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PubMedDate not supplied

Serum chromogranin-A assay in differential diagnosis of incidentally discovered adrenal masses.

Adrenal incidentalomas are defined as asymptomatic adrenal masses occasionally discovered during high-resolution imaging procedures such as computed tomography (CT) or magnetic resonance (MR). Pheochromocytoma, a potentially lethal chromaffin tumour, must be excluded before any invasive diagnostic procedures to avoid massive catecholamines release. Chromogranin A (CgA) is a member of the granin family contained in secretory vescicles of chromaffin adrenal cells. Consequently, serum CgA increases in patients affected by pheochromocytoma and other diseases of the chromaffin system. This study investigated the performance of serum CgA assay in diagnosis of pheochromocytoma among patients affected by adrenal incidentaloma. Additionally, we evaluated the role of the CgA assay in selection of patients for 123I-metaiodobenzyl-guanidine (MIBG) scintigraphy, a very accurate but high-cost and time-consuming imaging procedure. We enrolled 104 patients affected by adrenal incidentally discovered masses and 100 healthy blood donors as controls. Serum CgA was assayed by a specific immunoradiometric method (IRMA) and 123I-MIBG scan was performed in all patients. A cytological or histological diagnosis was obtained in all cases. Circulating CgA assay was positive in 12 out of 12 patients with pheochromocytoma and negative in 92 out of 92 patients with non-chromaffin adrenal nodules. Serum levels of CgA clearly increased from blood donors and patients with non-chromaffin adrenal nodules to patients with pheochromocytoma (p<0.0001). All patients with negative CgA assay showed a negative 1231-MIBG scan. Serum CgA assay is effective in evaluating the presence of chromaffin tumour among patients with adrenal incidentaloma. A negative serum CgA assay rules out successive 123I-MIBG imaging.

3-Iodobenzylguanidine↗
PubMed1996

Cholinergic agonists stimulate secretion of soluble full-length amyloid precursor protein in neuroendocrine cells.

The Abeta peptide of Alzheimer disease is derived from the proteolytic processing of the amyloid precursor proteins (APP), which are considered type I transmembrane glycoproteins. Recently, however, soluble forms of full-length APP were also detected in several systems including chromaffin granules. In this report we used antisera specific for the cytoplasmic sequence of APP to show that primary bovine chromaffin cells secrete a soluble APP, termed solAPPcyt, of an apparent molecular mass of 130 kDa. This APP was oversecreted from Chinese hamster ovary cells transfected with a full-length APP cDNA indicating that solAPPcyt contained both the transmembrane and Abeta sequence. Deglycosylation of solAPPcyt showed that it contained both N- and O-linked sugars, suggesting that this APP was transported through the endoplasmic reticulum-Golgi pathway. Secretion of solAPPcyt from primary chromatin cells was temperature-, time-, and energy-dependent and was stimulated by cell depolarization in a Ca2+-dependent manner. Cholinergic receptor agonists, including acetylcholine, nicotine, or carbachol, stimulated the rapid secretion of solAPPcyt, a process that was inhibited by cholinergic antagonists. Stimulation of solAPPcyt secretion was paralleled by a stimulation of secretion in catecholamines and chromogranin A, indicating that secretion of solAPPcyt was mediated by chromaffin granule vesicles. Taken together, our results show that release of the potentially amyloidogenic solAPPcyt is an active cellular process mediated by both the constitutive and regulated pathways. solAPPcyt was also detected in human cerebrospinal fluid. Combined with the neuronal physiology of chromaffin cells, our data suggest that cholinergic agonists may stimulate the release of this APP in neuronal synapses where it may exert its biological functions. Moreover, vesicular or secreted solAPPcyt may serve as a soluble precursor of Abeta.

Acetylcholine↗
PubMedDate not supplied

Serum chromogranin-alpha immunoradiometric assay in the diagnosis of pheochromocytoma.

BACKGROUND: The diagnosis of pheochromocytoma is based on laboratory tests that demonstrate an increase in urinary excretion of catecholamines or their metabolites. Chromogranin A (CgA) is a member of the granin family and is widely distributed in neuroendocrine cells and particularly in chromaffin adrenal cells. Consequently, serum CgA increases in patients affected by pheochromocytoma and other diseases of the chromaffin system. AIM: This study investigated the performance of serum CgA assay in the diagnosis of pheochromocytoma and compared serum CgA with 24-hour urinary epinephrine (E), norepinephrine (NE), vanillylmandelic acid (VMA) and metanephrines (MNs). METHODS: We enrolled 15 patients with histologically proven pheochromocytoma; 100 healthy blood donors and 148 patients with essential hypertension were enrolled as controls. Serum CgA was assayed by a specific immunoradiometric method (IRMA). Urinary tests were done with high performance liquid chromatography (HPLC). RESULTS: Circulating CgA showed a higher sensitivity (1.00), specificity (0.96) and accuracy (0.96) than all other tests. Serum levels of CgA clearly increased from blood donors and patients with essential hypertension to patients with pheochromocytoma (p<0.0001). Furthermore, a strong relationship between serum CgA and tumor mass was found (p<0.0001). In conclusion, our data suggest that the CgA assay might be used as a single test for the diagnosis of pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed2000

[Changes in gastric electric activity and serum catecholamine level under the influence of electromagnetic microwaves (experimental studies)].

Chronic experiments on 17 dogs revealed that ultrahigh-frequency electromagnetic waves applied on epigastric area and head induce a double-phase response: depressed electric activity of gaster and increased total catecholamines level during exposure, but higher gastric activity and lower levels of epinephrine and norepinephrine in 24 hours after each of 10 procedures and during 7 days after 10 procedures. Double-phase changes in electric activity of gaster could be explained by double-phase fluctuations of humoral division in chromaffin system.

Animals↗
PubMed1993

[Multiple paraganglioma].

Paragangliomas are tumors of the chromaffin system producing catecholamines and both the adrenal extra-adrenal type have a common origin at the neural crest, which has been supported by the similarities of the paraganglions both from a histological and functional perspective. Most of the extra-adrenal paragangliomas are bending and non-functional. In addition, they are usually confined to just one site. We present the case of a young patient with benign multiple paraglanglioma in two different locations, juxtahepatic and juxtacarotic (Chemodectoma) and, thus, far away from each other. The extra-abdominal location is very rare, with a frequency lower than 2%. In addition, one of paraganglions was functional and the other one was not. Initially, a surgical intervention was performed on the functional abdominal tumoration and latter, another intervention was performed at the cervical level, both with excellent results. We also highlight the good response to the postoperative therapy with Prazosin.

Abdominal Neoplasms↗
PubMed1984

Intrinsic GABAergic system of adrenal chromaffin cells.

Histochemical and biochemical studies demonstrate that gamma-aminobutyric acid (GABA), glutamic acid decarboxylase (EC 4.1.1.15), and GABA aminotransferase (EC 2.6.1.19) are present in bovine adrenal chromaffin cells. Moreover, [3H]GABA can be taken up and stored by primary cultures of adrenal chromaffin cells. Nicotinic receptor stimulation or KCl depolarization releases the [3H]GABA taken up by these cell cultures. GABA and benzodiazepine recognition sites located in chromaffin cells interact with each other with modalities similar to those described for GABA and benzodiazepine recognition sites located in synaptic membranes prepared from brain tissue. Bicuculline facilitates the release of catecholamine from chromaffin cells induced by nicotinic receptor stimulation but it fails to influence the release of catecholamine evoked by K+ depolarization. Since the GABA-benzodiazepine receptor system appears to modulate nicotinic receptor function, it is suggested that GABA transmission might participate in modulating responsiveness of chromaffin cells to incoming cholinergic stimuli.

4-Aminobutyrate Transaminase↗