Randi Marie Mohus1,2,3, Julie Paulsen4,5,6, Lise Gustad6,7, Åsa Askim8,6,9, Arne Mehl6,7, Andrew T DeWan6,10, Jan Egil Afset11,6, Bjørn Olav Åsvold12,6,13,14, Erik Solligård8,6,9, Jan Kristian Damås15,16,17,18. 1. Department of Circulation and Medical Imaging, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. randi.m.mohus@ntnu.no. 2. Mid-Norway Sepsis Research Center, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. randi.m.mohus@ntnu.no. 3. Clinic of Anaesthesia and Intensive Care, St. Olavs Hospital, 7006, Trondheim, Norway. randi.m.mohus@ntnu.no. 4. Centre of Molecular Inflammation Research, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. 5. Department of Medical Genetics, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. 6. Mid-Norway Sepsis Research Center, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. 7. Department of Medicine, Levanger Hospital, Nord-Trøndelag Hospital Trust, Levanger, Norway. 8. Department of Circulation and Medical Imaging, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. 9. Clinic of Anaesthesia and Intensive Care, St. Olavs Hospital, 7006, Trondheim, Norway. 10. Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA. 11. Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. 12. Department of Public Health and Nursing, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. 13. K.G. Jebsen Center for Genetic Epidemiology, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. 14. Department of Endocrinology, St. Olavs Hospital, Trondheim, Norway. 15. Centre of Molecular Inflammation Research, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. jan.k.damas@ntnu.no. 16. Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. jan.k.damas@ntnu.no. 17. Mid-Norway Sepsis Research Center, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. jan.k.damas@ntnu.no. 18. Department of Infectious Diseases, St. Olavs Hospital, 7006, Trondheim, Norway. jan.k.damas@ntnu.no.
Abstract
PURPOSE: As iron is essential for both immune function and microbial growth, alterations in iron status could influence the risk of infections. We assessed the associations of iron status with risk of bloodstream infections (BSIs) and BSI mortality. METHODS: We measured serum iron, transferrin saturation (Tsat) and total iron-binding capacity (TIBC) in 61,852 participants in the population-based HUNT2 study (1995-97). Incident BSIs (1995-2011) were identified through linkage with the Mid-Norway Sepsis Register, which includes prospectively registered information on BSI from local and regional hospitals. We assessed the risk of a first-time BSI and BSI mortality with the iron indices using Cox proportional hazards regression analysis. RESULTS: During a median follow-up of 14.8 years, 1738 individuals experienced at least one episode of BSI, and 370 died within 30 days after a BSI. In age- and sex-adjusted analyses, BSI risk was increased among participants with indices of iron deficiency, serum iron ≤ 2.5th percentile (HR 1.72, 95% CI 1.34-2.21), Tsat ≤ 2.5th percentile (HR 1.48, 95% CI 1.12-1.96) or TIBC ≥ 97.5th percentile (HR 1.46, 95% CI 1.06-2.01). The associations remained similar after adjusting for comorbidities and exclusion of BSI related to cancer, rheumatic illnesses and inflammatory bowel disease. BSI mortality showed similar associations. CONCLUSION: Indices of severe iron deficiency are associated with an increased risk of a future BSI.
PURPOSE: As iron is essential for both immune function and microbial growth, alterations in iron status could influence the risk of infections. We assessed the associations of iron status with risk of bloodstream infections (BSIs) and BSI mortality. METHODS: We measured serum iron, transferrin saturation (Tsat) and total iron-binding capacity (TIBC) in 61,852 participants in the population-based HUNT2 study (1995-97). Incident BSIs (1995-2011) were identified through linkage with the Mid-Norway Sepsis Register, which includes prospectively registered information on BSI from local and regional hospitals. We assessed the risk of a first-time BSI and BSI mortality with the iron indices using Cox proportional hazards regression analysis. RESULTS: During a median follow-up of 14.8 years, 1738 individuals experienced at least one episode of BSI, and 370 died within 30 days after a BSI. In age- and sex-adjusted analyses, BSI risk was increased among participants with indices of iron deficiency, serum iron ≤ 2.5th percentile (HR 1.72, 95% CI 1.34-2.21), Tsat ≤ 2.5th percentile (HR 1.48, 95% CI 1.12-1.96) or TIBC ≥ 97.5th percentile (HR 1.46, 95% CI 1.06-2.01). The associations remained similar after adjusting for comorbidities and exclusion of BSI related to cancer, rheumatic illnesses and inflammatory bowel disease. BSI mortality showed similar associations. CONCLUSION: Indices of severe iron deficiency are associated with an increased risk of a future BSI.
Entities:
Keywords:
Bacteraemia; Epidemiology; Iron; Population based; Sepsis
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