Chromogranin A in patients with acid hypersecretion and/or hypergastrinaemia

Hirschowitz, Basil I.; Worthington, Julie; Mohnen, Jean; Haber, Marian M.

doi:10.1111/j.1365-2036.2007.03439.x

Cited by 14 publications

(5 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on the ECL cell pathophysiology and the majority of published data, gastric ECL activation (hyperfunction/proliferation) seems to be the potential source of increased circulating CgA levels observed even after an ultra-short-term PPI treatment in our study, but in the study by Hirschowitz et al [33], serumCgA was elevated in patients with gastrinoma, even without any enterochromaffin-like cell proliferation.…”

Section: Discussioncontrasting

confidence: 51%

Effect of Proton-Pump Inhibitor Therapy on Serum Chromogranin A Level

et al. 2011

View full text Add to dashboard Cite

Background: The neuroendocrine marker, chromogranin A (CgA) increases during medium- or long-term proton-pump inhibitor (PPI) treatment. Aims: To analyze the effect of ultra-short-term and diverse dose of PPI therapy on serum CgA and gastrin levels and evaluate the effect of PPI treatment cessation. Patients and Methods: Fasting serum CgA and gastrin were determined in newly diagnosed gastroesophageal reflux disease (GERD) patients (n = 54) treated with diverse doses of PPI during a 28-day period, in patients treated with PPIs for at least 6 months (n = 42), and in subjects where PPI treatment could be stopped (n = 11). Results: A significant stepwise increase of CgA levels was observed after 5 days during the 28-day period treatment with all PPI doses. Gastrin increased significantly also in the standard and high-dose PPI subgroups. The most prominent increase of CgA was observed in the high-dose PPI subgroup. Serum CgA and gastrin were markedly elevated after 6 months of PPI treatment, and decreased significantly after 5 days of PPI discontinuation. Conclusions: Serum CgA increases significantly even after ultra-short-term (5 days) PPI therapy. After long-term treatment, 5-day cessation of PPI therapy is sufficient to decrease significantly both CgA and gastrin levels.

show abstract

Section: Discussioncontrasting

confidence: 51%

Effect of Proton-Pump Inhibitor Therapy on Serum Chromogranin A Level

et al. 2011

View full text Add to dashboard Cite

show abstract

“…There were two patients with gastrinoma and both of them had highest plasma CgA level. CgA is known to be much higher in gastrinoma (26). However, we should be careful in interpreting this result because the patients with gastrinoma had taken proton pump inhibitors at the time, which could cause plasma CgA level overestimated.…”

Section: Discussionmentioning

confidence: 99%

Clinical Usefulness of Plasma Chromogranin A in Pancreatic Neuroendocrine Neoplasm

et al. 2013

View full text Add to dashboard Cite

Chromogranin A (CgA) is widely used as an immunohistochemical marker of neuroendocrine neoplasms and has been measurable in plasma of patients. We assessed the clinical role of plasma CgA in diagnosing pancreatic neuroendocrine neoplasm (PNEN). CgA was checked in 44 patients with pancreatic mass who underwent surgical resection from 2009 through 2011. The cutoff value for diagnosing PNEN and the relationships between CgA and clinicopathologic variables were analyzed. Twenty-six patients were PNENs and 18 patients were other pancreatic disorders. ROC analysis showed a cutoff of 60.7 ng/mL with 77% sensitivity and 56% specificity, and the area under the curve (AUC) was 0.679. Among PNEN group, the sensitivity and specificity of diagnosing metastasis were 100% and 90% respectively when CgA cutoff was 156.5 ng/mL. The AUC was 0.958. High Ki-67 index (160.8 vs 62.1 ng/mL, P = 0.001) and mitotic count (173.5 vs 74.6 ng/mL, P = 0.044) were significantly correlated with plasma CgA, but the tumor size was not. In conclusion, CgA has a little value in diagnosing PNEN. However, the high level of CgA (more than 156.5 ng/mL) can predict the metastasis. Also, plasma CgA level correlates with Ki-67 index and mitotic count which represents prognosis of PNENs.

show abstract

“…One of the commonest causes of spuriously elevated Cg A levels is the proton pump inhibitor (PPI) administration [ 55 ]. As reported by Mosli et al, short-term PPI use results in a significant increase of Cg A in serum and plasma, an effect that is largely independent of the assay used [ 56 ].…”

Section: Granin Family and Biological Activitiesmentioning

confidence: 99%

Chromogranin A: From Laboratory to Clinical Aspects of Patients with Neuroendocrine Tumors

Giacinto

Rota

Rizzà

et al. 2018

International Journal of Endocrinology

View full text Add to dashboard Cite

Background. Neuroendocrine tumors (NETs) are characterized by having behavior and prognosis that depend upon tumor histology, primary site, staging, and proliferative index. The symptoms associated with carcinoid syndrome and vasoactive intestinal peptide tumors are treated with octreotide acetate. The PROMID trial assesses the effect of octreotide LAR on the tumor growth in patients with well-differentiated metastatic midgut NETs. The CLARINET trial evaluates the effects of lanreotide in patients with nonfunctional, well-, or moderately differentiated metastatic enteropancreatic NETs. Everolimus has been approved for the treatment of advanced pancreatic NETs (pNETs) based on positive PFS effects, obtained in the treated group. Sunitinib is approved for the treatment of patients with progressive gastrointestinal stromal tumor or intolerance to imatinib, because a randomized study demonstrated that it improves PFS and overall survival in patients with advanced well-differentiated pNETs. In a phase II trial, pasireotide shows efficacy and tolerability in the treatment of patients with advanced NETs, whose symptoms of carcinoid syndrome were resistant to octreotide LAR. An open-label, phase II trial assesses the clinical activity of long-acting repeatable pasireotide in treatment-naive patients with metastatic grade 1 or 2 NETs. Even if the growth of the neoplasm was significantly inhibited, it is still unclear whether its antiproliferative action is greater than that of octreotide and lanreotide. Because new therapeutic options are needed to counter the natural behavior of neuroendocrine tumors, it would also be useful to have a biochemical marker that can be addressed better in the management of these patients. Chromogranin A is currently the most useful biomarker to establish diagnosis and has some utility in predicting disease recurrence, outcome, and efficacy of therapy.

show abstract

Chromogranin A in patients with acid hypersecretion and/or hypergastrinaemia

Abstract: SUMMARY BackgroundChromogranin has been proposed as a marker for gastrin-dependent enterochromaffin-like cell proliferation.

Cited by 14 publications

References 35 publications

Effect of Proton-Pump Inhibitor Therapy on Serum Chromogranin A Level

Effect of Proton-Pump Inhibitor Therapy on Serum Chromogranin A Level

Clinical Usefulness of Plasma Chromogranin A in Pancreatic Neuroendocrine Neoplasm

Chromogranin A: From Laboratory to Clinical Aspects of Patients with Neuroendocrine Tumors

Contact Info

Product

Resources

About