Background and Objective: Hepcidin is an acute-phase protein produced by the liver, which inhibits the proliferation of pathogens by increasing iron sequestration in macrophages and decreasing iron absorption. Although several studies have been performed on the role of hepcidin, data on its role in brucellosis are scarce. The aim of this study was to compare the serum level of hepcidin in patients with brucellosis and healthy controls.
Materials and Methods: We recruited all the brucellosis patients referred to the clinic or Infectious Diseases Unit of Sina Hospital, Hamadan, Iran, from April 2016 to February 2017. The control group included age- and gender-matched individuals who visited the hospital for medical check-up examination or as patient companions. Blood samples were obtained from all the individuals and serum hepcidin level was measured using ELISA. A questionnaire on demographic characteristics and clinical symptoms and signs of brucellosis was completed for each subject. Data were analyzed using Stata 11 software.
Results: In this case-control study, 42 patients with brucellosis and 42 healthy controls were enrolled. The most common clinical symptoms of brucellosis were fever (76%) and arthralgia (69%). Further, Wright > 1.160 and 2ME > 1.80 were found in 55% and 60% of the patients, respectively. Symptomatic brucellosis was detected in 12 (28%) patients. The mean serum levels of hepcidin in the patients and controls were 42.6±11.7 and 17.3±4.2, respectively, showing that hepcidin level was significantly higher in the patient group compared to the control group (P<0.001). Of the 42 patients, 12 suffered from symptomatic brucellosis. The mean serum levels of hepcidin in the symptomatic and asymptomatic patients were 41±10.1 and 43±12.4, respectively, indicating no significant differences between the two groups in this regard.
Conclusion: Increased serum level of hepcidin in brucellosis patients can be considered as a diagnostic biomarker of inflammation and active disease. Further studies are required to identify the role of hepcidin as a host defense mechanism and its potential effect on brucellosis pathogenesis.