs tend to experience a longer indolent duration of their condition. Although the incidence of NETs is low (3 -4 cases per 100 000 per annum) (Ramage et al, 2005), the good prognosis of many with these tumours has resulted in an increasing prevalence.…”

mentioning

confidence: 99%

“…In such patients, alleviation of hormonal symptoms and prolongation of survival are key goals (Plockinger et al, 2004;Ramage et al, 2005). Palliative treatment options include surgical resection of the primary tumour if symptomatic, treatment of liver metastases (by debulking surgery, hepatic artery embolisation or radiofrequency ablation), chemotherapy, interferon-a, somatostatin analogues and radionuclide therapies (Plockinger et al, 2004;Ramage et al, 2005).…”

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confidence: 99%

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Assessment of the efficacy and toxicity of 131I-metaiodobenzylguanidine therapy for metastatic neuroendocrine tumours

et al. 2008

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131 I-metaiodobenzylguanidine ( 131 I-MIBG) is a licensed palliative treatment for patients with metastatic neuroendocrine tumours. We have retrospectively assessed the consequences of 131 I-MIBG therapy in 48 patients (30 gastroenteropancreatic, 6 pulmonary, 12 unknown primary site) with metastatic neuroendocrine tumours attending Royal Liverpool University Hospital between 1996 and 2006. Mean age at diagnosis was 57.6 years (range 34 -81). 131 I-MIBG was administered on 88 occasions (mean 1.8 treatments, range 1 -4). Twenty-nine patients had biochemical markers measured before and after 131 I-MIBG, of whom 11 (36.7%) showed 450% reduction in levels post-therapy. Forty patients had radiological investigations performed after 131 I-MIBG, of whom 11(27.5%) showed reduction in tumour size post-therapy. Twenty-seven (56.3%) patients reported improved symptoms after 131 I-MIBG therapy. Kaplan -Meier analysis showed significantly increased survival (P ¼ 0.01) from the date of first 131 I-MIBG in patients who reported symptomatic benefit from therapy. Patients with biochemical and radiological responses did not show any statistically significant alteration in survival compared to non-responders. Eleven (22.9%) patients required hospitalisation as a consequence of complications, mostly due to mild bone marrow suppression. 131 I-MIBG therefore improved symptoms in more than half of the patients with metastatic neuroendocrine tumours and survival was increased in those patients who reported a symptomatic response to therapy.

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“…(Oberg et al, 2004) Ramage and colleagues advocate a constant intravenous infusion of octreotide at a dose of 50mg/h for 12h prior to and at least 48h after surgery for symptomatic patients in 2005. (Ramage et al, 2005) Furthermore, the authors raise cautions for carcinoid crisis in asymptomatic patients and suggest constant preparation of somatostatin analogues before interventional procedures in 2012. (Ramage et al, 2012) Nevertheless, the efficacy regarding the prophylactic usage of SSTA has not been fully assessed and the schemes are generally based on the authors' personal experience.…”

Section: Introductionmentioning

confidence: 99%

Somatostatin Analogues Do Not Prevent Carcinoid Crisis

Guo

Tang²

2014

Asian Pacific Journal of Cancer Prevention

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Background: Carcinoid crisis is a life-threating syndrome of neuroendocrine tumors (NETs) characterized by dramatic blood pressure fluctuation, arrhythmias, and bronchospasm. In the era of booming anti-tumor therapeutics, this has become more important since associated stresses can trigger carcinoid crisis. Somatostatin analogues (SSTA) have been recommended for prophylactic administration before intervention procedures for functioning NETs. However, the efficacy is still controversial. The aim of this article is to review efficacy of SSTA for preventing carcinoid crisis. Materials and Methods: PubMed, Cochrane Controlled trials Register, and EMBASE were searched using 'carcinoid crisis' as a search term combining terms with 'somatostatin'; 'octreotide'; 'lanreotide' and 'pasireotide' until December 2013. Results: Twenty-eight articles were retrieved with a total of fifty-three unique patients identified for carcinoid crisis. The most common primary sites of NETs were the small intestine and respiratory tract. The triggering factors for carcinoid crisis included anesthesia/ surgery (63.5%), interventional therapy (11.5%), radionuclide therapy (9.6%), examination (7.7%), medication (3.8%), biopsy (2%) and spontaneous (2%). No randomized controlled trials (RCTs) were identified and two case-control studies were included to assess the efficacy of SSTA for preventing carcinoid crisis by meta-analysis. The overall pooled risk of perioperative carcinoid crisis was similar despite the prophylactic administration of SSTA (OR 0.44, 95% CI: 0.14 to 1.35, p=0.15). Conclusions: SSTA wasnot helpful for preventing carcinoid crisis based on a meta-analysis of retrospective studies. Attentive monitoring and careful intervention are essential. Future studies with better quality are needed to clarify any effect of SSTA for preventing carcinoid crisis.

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Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours

Cited by 326 publications

References 171 publications

For Which Cancer Types can Neuron-Specific Enolase be Clinically Helpful in Turkish Patients?

For Which Cancer Types can Neuron-Specific Enolase be Clinically Helpful in Turkish Patients?

Assessment of the efficacy and toxicity of 131I-metaiodobenzylguanidine therapy for metastatic neuroendocrine tumours

Somatostatin Analogues Do Not Prevent Carcinoid Crisis

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