ObjectiveVitamin D deficiency is prevalent in critically ill patients and may contribute to suboptimal clinical outcomes, but little is known about alterations of the calcium-parathyroid hormone (PTH)-vitamin D axis and prognosis in these individuals.MethodsA prospective observational study was conducted on 216 patients admitted to a university-affiliated, tertiary-care medical intensive care unit(MICU) between June 2011 and December 2012. Serum levels of 25-hydroxyvitamin D, ionised calcium and intact PTH were determined within 24 h of MICU admission. The primary end point was all-cause hospital mortality within 90-days of admission.Results95 patients (44%) showed 25-hydroxyvitamin D deficiency. Patients deficient in vitamin D showed significantly higher Acute Physiology and Chronic Health Evaluation II (APACHE II) score, rate of positive blood culture, incidence of multiple organ dysfunction syndrome, and 90-day mortality rate than did patients with vitamin D insufficiency or sufficiency (P<0.05), as well as lower levels of serum IgG. 25-Hydroxyvitamin D deficiency was identified as an independent risk factor for mortality (OR = 3.018, 95%CI 1.329–6.854, P = 0.008). Hypovitaminosis D in PTH-responders was associated with higher mortality than was the same condition in non-responders (P<0.05).ConclusionsThese results suggest that vitamin D deficiency is prevalent among MICU patients, suggesting a significant derangement of the calcium-PTH-vitamin D axis in critically ill patients. Vitamin D deficiency is an independent risk factor for 90-day mortality, and hypovitaminosis D in PTH-responders is associated with higher mortality than is the same condition in non-responders.

Lower serum 25OHD levels at ICU admission were associated with 28-day mortality in septic patients. Serum 25OHD levels were inversely correlated with PCT levels. Hypovitaminosis D was associated with higher mortality rates in PTH responders than in nonresponders.

Adrenocortical carcinoma (ACC) is a rare malignancy with a poor prognosis. The presently available understanding of the pathogenesis of ACC is incomplete and the treatment options for patients with ACC are limited. Gene marker identification is required for accurate and timely diagnosis of the disease. In order to identify novel candidate genes associated with the occurrence and progression of ACC, the microarray datasets, GSE12368 and GSE19750, were obtained from Gene Expression Omnibus. Differentially expressed genes (DEGs) were identified, and functional enrichment analysis was performed. A protein-protein interaction network (PPI) was constructed to identify significantly altered modules, and module analysis was performed using Search Tool for the Retrieval of Interacting Genes and Cytoscape. A total of 228 DEGs were screened, consisting of 29 up and 199 downregulated genes. The enriched functions and pathways of the DEGs primarily included ‘cell division’, ‘regulation of transcription involved in G1/S transition of mitotic cell cycle’, ‘G1/S transition of mitotic cell cycle’, ‘p53 signaling pathway’ and ‘oocyte meiosis’. A total of 14 hub genes were identified, and biological process analysis revealed that these genes were significantly enriched in cell division and mitotic cell cycle. Furthermore, survival analysis revealed that AURKA, TYMS, GINS1, RACGAP1, RRM2, EZH2, ZWINT, CDK1, CCNB1, NCAPG and TPX2 may be involved in the tumorigenesis, progression or prognosis of ACC. In conclusion, the 14 hub genes identified in the present study may aid researchers in elucidating the molecular mechanisms associated with the tumorigenesis and progression of ACC, and may be powerful and promising candidate biomarkers for the diagnosis and treatment of ACC.