Circulating biomarkers in gastroenteropancreatic neuroendocrine tumours

Öberg, Kjell

doi:10.1530/erc-10-0280

Cited by 86 publications

(56 citation statements)

References 43 publications

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“…2 According to this evidence the presentation and findings can change based on the embryonic origin of the tumor; the foregut lesions account for 20-25% of all carcinoid tumors in which normally the primary lesions are found in the lung, thymus, stomach, or proximal duodenum with few cases along the hepatobiliary tract or pancreas. 7 There are usually associated with low serotonin levels but also they are able to produce serotonin precursors, histamine, corticotropin releasing hormone, adrenocorticotropic hormone (ACTH), gastrin, and CgA. Moreover midgut carcinoid tumors that are considered the most prevalent variation account for 40-50% of cases.…”

Section: Discussionmentioning

confidence: 99%

“…[11][12][13] Specifically in the case of carcinoid tumors, CgA is highly remarkable; it has been shown to be an independent prognostic factor because it correlates with the tumor load and illustrates the biological activity potency of the tumor. 7,14 However, other non-oncologic medical conditions that are able to raise the blood CgA levels develop several clinical symptoms that can mimic a NET. This increment is commonly seen in some medical conditions like impaired kidney function or even more common in individuals with chronic atrophic gastritis treated with proton pump inhibitors medications.…”

Section: Discussionmentioning

confidence: 99%

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Non oncologic elevated levels of chromogranin A in a symptomatic patient without a carcinoid tumor

2013

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The diagnosis of neuroendocrine tumors requires a highly suspicious level due to its variable symptoms and clinical presentation. Early diagnosis, prompt and appropriate treatments are clues to success preventing the eventual disease progression and the devastating consequences of the carcinoid syndrome. Measurement of the chromogranin A, plays an important role in the diagnosis of carcinoid tumors, during the clinical evolution and even more to evaluate the treatment response to somatostatin analogues. However, in some situations like our case, the serum levels evaluation could be a confounding factor imitating the clinical scenario of the disease especially when the chromogranin level is elevated but not in the typical oncologic range and moreover when the symptoms magnitude is really convincing and similar to the tumor disease instances. Case ReportA 58-year-old Hispanic woman with non-past medical history and negative history of risk factors presented to the emergency department with one-day history of lower extremity edema, shortness of breath and tachycardia. She has a history of mammary prosthesis replacement 28 days ago. An initial diagnosis of pulmonary embolism was made; a pulmonary angio computed tomography (CT) was performed showing no vascular occlusion. Transthoracic echocardiogram has shown normal EF of 60% and no valvular disease. Coronary pharmacologic perfusion echocardiogram showed normal heart function and finally renal function was normal. The patient was treated for acute heart failure and discharged with ambulatory control. Six months later, upper gastric endoscopy was performed evidencing multiple polyps. Immediately after the procedure, the patient presented an episode of upper body flushing and an intense diffuse dull abdominal pain without rebound and tenderness. She concern that she had experienced explosive episodes of non bloody diarrhea, self limited episodes of dry cough, frequent episodes of flushing in the upper trunk and face with profuse sweating and intense pruritus lasting 15 minutes associated with significant unintentional weight loss over the last 6 month. Further workup included negative brain MRI, negative chest CT and abdominal MRI that only showed multiple benign liver cysts, (Figure 1) pancreatic and rectal endosonography were also normal. Somatostatin receptor scintigraphy (SRS) with Indium-111-DPA-octreotide was negative, capsule endoscopy negative for masses, 24-hour urine level of 5-HIAA appeared borderline 9.8 mg/24 hr (range levels 1.9-10.0 mg/24 hr) and plasma chromogranin A were above the reference range 92.0 ng/mL (range levels 1.9-15.0 ng/mL by electrochemilumiscent method) ( Table 1). An endoscopic polypectomy was done and histopathology reported hyperplasic polyps. Three months later, due to the persistent and more intense symptoms, a SRS with Indium-111-DPA-octreotide was repeated showing positive reactivity at the epigastric area and chromogranin A control persists elevated. The patient was placed on monthly intramuscular octreotide with dramati...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Non oncologic elevated levels of chromogranin A in a symptomatic patient without a carcinoid tumor

2013

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“…Currently, the most frequently used biomarker for the diagnosis and follow-up of GEP-NETs is CgA (19,20,21). CgA is an acidic glycoprotein that is exclusively expressed in the secretory dense core granules of most normal en neoplastic neuroendocrine cells and upon stimulation is co-released with peptide hormones and neuropeptides (12,22,23).…”

Section: Generalmentioning

confidence: 99%

GEP-NETs UPDATE: Secreting gastro-enteropancreatic neuroendocrine tumours and biomarkers

Verbeek¹,

Korse²,

Tesselaar

2016

European Journal of Endocrinology

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Neuroendocrine tumours (NETs) are rare tumours with an annual incidence in the population in a range of 2-5 new cases per 100 000 inhabitants. NETs are widely variable in terms of anatomical location, hormone production, clinical behaviour and syndromes they can cause. This article reviews the many localizations and clinical presentations of NETs with a main focus on clinical biomarkers and their use in medical practice.

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“…Several studies report on the utility of tumor markers, such as chromogranin A (CgA) and neuron specific enolase (NSE) in the setting of pNETs [21][22][23]. It is worth noting that CgA is hindered by a moderate specificity (sensitivity: 72-100 %; specificity: 50-80 %), and NSE has been reported to have a poor sensitivity (sensitivity: 30-40 %; specificity: ∼100 %) limiting their utility as reliable diagnostic tools.…”

Section: Diagnosismentioning

confidence: 99%

“…Unfortunately, even after removal of all metastatic disease with microscopic negative margin (R0), the recurrence (or persistence) rate remains high with 1-year and 5-year disease free survival (DFS) of 53.7 and 10.7 %, respectively [23].…”

Section: Advanced Diseasementioning

confidence: 99%

Pancreatic Neuroendocrine Tumors: an Update

2015

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Pancreatic neuroendocrine tumors (pNETs) are rare and comprise only 1-2 % of all pancreatic neoplastic disease. Although the majority of these tumors are sporadic (90 %), pNETs can arise in the setting of several different hereditary genetic syndromes, most commonly multiple endocrine neoplasia type 1 (MEN1). The presentation of pNETs varies widely, with over 60 % having malignant distant disease at the time of initial diagnosis involving the liver or other distant sites. Functioning pNETs represent approximately 10 % of all pNETs, secrete a variety of peptide hormones, and are responsible for several clinical syndromes caused by profound hormonal derangement. Surgery remains the cornerstone of therapy and the only curative approach. It should be pursued for localized disease and for metastatic lesions amenable to resection. Multimodality therapies, including liver-directed therapies and medical therapy, are gaining increasing favor in the treatment of advanced pNETs. Their utility is multifold and spans from ameliorating symptoms of hormonal excess (functional pNETs) to controlling the local and systemic disease burden (non-functional pNETs). The recent introduction of target molecular therapy has promising results especially for the treatment of progressive well-differentiated G1/G2 tumor. In this review, we summarize the current knowledge and give an update on recent advancements made in the therapeutic strategies for pNETs.

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Circulating biomarkers in gastroenteropancreatic neuroendocrine tumours

Cited by 86 publications

References 43 publications

Non oncologic elevated levels of chromogranin A in a symptomatic patient without a carcinoid tumor

Non oncologic elevated levels of chromogranin A in a symptomatic patient without a carcinoid tumor

GEP-NETs UPDATE: Secreting gastro-enteropancreatic neuroendocrine tumours and biomarkers

Pancreatic Neuroendocrine Tumors: an Update

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