Prospective study of the value of serum chromogranin A or serum gastrin levels in the assessment of the presence, extent, or growth of gastrinomas

Abstract

BACKGROUND Serum chromogranin A levels (CgA) are reported by some authors to be of clinical utility for assessing the presence or absence of a pancreatic endocrine tumor and tumor extent or growth. The aim of the current study was to assess this finding and compare the results with those from serum gastrin determinations (FSG) in a large cohort of patients with gastrinomas. METHODS In 112 consecutive patients with the Zollinger–Ellison syndrome serum CgA and FSG levels were measured and correlated with disease activity, extent of disease, and the presence of multiple endocrine neoplasia type‐1 (MEN‐1) or gastric carcinoid tumors. RESULTS Serum CgA levels drawn on 2 consecutive days correlated closely (P < 0.00001) as did serum gastrin levels. Serum CgA levels correlated significantly with FSG levels (P < 0.00001). Serum CgA and FSG levels were significantly higher in patients with active disease than in disease free patients (P < 0.00001). The sensitivity for the presence of disease was higher for CgA compared with FSG (92% vs. 80%; P = 0.021). However, the specificity of CgA was 67%. Serum CgA levels were not significantly different in the four disease categories (stable extrahepatic disease, increasing extrahepatic disease, stable liver metastases, and increasing liver metastases). FSG levels were significantly lower in patients with stable extrahepatic disease compared with those with increasing extrahepatic disease. However, both tumor markers decreased significantly with a gastrinoma resection in five patients. The presence of MEN‐1 or a gastric carcinoid tumor did not influence the results. CONCLUSIONS The results of the current study showed that serum CgA and FSG levels both are sensitive tumor markers for the detection of a gastrinoma; however, CgA levels have a relatively low specificity. Neither the magnitude of the serum CgA nor gastrin level correlated with tumor growth or tumor extent and therefore cannot be used to determine these variables. However, in contrast to some other studies, the results of the current study show that changes in serum CgA or gastrin in a given patient with time are related to the tumor extent and not to gastric mucosal changes due to hypergastrinemia. Cancer 1999;85:1470–83. © 1999 American Cancer Society.

Plasma chromogranin A in patients with sporadic gastro-entero-pancreatic neuroendocrine tumors or multiple endocrine neoplasia type 1

“…Moreover, plasma CgA levels correlated significantly with urinary 5-HIAA levels in our patients with midgut carcinoids and with plasma gastrin levels in those with gastrinoma. Similar correlations have already been reported by Nobels et al (4,8,13,14). It has therefore been suggested that elevations in CgA levels in patients with Zollinger-Ellison syndrome may be due to hyperplasia of the gastric enterochromaffine-like cells caused by chronic hypergastrinemia (14).…”

“…However, our results do not support this interpretation as we found no correlation between CgA and gastrin plasma levels in patients with gastric carcinoid and hypergastrinemia due to chronic atrophic gastritis. Moreover, Goebel et al (13) demonstrated recently that gastrinoma resection significantly reduced CgA levels in patients with Zollinger-Ellison syndrome.…”

Chromogranin A in patients with acid hypersecretion and/or hypergastrinaemia

“…Chromogranin A was measured twice in the hypersecretors during the study, between 2002 and 2005. As reproducibility for both gastrin and CgA from day to day has been shown to be high, 6,18 only single samples were measured on each occasion. Serum CgA was measured by an immunochemiluminometric assay (ICMA) with a normal range of 6-39 ng ⁄ mL performed by Quest Diagnostics (San Juan Capistrano, CA, USA).…”

“…2,3 Various studies have examined the clinical value of measuring circulating CgA as a surrogate marker for screening, diagnosis, prognosis, treatment response 4 and disease progression of neuroendocrine tumors 2, 4-13 including gastrinoma. 4,6 In some cases, especially in CgA-rich pheochromocytomas, circulating levels reflect tumour mass. 7,10 However, CgA has been shown to be of little value in diagnosing CgA-poor neuroendocrine tumours such as parathyroid adenoma.…”

The importance of the measurement of circulating markers in patients with neuroendocrine tumours of the pancreas and gut.

“…CgA is, however, considered to be the best general marker for neuroendocrine tumours, particularly the carcinoid group (Ö berg 1997(Ö berg , Tomossetti et al 2001. It is raised in pancreatic neuroendocrine tumours, where more than 92% of active gastrinomas have been shown to have elevated CgA (Goebel et al 1999), and also in more than 60% of patients with multiple endocrine neoplasia type 1(MEN-1) (Ö berg & Skogseid 1998). CgA is a large molecule and may be processed differently by different tumour cells.…”