Objective: To compare the prohepcidin and hepcidin levels in the afebrile neutropenic period and neutropenic fever in patients with hematological malignancy.
Study Design: Descriptive study.
Place And Duration Of Study: Department of Hematology, Pamukkale University Hospital, Denizli, Turkey, between January 2018 and December 2019.
Methodology: Neutropenic patients were compared with a healthy control group. Prohepcidin and hepcidin serum levels were to be measured in neutropenic and control groups. When fever occurred in neutropenic group, serum was taken again and the same values were compared, in addition to procalcitonin and CRP values.
Results: Prohepcidin and hepcidin levels were found to be significantly higher in the neutropenic group (n = 53) than the control group [n = 44, (med:166.65 ng/ml, IQR:147.66 - 187.38 ng/ml vs. med:47.49 ng/ml, IQR:15.61 - 82.51 ng/ml; p <0.001); (med:315 ng/ml, IQR:314.92 - 315 ng/ml vs. med:26.61 ng/ml, IQR:4.69 - 66.83 ng/ml; p <0.001)]. No significant difference was found in terms of these two analyses (167.29 ± 29.31 ng/ml vs. 167.15 ± 27.61 ng/ml; p = 0.979; 296.21 ± 37.19 ng/ml vs 299.16 ± 37.68 ng/ml; p= 0.629) in the neutropenic fever period compared to the afebrile neutropenic period. In neutropenic fever patients, procalcitonin and CRP (C-reactive protein) were found significantly higher than the afebnile neutropenic group (0.7 ± 1.2 ng/ml vs. 0.25 ± 0.76 ng/ml; p = 0.034; 10.27 ± 9.93 mg/dl vs 2.61 ± 2.78 mg/dl; p <0.001).
Conclusion: Although there was no significant difference between afebnile neutropenia and neutropenic fever in patients in terms of hepcidin and prohepcidin levels, higher levels were found in both groups compared to the control group. Key Words: Hepcidin, Prohepcidin, Neutropenia, Febrile neutropenia.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.29271/jcpsp.2021.11.1303 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Hepcidin inhibits hepatocyte apoptosis through the PERK pathway in acute liver injury and fibrosis.
Hepatol Commun
January 2025
Liver Research Center, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health and National Clinical Research Center of Digestive Diseases, Beijing, China.
Background: Hepcidin, a peptide hormone primarily produced by the liver, regulates iron metabolism by interacting with its receptor, ferroportin. Studies have demonstrated that hepcidin participates in the progression of liver fibrosis by regulating HSC activation, but its regulatory effect on hepatocytes remains largely unknown.
Methods: A carbon tetrachloride (CCl4)-induced liver fibrosis model was established in C57BL/6 wild-type (WT) and hepcidin knockout (Hamp-/-) mice.
Cutaneous leishmaniasis and iron metabolism: current insights and challenges.
Front Immunol
December 2024
Health and Environment Laboratory, Hassan II University of Casablanca, Biochemistry, Biotechnology and Immunophysiopathology Research Team, Ain Chock Faculty of Sciences, Casablanca, Morocco.
Leishmaniasis is a vector-borne parasitic infection induced by protozoa of the genus The disease spectrum ranges from skin lesions to visceral leishmaniasis, which is fatal if untreated. The cutaneous leishmaniasis is characterized by a clinical polymorphism of lesions with a broad range of severity ranging from a self-limited lesion to multiple disfiguring lesions stigmatizing the patient for life. Although iron is required for several process of infection including survival, growth and virulence, the number of studies on host iron metabolism during this infection remains limited.
View Article and Find Full Text PDFNovel loci and biomedical consequences of iron homoeostasis variation.
Commun Biol
December 2024
BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Iron homoeostasis is tightly regulated, with hepcidin and soluble transferrin receptor (sTfR) playing significant roles. However, the genetic determinants of these traits and the biomedical consequences of iron homoeostasis variation are unclear. In a meta-analysis of 12 cohorts involving 91,675 participants, we found 43 genomic loci associated with either hepcidin or sTfR concentration, of which 15 previously unreported.
View Article and Find Full Text PDFRecurrent BMP4 variants in exon 4 cause non-HFE-associated hemochromatosis via the BMP/SMAD signaling pathway.
Orphanet J Rare Dis
November 2024
Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Background: Hereditary hemochromatosis (HH) is an iron overload disorder and can be caused by variants in non-HFE genes in Chinese patients. However, there is still a considerable proportion of patients suffering from unexplained iron overload. In our previous study, we had identified the p.
View Article and Find Full Text PDFRAS signaling pathway is essential in regulating PIEZO1-mediated hepatic iron overload in dehydrated hereditary stomatocytosis.
Am J Hematol
January 2025
Department of Molecular Medicine and Medical Biotechnologies, "Federico II" University of Naples, Naples, Italy.
PIEZO1 encodes a mechanoreceptor, a cation channel activated by mechanical stimuli. Gain-of-function (GoF) variants in PIEZO1 cause dehydrated hereditary stomatocytosis (DHS), or xerocytosis, a pleiotropic syndrome characterized by anemia and iron overload. DHS patients develop hepatic iron overload independent of the degree of anemia and transfusion regimen.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!