Reference intervals for the Kryptor second-generation chromogranin A assay

Ferraro, Simona; Borille, Simona; Panteghini, Mauro

doi:10.1515/cclm-2016-0083

Cited by 5 publications

(3 citation statements)

References 8 publications

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“…(Figure E1). These data are consistent with the conclusions that adult patients with mastocytosis not taking PPIs have serum CgA levels within the normal reference range and that the serum levels of CgA are significantly influenced by the use of PPIs (8). Serum gastrin levels correlated with CgA levels (p=0.020, r = 0.51) (Figure 1B) (5).…”

Section: To the Editorsupporting

confidence: 90%

Chromogranin A is not a biomarker of mastocytosis

Hanjra

Lee²,

Marić

et al. 2018

The Journal of Allergy and Clinical Immunology: In Practice

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Section: To the Editorsupporting

confidence: 90%

Chromogranin A is not a biomarker of mastocytosis

Hanjra

Lee²,

Marić

et al. 2018

The Journal of Allergy and Clinical Immunology: In Practice

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“…impact of protein folding on CgA measurement (Ferraro et al 2016). Utility of this improved method has also been demonstrated in studies exploring the value of CgA as a predictive marker in tumors different from NENs (Niedworok et al 2017).…”

Section: Methods For Circulating Cga Determinationmentioning

confidence: 92%

Chromogranin A as circulating marker for diagnosis and management of neuroendocrine neoplasms: more flaws than fame

Marotta

Zatelli

Sciammarella³

et al. 2018

Endocrine-Related Cancer

128

104

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Owing to the heterogeneity of neuroendocrine neoplasms (NENs), the availability of reliable circulating markers is critical for improving diagnostics, prognostic stratification, follow-up and definition of treatment strategy. This review is focused on chromogranin A (CgA), a hydrophilic glycoprotein present in large dense core vesicles of neuroendocrine cells. Despite being long identified as the most useful NEN-related circulating marker, clinical application of CgA is controversial. CgA assays still lack standardization, thus hampering not only clinical management but also the comparison between different analyses. In the diagnostic setting, clinical utility of CgA is limited as hampered by (a) the variety of oncological and non-oncological conditions affecting marker levels, which impairs specificity; (b) the fact that 30-50% of NENs show normal CgA, which impairs sensitivity. Regarding the prognostic phase, there is prospective evidence which demonstrates that advanced NENs secreting CgA have poorer outcome, as compared with those showing non-elevated marker levels. Although the identification of cut-offs allowing a proper risk stratification of CgA-secreting patients has not been performed, this represents the most important clinical application of the marker. By contrast, based on prospective studies, the trend of elevated circulating CgA does not represent a valid indicator of morphological evolution and has therefore no utility for the follow-up phase. Ultimately, current knowledge about the role of the marker for the definition of treatment strategy is poor and is limited by the small number of available studies, their prevalent retrospective nature and the absence of control groups of untreated subjects.

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“…Interestingly, while P2 values obtained by two statistical methods resulted quite similar at P1 of 50 μg/L (corresponding approx. to the average concentration of a reference population [22]), for P1 concentrations around the upper reference limit (90 μg/L) or frankly abnormal (200 μg/L) the P2 estimate significantly differed, indicating a higher sensitivity of the Method 2 for detecting significant changes in CgA values (Table 1).…”

Section: Example 2: Cgamentioning

confidence: 99%