Chromogranin A as a diagnostic marker of pheochromocytoma and paraganglioma: A systematic review and meta-analysis.

OBJECTIVES: This work aims to assess the diagnostic value of chromogranin A (CgA) in the laboratory diagnosis of neuroendocrine tumors classified as pheochromocytoma and paraganglioma (PPGL). METHODS: A comprehensive search was performed in PubMed, Embase, the Cochrane Library, and Web of Science databases to obtain relevant studies reporting the diagnostic accuracy of CgA in patients with PPGL. The search involved studies written in English between the time of library inception and May 1, 2023. We computed the pooled sensitivity, specificity, and diagnostic odds ratio (DOR). Additionally, the receiver operating characteristic curve and area under the curve (AUC) were determined. The heterogeneity was assessed using the Chi-square test and the I2 test. The subgroup analyses were performed to investigate the origins of heterogeneity. Stata 15.1 statistical software was used in all data analyses. RESULTS: This meta-analysis included 13 studies involving 1470 patients. CgA had a pooled diagnostic sensitivity of 0.86 (95% CI 0.81-0.91), a specificity of 0.90 (95% CI 0.81-0.95), and a DOR of 57 (95% CI 23-142). CgA had an AUC of 0.93. The studies did not reveal any threshold effect (r = -0.165; p > 0.05). The subgroup analyses revealed that the control group category and the detection method caused the overall heterogeneity. CONCLUSIONS: Our study suggests that CgA is a helpful PPGL biomarker. However, relying solely on CgA for diagnosis is not advisable. A comprehensive approach is essential for accurate diagnosis. Future large-scale research is needed to refine CgA's clinical application.

Pro-apoptotic role of nuclear factor-κB in adriamycin-induced acute myocardial injury in rats.

Nuclear factor κB (NF-κB) is activated by a wide range of inducers and is able to mediate gene transcription. We investigated the role of NF-κB in adriamycin-induced myocardial injury in rats and its mechanism of action. A total of 30 male Wistar rats were randomly divided into 3 groups: control, anthracycline antibiotic adriamycin (ADR) and ADR + pyrrolidine dithiocarbamate (PDTC). Myocardial apoptosis was detected by TUNEL assay; myocardium p53 gene expression was examined by RT-PCR analysis; location and distribution of p53 was observed by immunohistochemical assay; myocardial expression of p53 protein was assessed by Western blot analysis and activity of NF-κB was evaluated by electrophoretic mobility shift assay. The binding activity of NF-κB, myocardial apoptotic index and expression of p53 increased significantly in the ADR groups. All of these changes induced by ADR were inhibited by PDTC. It was concluded that NF-κB activation may be pro-apoptotic through regulation of the expression of p53 in adriamycin-induced myocardial injury.