Version May 2024
INTRODUCTION — Neuroendocrine cells are distributed widely throughout the body, and neuroendocrine neoplasms can arise at many sites. While there are differences in terminology and grading for tumors arising at different sites, all commonly used classification systems reflect a basic separation between more indolent, well-differentiated neuroendocrine tumors (NETs; which in the past, were referred to as carcinoid tumors when arising in the digestive system [now termed gastrointestinal NETs], or pancreatic islet cell tumors [pancreatic NETs]) and far more aggressive, poorly differentiated neoplasms that behave clinically more like small cell carcinoma of the lung (termed neuroendocrine carcinomas). (See "High-grade gastroenteropancreatic neuroendocrine neoplasms" and "Pathobiology and staging of small cell carcinoma of the lung".)
The clinical presentation, prognosis, radiographic imaging, and tumor marker evaluation of patients with well-differentiated NETs arising in the digestive system are discussed in this topic review. Pathology and nomenclature of gastroenteropancreatic NETs, treatment options for advanced or metastatic NETs, as well as issues relating to the presentation, localization, and treatment of early stage gastrointestinal NETs and pancreatic NETs are presented elsewhere, as are small cell lung cancer, high-grade gastroenteropancreatic neuroendocrine carcinoma, and neuroendocrine carcinoma of unknown primary site.
●(See "Pathology, classification, and grading of neuroendocrine neoplasms arising in the digestive system".)
●(See "Diagnosis of carcinoid syndrome and tumor localization".)
●(See "Insulinoma".)
●(See "Glucagonoma and the glucagonoma syndrome".)
●(See "Somatostatinoma: Clinical manifestations, diagnosis, and management".)
●(See "VIPoma: Clinical manifestations, diagnosis, and management".)
●(See "Neuroendocrine neoplasms of unknown primary site".)
●(See "High-grade gastroenteropancreatic neuroendocrine neoplasms".)
●(See "Pathobiology and staging of small cell carcinoma of the lung".)
CLASSIFICATION AND NOMENCLATURE — The World Health Organization (WHO) classification of neuroendocrine neoplasms arising in the digestive system separates these tumors into two broad categories (table 1) [1] (see "Pathology, classification, and grading of neuroendocrine neoplasms arising in the digestive system", section on 'Pathology, tumor classification, and nomenclature'):
●Well-differentiated NETs, which show a solid, trabecular, gyriform, or glandular pattern, with fairly uniform nuclei, salt-and-pepper chromatin, and finely granular cytoplasm. They are divided into low-grade (G1), intermediate-grade (G2), and high-grade (G3) subtypes based on proliferative rate.
●Poorly differentiated neuroendocrine carcinomas, which are G3 carcinomas that resemble small cell or large cell neuroendocrine carcinoma of the lung (picture 1) [2]. (See "High-grade gastroenteropancreatic neuroendocrine neoplasms" and "Pathology of lung malignancies", section on 'Neuroendocrine tumors'.)
Poorly differentiated neuroendocrine carcinomas are often associated with a rapid clinical course; as such, their clinical behavior is similar to that of small cell carcinoma of the lung, and they are treated similarly with platinum-based chemotherapy. (See "High-grade gastroenteropancreatic neuroendocrine neoplasms".)
By contrast, most well-differentiated gastroenteropancreatic NETs generally have a much better prognosis. Even in the presence of liver metastases, some patients may survive for many years. However, these tumors are not a homogeneous group, but instead display a spectrum of aggressiveness. Within the subgroup of well-differentiated NETs, morphology alone cannot predict tumor behavior. Proliferative rate, as assessed by mitotic count and/or Ki-67 labeling index, is of prognostic significance, independent of tumor stage [3,4].
There is a small subset of patients with NETs that appear histologically well differentiated, with fewer than 20 mitoses per 10 high-power fields (G2 by mitotic count), but are associated with high Ki-67 proliferation indices (>20 percent) that fall into the G3 range. The clinical behavior of these grade-discordant tumors is somewhat worse than grade-concordant well-differentiated G2 NETs but is better than that of bona fide poorly differentiated neuroendocrine carcinomas. (See "Pathology, classification, and grading of neuroendocrine neoplasms arising in the digestive system", section on 'High-grade, well-differentiated neoplasms'.)
Digestive tract NETs can also be defined by their functional, or hormone-secreting, status. Functioning NETs are characterized by the presence of clinical symptoms due to excess hormone secretion by the tumor. Functioning (hormone-secreting) pancreatic NETs are classified according to the predominant hormone they secrete and the resulting clinical syndrome (eg, insulinoma, gastrinoma, glucagonoma, VIPoma, somatostatinoma). Functioning gastrointestinal NETs (ie, those associated with the carcinoid syndrome) are not classified differently than nonfunctioning tumors. Although functionality may impact prognosis (eg, insulinomas are generally indolent tumors), the biologic behavior of most functioning NETs is defined by the grade and stage of the tumor, just as it is in nonfunctioning tumors. The vast majority of functioning tumors are well differentiated. (See "Insulinoma" and "Zollinger-Ellison syndrome (gastrinoma): Clinical manifestations and diagnosis" and "Glucagonoma and the glucagonoma syndrome" and "VIPoma: Clinical manifestations, diagnosis, and management" and "Somatostatinoma: Clinical manifestations, diagnosis, and management" and "Clinical features of carcinoid syndrome" and "Diagnosis of carcinoid syndrome and tumor localization" and "Pathology, classification, and grading of neuroendocrine neoplasms arising in the digestive system", section on 'Functionality and nomenclature'.)
CLINICAL PRESENTATION — The clinical course of patients with metastatic well-differentiated gastroenteropancreatic NET is highly variable. Some untreated patients with indolent tumors remain symptom free for years, while others have symptomatic disease, either from tumor bulk or peptide hormone hypersecretion. Patients with functioning pancreatic NETs typically have symptoms caused by the specific type of hormone being produced by the tumor. (See "Glucagonoma and the glucagonoma syndrome", section on 'Clinical features' and "Insulinoma", section on 'Symptoms and misdiagnosis' and "Somatostatinoma: Clinical manifestations, diagnosis, and management", section on 'Clinical manifestations' and "VIPoma: Clinical manifestations, diagnosis, and management", section on 'Clinical features'.)
For patients with metastatic gastrointestinal NETs, the secretion of serotonin and other vasoactive substances causes carcinoid syndrome, which is manifested by episodic flushing, wheezing, diarrhea, and eventual right-sided valvular heart disease [5]. The carcinoid syndrome is most commonly seen with midgut NETs (small intestine, appendix, proximal large bowel), almost exclusively in the setting of metastatic (usually liver) disease. It is rare with foregut (gastric, bronchial) and hindgut (distal colon, rectum, genitourinary) NETs. In addition, foregut NETs can be associated with an atypical variant of carcinoid syndrome. Patients with extraintestinal (eg, ovarian and bronchial) NETs can develop carcinoid syndrome in the absence of liver metastases (table 2). (See "Clinical features of carcinoid syndrome" and "Clinical characteristics of well-differentiated neuroendocrine (carcinoid) tumors arising in the gastrointestinal and genitourinary tracts" and "Diagnosis of carcinoid syndrome and tumor localization".)
PROGNOSIS — Even when advanced, survival times for patients with well-differentiated gastroenteropancreatic NETs are generally better than those for patients with other malignancies [6], although prognosis can be highly variable. A major factor impacting overall survival is primary tumor site [6]. In an analysis of cases in the National Cancer Institute (NCI) Surveillance, Epidemiology, and End Results (SEER) database of NETs diagnosed between 2000 and 2012, the median survival for patients with distant metastases from grade 1 to 2 pancreatic NETs was 50 months. For patients with distant metastases from grade 1 to 2 small intestinal NETs, median survival was 103 months; by contrast, it was only 14 months for patients with colonic primary tumors [7].
Another major prognostic factor is histologic grade, which is assigned based on the mitotic rate or Ki-67 labeling index [7,8]. As an example, in the SEER database analysis, patients with a grade 1 or 2 appendiceal NET, or a grade 1 rectal NET had a median survival >30 years. By contrast, patients with grade 3 neuroendocrine carcinoma had poor overall survival irrespective of primary tumor site, ranging from 30 to 33 months for small intestine and appendix, respectively, to 8 months for cecum and colon [7]. (See "Pathology, classification, and grading of neuroendocrine neoplasms arising in the digestive system", section on 'Staging system'.)
Other prognostic factors in patients with metastatic disease include disease burden, the presence of distant extrahepatic metastases, race, and older age [7,9].
IMAGING — The predominant site of metastatic spread well-differentiated NETs is the liver (picture 2). Liver function tests are an unreliable indicator of tumor involvement; the serum total bilirubin and/or alkaline phosphatase are frequently normal despite extensive liver involvement. Imaging is therefore an important aspect of monitoring patients with advanced gastroenteropancreatic NETs for evidence of disease progression or treatment response.
Well-differentiated neuroendocrine tumors
Cross-sectional imaging — For patients with advanced gastroenteropancreatic NETs, cross-sectional anatomic imaging is the standard approach to monitoring patients and is generally performed with either multiphasic computed tomography (CT) or magnetic resonance imaging (MRI). Triphasic helical CT of the abdomen and pelvis is recommended to image metastatic gastrointestinal and pancreatic NETs [10,11]. These tumors are highly vascular and may appear isodense with the liver during certain contrast phases (image 1). They generally enhance most intensely with intravenous contrast during the early arterial phases of imaging, with washout during the delayed portal venous phase.
MRI is a reasonable alternative, as lesions can be visualized without contrast in T1 and T2-weighted sequences, reducing the variability sometimes seen with CT-based imaging results (image 2 and image 3). In one study, MRI detected significantly more metastases than either planar somatostatin receptor scintigraphy (SRS) using indium-111 (111-In) pentetreotide (OctreoScan) or CT (sensitivity rates for MRI, planar SRS, and CT were 95, 79, and 49 percent, respectively) [12]. As a result of this greater sensitivity for liver metastases, some clinicians prefer MRI over CT. Consensus-based guidelines from the European Neuroendocrine Tumor Society (ENETS) state that MRI should be considered superior to CT for the detection and follow-up of liver metastases from NETs [13,14].
Somatostatin receptor-based imaging techniques — Over 90 percent of gastroenteropancreatic NETs, including nonfunctioning NETs (with the exception of insulinomas), have high concentrations of somatostatin receptors and can be imaged using a radiolabeled form of the somatostatin analog octreotide (111-In pentetreotide). More recently, a number of positron emission tomography (PET)-based, somatostatin receptor-based imaging techniques have also been evaluated. One of these radionuclides, gallium Ga-68 DOTATATE (Ga-68 DOTATATE), was approved by the US Food and Drug Administration (FDA) for routine use in patients with NETs in June 2016 [15]. The higher sensitivity of Ga-68 DOTATATE suggests that this is the preferred option for most clinical scenarios, particularly in patients with smaller tumor volume or an occult primary tumor [16]. Two other radionuclides, gallium Ga-68 DOTATOC (Ga-68 DOTATOC) and copper Cu-64 DOTATATE (Cu-64 DOTATATE), were subsequently approved.
Clinical use — Baseline imaging using one of the somatostatin receptor-based imaging techniques is generally recommended in patients with advanced NETs, both as an adjunct to routine cross-sectional imaging and because evidence of somatostatin receptor expression (based on a positive scan) can be predictive of a clinical response to therapy with somatostatin analogs, such as octreotide and lanreotide [17], as well as peptide receptor radioligand therapy. (See "Metastatic well-differentiated gastrointestinal neuroendocrine (carcinoid) tumors: Systemic therapy options to control tumor growth", section on 'Somatostatin analogs' and "Metastatic well-differentiated pancreatic neuroendocrine tumors: Systemic therapy options to control tumor growth and symptoms of hormone hypersecretion", section on 'Somatostatin analogs' and "Metastatic well-differentiated pancreatic neuroendocrine tumors: Systemic therapy options to control tumor growth and symptoms of hormone hypersecretion", section on 'Peptide receptor radioligand therapy' and "Metastatic well-differentiated gastrointestinal neuroendocrine (carcinoid) tumors: Systemic therapy options to control tumor growth", section on 'Somatostatin receptor-expressing tumors'.)
Whether either of these techniques should be used to assess tumor response or progression in patients with advanced disease is unclear, and this has not yet been formally studied [16]. These imaging techniques rely in part on the assessment of somatostatin receptor density, rather than direct measurements of tumor volume. Using somatostatin receptor-based techniques may, in theory, not always correlate with disease progression or response to therapy, and further studies are needed to assess the utility of these technologies (including Ga-68 DOTATATE, Ga-68 DOTATOC, and Cu-64 DOTATATE) in this setting.
For patients treated with somatostatin analogs, it has generally been recommended that therapy with short-acting analogs be discontinued for 24 hours before somatostatin receptor-based imaging, with treatment resumed the day after, when clinically feasible [18]. For patients receiving long-acting preparations (Sandostatin LAR, lanreotide) the recommendation has been to allow a wash-out period of four weeks before imaging or to image just prior to dosing with long-acting somatostatin analogs. However, these recommendations preceded the availability of more sensitive imaging techniques using PET. Several studies have found that treatment with long-acting somatostatin analogs (lanreotide, octreotide) did not alter Ga-68 DOTATATE uptake into tumors or affect imaging results, suggesting that the recommended dose separation of these agents may not be needed in this setting [19-21]. We no longer recommend holding the somatostatin analog for a period of time prior to PET imaging.
Clinical studies — Scanning using 111-In pentetreotide has been widely available and has been commonly used to perform whole-body somatostatin receptor-based imaging in patients with NETs [22-24].
However, several PET tracers for functional imaging have emerged (Ga-68 DOTATATE, Ga-68 DOTATOC, Cu-64 DOTATATE, 18-F-dihydroxy-phenyl-alanine [18F-DOPA], and 11-C-5-hydroxytryptophan [11-C-5-HTP]), which in combination with high-resolution PET and integrated CT, improve the detection and staging of NETs. Novel PET modalities such as Ga-68 DOTATATE, Ga-68 DOTATOC and Cu-64 DOTATATE PET offer higher spatial resolution than conventional 111-In pentetreotide imaging and are more sensitive for detection of small lesions (image 4) [25-34].
Ga-68 DOTATATE is a positron-emitting analog of somatostatin that works by binding to these receptors; its highest affinity is for subtype 2 receptors (sstr2). The higher sensitivity of Ga-68 DOTATATE PET for the detection of gastroenteropancreatic NETs was best shown in a prospective study in which 131 patients with a known or suspected gastroenteropancreatic NET underwent conventional anatomic imaging with CT and/or MRI, 111-In pentetreotide SPECT/CT imaging, and Ga-68 DOTATATE PET/CT [25]. The following findings were noted:
●When all of the lesions demonstrated by any of the imaging studies were used as the imaging denominator, Ga-68-DOTATATE PET/CT imaging detected significantly more (95 percent, 95% CI 92.4-96.8) than did anatomic imaging (45 percent, 95% CI 37.9-52.9 percent) or 111-In pentetreotide SPECT/CT (30.9 percent, 95% CI 25.0-37.5 percent). Overall, 422 of the total 891 lesions were detected by 68-Ga-DOTATATE PET/CT and missed both by 111-In pentetreotide SPECT/CT and anatomic imaging.
●Of the 14 patients with an unknown primary tumor, four were identified using Ga-68 DOTATATE (none of which were seen with 111-In pentetreotide and two of which were not seen on cross sectional imaging). (See "Neuroendocrine neoplasms of unknown primary site".)
●The 25 patients who underwent surgery had 113 lesions that were histologically proven to be gastroenteropancreatic NETs (37 primary tumors, 69 lymph nodes, and 7 distant metastases). On a per-lesion analysis, Ga-68 DOTATATE had the highest true positive rate (72 of 113 [64 percent] versus 25 of 113 [22 percent] for 111-In pentetreotide and 44 of 113 [39 percent] for anatomic imaging). All 38 lesions that were not detected by any imaging study represented lymph node metastases.
●The addition of Ga-68-DOTATATE scanning to cross-sectional imaging and 111-In pentetreotide resulted in a clinically significant change in management in 43 of 131 patients (33 percent).
A newer PET radiotracer, Ga-68 DOTATOC, appears to have comparable diagnostic accuracy to Ga-68 DOTATATE for the detection of neuroendocrine neoplasms that express somatostatin receptors [35]. Although FDA approved in the United States in 2019 [36], it is not yet commercially available.
A third PET radiotracer, Cu-64 DOTATATE, appears also to have comparable diagnostic accuracy to Ga-68 DOTATATE [37] and was approved in the United States in September 2020.
Whole-body imaging using radiolabeled somatostatin analogs such as Ga-68 DOTATATE and DOTATOC, or Cu-64 DOTATATE may unexpectedly reveal other somatostatin receptor-expressing tumor types, including meningiomas [38]. The differential diagnosis includes a wide range of neoplastic and nonneoplastic entities, including metastatic NET (table 3). (See "Epidemiology, pathology, clinical features, and diagnosis of meningioma", section on 'Diagnostic evaluation' and "Management of known or presumed benign (WHO grade 1) meningioma", section on 'Small, asymptomatic tumors'.)
Poorly differentiated neuroendocrine tumors — Imaging for high-grade poorly differentiated neuroendocrine carcinomas arising in the gastrointestinal tract is discussed elsewhere. (See "High-grade gastroenteropancreatic neuroendocrine neoplasms", section on 'Diagnosis and staging'.)
BIOCHEMICAL MONITORING
Hormonal biomarkers
Urinary 5-HIAA — Elevated urinary levels of 5-hydroxyindoleacetic acid (5-HIAA) are highly specific for serotonin-producing NETs (ie, those arising in the midgut), but they are not particularly sensitive. In one study, only 73 percent of patients with metastatic NETs had elevated levels [39]. Furthermore, 5-HIAA levels are generally most useful in patients with primary midgut NETs. Foregut and hindgut NETs only rarely secrete serotonin; they lack the enzyme DOPA decarboxylase and cannot convert 5-hydroxytryptophan to serotonin and, therefore, to 5-HIAA (figure 1).
Clinical utility can also be limited by false positives. The normal rate of 5-HIAA excretion ranges from 2 to 8 mg (10 to 42 micromol) per day. Values of up to 30 mg (157 micromol) per day may be found in patients with malabsorption syndromes (eg, celiac disease), and following ingestion of large amounts of tryptophan/serotonin-rich foods; use of certain drugs also interferes with assay of urinary 5-HIAA (table 4). Although many patients with advanced well-differentiated midgut NETs have values above 100 mg (523 micromol) per day, some have more modest elevations. In one study, urinary 5-HIAA excretion in patients with carcinoid syndrome ranged from 99 to 2070 mg (518 to 10826 micromol) per day [40]. Lower but still elevated values were seen in patients with metastatic NETs without carcinoid syndrome (50 to 260 mg [262 to 1360 micromol] per day).
Urinary 5-HIAA is the most sensitive test for establishing the diagnosis of carcinoid syndrome. (See "Diagnosis of carcinoid syndrome and tumor localization", section on 'Biochemical testing for carcinoid syndrome'.)
For patients with advanced disease, serial measurements of 24-hour urine 5-HIAA do not correlate with symptomatic benefit from various treatments [41].
Functioning pancreatic neuroendocrine tumors — While they are specific for the individual hormonal syndrome, the hormones produced by functioning pancreatic NETs (ie, insulin, glucagon, somatostatin, VIP) may not be easily measurable. Assessment of specific hormone levels should be performed based on patient symptoms and suspicion for a functional NET. (See "Insulinoma", section on 'Diagnosis and staging' and "Glucagonoma and the glucagonoma syndrome", section on 'Serum glucagon' and "Zollinger-Ellison syndrome (gastrinoma): Clinical manifestations and diagnosis", section on 'Serum gastrin concentration' and "VIPoma: Clinical manifestations, diagnosis, and management", section on 'Diagnosis' and "Somatostatinoma: Clinical manifestations, diagnosis, and management", section on 'Diagnosis'.)
Nonhormonal biomarkers
Chromogranin A — Chromogranin A (CgA) is a 49-kD protein that is contained in the neurosecretory vesicles of NET cells and is detectable in the plasma of patients with a range of neuroendocrine neoplasms, including nonfunctioning pancreatic NETs. Because it does not rely on serotonin secretion, serum CgA is a more sensitive and broadly applicable tumor marker for NETs than is urinary 5HIAA, but it is less specific (table 5). (See "Overview of tumor biomarkers in gastroenteropancreatic neuroendocrine tumors", section on 'Chromogranin A (CgA)'.)
Among the clinical scenarios where CgA may be used includes patients with foregut and rectal NETs (in whom urinary 5HIAA levels are less likely to be elevated), as well as in patients with pancreatic NETs, in whom CgA is more often elevated than it is with gastrointestinal tract NETs [42-52]. Levels are higher in patients with diffuse metastases than with localized disease or isolated hepatic involvement [46,52]. (See "Clinical characteristics of well-differentiated neuroendocrine (carcinoid) tumors arising in the gastrointestinal and genitourinary tracts", section on 'Foregut tumors' and "Clinical characteristics of well-differentiated neuroendocrine (carcinoid) tumors arising in the gastrointestinal and genitourinary tracts", section on 'Hindgut tumors'.)
Plasma CgA levels have been shown to correlate with treatment response and may also have prognostic value. Elevated CgA levels have been associated with shorter overall survival times in several studies [3,53-56]. However, the utility of CgA as a marker of prognosis has been limited by wide variability in CgA ranges in the setting of metastatic disease, as well as variability in CgA assays in the United States and Europe. Caution is also needed when using serum CgA as a marker of disease activity in patients treated with somatostatin analogs. These agents significantly reduce plasma CgA levels, a change that may be more reflective of changes in hormonal synthesis and release from tumor cells than an actual reduction in tumor mass [45]. Finally, CgA is not recommended as a diagnostic marker for NETs, as it can be elevated in a number of unrelated conditions. These conditions include use of proton pump inhibitors, renal insufficiency, and hepatic insufficiency. For patients who are receiving treatment with a proton pump inhibitor, the drug should be stopped or replaced with an H2 receptor blocker if possible in order to obtain reliable CgA values [57]. The utility of measuring CgA levels in patients undergoing radiographic surveillance for detection of recurrence following surgery is debatable, as is its role in the routine follow-up of patients with advanced disease [58]. (See "Overview of tumor biomarkers in gastroenteropancreatic neuroendocrine tumors", section on 'Chromogranin A (CgA)'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Well-differentiated gastroenteropancreatic neuroendocrine tumors".)
SUMMARY
●Neuroendocrine neoplasms arising at different sites within the body are classified according to their histologic features. All commonly used classification systems reflect a basic separation between more indolent, well-differentiated tumors and far more aggressive, high-grade, poorly differentiated neoplasms (neuroendocrine carcinomas) that behave clinically more like small cell lung cancer (table 1). (See 'Classification and nomenclature' above.)
●The clinical course of patients with metastatic well-differentiated gastroenteropancreatic neuroendocrine tumors (NETs) is highly variable. Some patients with indolent tumors may remain symptom free for years, even without treatment. Others have symptomatic metastatic disease, either from tumor bulk or peptide hormone hypersecretion, and require therapy. (See 'Clinical presentation' above.)
●Even when advanced, survival times for patients with well-differentiated gastroenteropancreatic NETs are generally better than those for patients with other malignancies, although highly variable. The main prognostic factors are differentiation and grade (table 1), tumor site (table 6), disease burden, and the presence of extrahepatic metastases. (See 'Prognosis' above.)
●The predominant site of metastatic spread is the liver. Patients in whom metastatic disease is suspected should be evaluated with a triple-phase contrast-enhanced helical computed tomography (CT) or magnetic resonance imaging (MRI) scan to rule out liver metastases. Some clinicians prefer MRI because of its greater sensitivity for liver metastases. (See 'Cross-sectional imaging' above.)
●Uptake of radiolabeled somatostatin analogs is predictive of a clinical response to therapy with somatostatin analogs and to peptide receptor radionuclide therapy, and it can assist in identifying an otherwise occult primary site. The greater sensitivity of gallium Ga-68 DOTATATE, Ga-68 DOTATOC, or copper Cu-64 DOTATATE positron emission tomography (PET)/CT makes these methods for somatostatin receptor-based imaging preferred over indium-111 (111-In) pentetreotide (OctreoScan) where available. (See 'Somatostatin receptor-based imaging techniques' above.)
●Changes in biochemical markers may be associated with disease progression and/or response to treatment. Elevated urinary levels of 5-hydroxyindoleacetic acid (5-HIAA) are highly specific for serotonin-producing NETs (ie, those arising in the midgut), although they are not sensitive. (See 'Urinary 5-HIAA' above.)
●For non-serotonin-producing NETs, serum chromogranin A (CgA) may be more useful than 5-HIAA. However, serum CgA is not specific to NETs and can also be elevated in non-neuroendocrine-related conditions. The utility of measuring CgA levels in patients undergoing radiographic surveillance for detection of recurrence following surgery, and the role of CgA in the follow-up of patients with advanced disease are debatable. (See 'Chromogranin A' above.)
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