Chromogranin A (CgA) tests measure the level of chromogranin A, a protein secreted by neuroendocrine cells, in the blood. Elevated CgA can indicate the presence of neuroendocrine tumors (NETs) because many NETs release CgA; clinicians use the test as a tumor marker to support diagnosis, assess tumor burden, and monitor response to treatment or disease progression.

However, CgA is not specific for cancer: levels can be raised by non‑tumor conditions (for example proton pump inhibitor use, renal or hepatic impairment, chronic atrophic gastritis, and heart failure) and by different types of neuroendocrine activity, so results must be interpreted alongside clinical findings, imaging, and other laboratory tests.

The Chromogranin A test is performed with a routine blood draw (venipuncture). A healthcare professional will take a small sample of blood—usually from a vein in your arm—into a vacuum tube; the lab then separates serum or plasma and measures Chromogranin A concentration.

Before the draw you may be given simple preparation instructions because certain medications and conditions can raise CgA. Common recommendations include telling your provider about proton pump inhibitors and other medicines (you may be asked to stop PPIs for about 1–2 weeks if clinically appropriate), avoiding vigorous exercise immediately before the test, and following any fasting instructions your lab provides. Always inform the testing site of current medications and medical conditions so results are interpreted correctly.

Chromogranin A (CgA) is a protein secreted by neuroendocrine cells, so an elevated blood CgA can suggest the presence of a neuroendocrine tumor (NET) or active neuroendocrine disease; however, it is not a standalone diagnostic test. Clinicians use CgA results as one piece of information alongside symptoms, imaging, and biopsy — a markedly and persistently high CgA raises suspicion, but a single abnormal value does not prove cancer.

CgA results have important limitations: reference ranges vary by laboratory, and levels can be raised by many noncancer causes (most notably proton‑pump inhibitor use, chronic kidney disease, atrophic gastritis, liver disease, heart failure and some inflammatory conditions), while some NETs produce little or no CgA and can yield normal results. Trends over time are generally more informative than a single measurement, and CgA is most useful for monitoring disease activity or treatment response in patients with a known NET rather than for screening the general population.

Interpretation of your result depends on the magnitude of elevation, your medications and medical history, and other test or imaging findings. A clinician will often repeat the test (sometimes after stopping PPIs), compare it with prior values, and combine it with imaging or biopsy if there is clinical concern; a normal CgA does not completely rule out cancer, and an isolated mild elevation does not confirm it.

Chromogranin A (CgA) can be a useful tumor marker for many neuroendocrine tumors, but it is neither perfectly sensitive nor specific: some NETs do not raise CgA, and the degree of elevation correlates with tumor type, burden and activity. Because of this variability, a single CgA result cannot reliably confirm or rule out cancer on its own.

CgA levels are affected by many noncancer factors (notably proton‑pump inhibitors, kidney or liver dysfunction and some inflammatory or cardiac conditions) and by differences between assays and laboratories. Clinicians therefore interpret CgA together with clinical evaluation, imaging and histology; serial measurements are more informative for monitoring disease or treatment response than one isolated value. When possible, confounding factors (for example unnecessary acid‑suppressing drugs) should be addressed before testing to improve reliability.

There’s no one-size-fits-all interval — frequency depends on the type and stage of the neuroendocrine tumor, whether you’re receiving or changing treatment, and how stable your disease is. Common approaches are a baseline measurement at diagnosis, then repeat testing every 3 months during active treatment or when progression is suspected; if the disease is stable, many clinicians extend monitoring to every 6–12 months. Trends over time are more informative than single values.

Results can be affected by medications (notably proton‑pump inhibitors), renal function and other non‑cancer conditions, so use the same laboratory/assay for serial tests and interpret CgA alongside imaging and clinical findings. If feasible, stop PPIs 1–2 weeks before a test to reduce false elevations, and follow the schedule recommended by your treating clinician.

No — Chromogranin A (CgA) test results highlight patterns of imbalance or resilience rather than providing a definitive medical diagnosis.

CgA levels must be interpreted alongside symptoms, clinical history, imaging, and other lab or biomarker data by a qualified clinician to inform diagnostic and treatment decisions.

How you improve Chromogranin A (CgA) depends on why it’s high. CgA can be elevated by medications (notably proton-pump inhibitors), kidney dysfunction, inflammatory or metabolic conditions, and neuroendocrine tumors (NETs). The first step is to review medications and medical problems with your clinician — many providers will advise stopping or switching a PPI (under medical supervision) before repeating the test because PPIs commonly raise CgA; correcting reversible causes (e.g., uncontrolled inflammation or renal issues) can also lower levels.

If a NET is the cause, treating the underlying tumor (surgery, somatostatin analogues, or other oncologic therapies as recommended by your specialist) typically reduces CgA over time. Serial measurements and clinical context are more informative than a single value, so follow-up testing and specialist care (endocrinology or oncology) are important. Do not change medications or treatment without consulting your provider.