High Plasma Levels of Human Chromogranin a and Adrenomedullin in Patients with Pheochromocytoma

Cotesta, Dario; Caliumi, Chiara; Alò, Piero Luigi; Petramala, Luigi; Reale, M. G.; Masciangelo, Raffaele; Signore, Alberto; Cianci, Rosario; D'Erasmo, E; Letizia, Claudio

doi:10.1177/030089160509100110

Cited by 26 publications

(20 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This would suggest decreased catestatin is serving a pathophysiological role in the development of hypertension rather than being a consequence of elevated blood pressure. In contrast, plasma chromogranin A levels are increased in patients with pheochromocytoma or other chromaffin tumors [40], although catestatin levels have not yet been analyzed in these patients. Interestingly, a naturally occurring amino acid variant of catestatin, Gly364Ser, causes significant changes in human autonomic function and blood pressure.…”

Section: Catestatin and Catecholamine Releasementioning

confidence: 98%

Recent Insights on Circulating Catecholamines in Hypertension

Ton

Hammes

2014

Curr Hypertens Rep

View full text Add to dashboard Cite

Pheochromocytomas are neuroendocrine tumors that commonly lead to excess catecholamine secretion, resulting in elevated blood pressure. In addition to potentiating vasoconstriction, catecholamines promote endothelial dysfunction, as evidenced by elevated markers of endothelial dysfunction, ADMA and sVCAM-1, in patients with pheochromcytoma. Importantly, catecholamine-induced endothelial dysfunction and hypertension may not only be due to catecholamine production by neuroendocrine tumors, as vascular endothelial cells have now been demonstrated to synthesize and secrete catecholamines. This local vascular catecholamine release appears to be triggered by hypoxia. In fact, chronic intermittent hypoxia both in vitro and in vivo leads to stabilization of hypoxic-inducible factors that increase gene expression of catecholamine-synthesizing enzymes. In an effort to target catecholamines as a means of treating hypertension, novel therapeutic options are being explored, including the generation of pharmacophores that mimic the suppressive effects of catestatin on catecholamine release as well as the use of renalase enhancers to increase catecholamine metabolism.

show abstract

Section: Catestatin and Catecholamine Releasementioning

confidence: 98%

Recent Insights on Circulating Catecholamines in Hypertension

Ton

Hammes

2014

Curr Hypertens Rep

View full text Add to dashboard Cite

show abstract

“…Giovanella [12] suggested that a negative serum chromogranin A could rule out successive 123 I-MIBG imaging, but there are still too few studies to recommend the use of chromogranin A for pheochromocytoma screening. In one study the sensitivity of chromogranin A level was 90.2%, and its specificity 99.0%, with a significant relationship between serum levels of chromogranin A and tumor mass [13], whereas in another study chromogranin A had a sensitivity of 76.2%, a specificity of 97.7%, and an accuracy of 91% [14]. Larger studies are needed to better define the usefulness of chromogranin A in the diagnosis of pheochromocytoma.…”

mentioning

confidence: 99%

A pheochromocytoma with normal clonidine-suppression test: how difficult the biochemical diagnosis?

et al. 2008

View full text Add to dashboard Cite

Pheochromocytomas are rare but clinically important tumors of chromaffin cells that take up, produce, store, release, and metabolize catecholamines, and constitute a potentially surgically curable cause of hypertension [1]. Failure to diagnose the tumor can result in devastating consequences. The diagnosis of pheochromocytoma depends crucially on the biochemical evidence of catecholamine production by the tumor [2]. The clonidinesuppression test is widely used for distinguishing high plasma catecholamine levels caused by increased sympathetic nervous system outflows from high levels caused by a high rate of secretion by a pheochromocytoma [3]. We report the case of a 50-year-old white man referred to the Padua hypertension unit for the clinical evaluation of hypertension and adrenal mass with increased urinary metanephrines and negative clonidine-suppression test.The patient was a heavy smoker; his LDL cholesterol was 162 mg/dL. Blood pressure had not been measured in the last 3 years. One month before, he had been admitted to another hospital for abdominal pain and vomits. Arterial blood pressure was 200/102 mmHg with heart rate of 72 beats/min. Abdomen radiograph was negative. Results of initial laboratory tests were significant for a troponin I level of 4.0 lg/L (normal range, \0.1 lg/L). Serum chemistry and complete blood count were also normal or non-contributory. Electrocardiography showed 2-mm ST-segment depression in leads V1, V2 and V3. At echocardiographic examination, left ventricular ejection fraction was 60% and left ventricle concentric hypertrophy present. Since he complained of several episodes of abdominal pain associated with nausea and vomits, he underwent an abdominal computed tomography that showed a right adrenal mass of 2.5 cm 9 3 cm. Plasma renin, serum aldosterone, serum and urinary corisol, and 24-h urinary excretion rates of catecholamines were described as normal. Upon discharge he was on amlodipine 10 mg o.d., pravastatin 40 mg o.d., acetylsalicylic acid 100 mg o.d., and trans-dermal nitroglycerine. The patients quitted to smoke and he was referred to our unit for adrenal mass and hypertension.Arterial blood pressure was persistently elevated (Table 1). Twenty-four hours non-invasive ambulatory blood pressure was 136/79 mmHg, with several peaks of systolic blood pressure, the highest reaching 198 mmHg. Repeated 24-h urinary excretion rates of catecholamines were non-contributory, as were plasma aldosterone, plasma and urinary cortisol, within the normal range (Table 2). Plasma renin activity, plasma concentration of norepinephrine and epinephrine were slightly elevated (Table 2). Urinary levels of metanephrines and plasma chromogranin A were above our normal cut-off (Table 2). Urinary normethanephrines and methanephrines were elevated beyond four-fold of normal cut-off, and were diagnostic of pheochromocytoma. A clonidine-suppression test was, also, carried out after an overnight fast in supine position. The patient was instructed to abstain from caffeinated and decaffeinated beverage...

show abstract

“…Our data does not support the use of CgA in the diagnosis of these tumors. Future collaborative studies to further investigate CgA in PCC/PGL diagnosis could involve CgA antisera from those centers where a positive role for CgA has been described (37,49,50). Adding plasma CART to the laboratory biochemical work-up for PCC/PGL diagnosis may be particularly valuable.…”

Section: Discussionmentioning

confidence: 99%