Marked chromogranin A elevation in a patient with bilateral adrenal incidentalomas, and its rapid normalization after discontinuation of proton pump inhibitor therapy

Abstract

Fig. 1Changes in serum CgA after withdrawal and 1 day after reintroduction of PPI-therapy. The broader horizontal line represents the upper normal level (98·1 ng/ml).

Malignant Range Elevation of Serum Chromogranin A due to Inadvertent Use of Proton Pump Inhibitor in a Subject with Pancreatic Incidentaloma

“…Similar findings were reported in subjects with bilateral adrenal incidentaloma in which persistently elevated CgA after adrenalectomy for phaeochromocytoma was normalized only following suspension of PPI [3]. Our report as well as others observations serve as a reminder to clinicians to pay great attention to confounding factors before pursuing invasive and costly procedures in suspected cases of NETs.…”

“…Furthermore, other nonmalignant endocrine conditions leading to hypergastrinemia were reported to cause increased serum CgA [7]. Interestingly, recent reports have suggested that chronic use and dose escalation of PPI correlates with increased level of both CgA and serum gastrin [3, 5]. Our patient was maintained on the same dose of PPI throughout the period of use yet; in the last 4 months there was an alarmingly marked elevation of CgA.…”

“…Other confounding factors including use of non-PPI medications such as glucocorticoids were not contributory. On the other hand, the period from withdrawal of PPI to subsequent CgA decline was suggested in a recent report to be one week [3] while others earlier proposed 7–10 days [2]. In our subject, the decisive fasting serum CgA was analysed after complete suspension of the PPI for a period of 3 weeks which led to dramatic normalization of the tumor marker.…”

“…While rising level of CgA is not new in the literature [1, 2], the progressive rise of CgA in association with symptoms particularly in an individual with pancreatic mass was an interesting aspect of our report. Igaz et al reported a 7-fold rise of CgA due to PPI which was normalized upon stoppage of the medication [3]. To our knowledge, this is the first report of a very high level of serum CgA of 10-fold magnitude due to ingestion of PPI.…”

Subtyping of primary aldosteronism by adrenal vein sampling: effect of acute D2 receptor dopaminergic blockade on adrenal vein cortisol and chromogranin A levels

“…As proton pump inhibitors raise ChA (15,16), the exclusion criteria entailed need for such treatment and a concurrent pheochromocytoma, because metoclopramide can trigger hypertensive crises in these patients, besides refusal of the patients to undergo AVS and/or adrenalectomy. Peripheral plasma ChA and urinary free catecholamines, normetanephrine, and metanephrine were systematically measured before AVS to exclude pheochromocytoma.…”