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Soluble Transferrin Receptor (sTfR) Identifies Iron Deficiency Anemia (IDA) in Pulmonary Tuberculosis Patients.
Ratnaningsih, T, Sukirto, NW, Wahyuningsih, AT
Acta medica Indonesiana. 2020;(4):334-343
Abstract
BACKGROUND iron deficiency in pulmonary tuberculosis (TB) patients may weaken their immune system, causing difficulty in overcoming the infection. Accurate diagnosis of iron deficiency anemia (IDA) in pulmonary TB patients is essential. In order to prove the iron deficient state, diagnosis should focus on inflammatory factors, which could highly affect the outcome of iron status, such as measurement of serum ferritin (SF). Soluble Transferrin Receptor (sTfR) is the best parameter to diagnose iron deficiency in the inflammatory condition. This study aimed to understand the role of sTfR to identify IDA in TB patients. METHODS cross-sectional study were applied to 3 study groups: anemic pulmonary TB (68 subjects), IDA (7 subjects), and non-anemic pulmonary TB (15 subjects). The test averages and correlations between sTfR, SF, and other hematological parameters were measured and analyzed. RESULTS significant differences of sTfR were found in the anemic TB group compared to the IDA group and also between the IDA and non-anemic TB groups (p<0.0001). However, there was no significant difference (p>0.05) between TB anemic and non-anemic groups. We also found no significant difference between the TB anemic sub-group with normal levels of sTfR compared with the non-anemic group. There was no significant difference of sTfR levels between sub-group of increasing sTfR and group IDA (p>0.05). However, there was strong correlation between sTfR and SF in the IDA group (r=-0.89; p=0.007). CONCLUSION the findings suggest verifying the sTfR amount in anemic patients with pulmonary TB suffering from inflammation, so that the iron deficiency could be more accurately identified and properly treated.
2.
Increased ferritin levels in non-transfusion-dependent β°-thalassaemia/HbE are associated with reduced CXCR2 expression and neutrophil migration.
Thiengtavor, C, Siriworadetkun, S, Paiboonsukwong, K, Fucharoen, S, Pattanapanyasat, K, Vadolas, J, Svasti, S, Chaichompoo, P
British journal of haematology. 2020;(1):187-198
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Abstract
Severe bacterial infection is a major complication causing morbidity and mortality in β-thalassaemia/HbE patients. Innate immunity constitutes the first line of defence against bacterial infection. This study aimed to comprehensively investigate the innate immune phenotype and function related to factors predisposing to infection in non-transfusion-dependent (NTD) β°-thalassaemia/HbE patients. Twenty-six patients and 17 healthy subjects were recruited to determine complement activity (C3, C4, mannose-binding lectin and CH50) and surface receptor expression including markers of phagocytosis (CD11b, CD16 and C3bR), inflammation (C5aR) and migration (CD11b, CXCR1 and CXCR2) on neutrophils and monocytes. In addition, phagocytosis and oxidative burst activity of neutrophils and monocytes against Escherichia coli and neutrophil migration were examined. Decreased C3 and surface expression of CD11b and C3bR on neutrophils were found in patients. However, phagocytosis of neutrophils in patients was still in the normal range. Interestingly, patients displayed a significant reduction of surface expression of CXCR2 [1705 ± 217 mean fluorescent intensity (MFI)] on neutrophils, leading to impaired neutrophil migration (9·2 ± 7·7%) when compared to neutrophils from healthy subjects (2261 ± 627 MFI and 27·8 ± 9% respectively). Moreover, surface expression of CXCR2 on neutrophils was associated with splenectomy status, serum ferritin and haemoglobin levels. Therefore, impaired neutrophil migration could contribute to the increased susceptibility to infection seen in NTD β°-thalassaemia/HbE patients.
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Hyperferritinaemia: An Iron Sword of Autoimmunity.
Giemza-Stokłosa, J, Islam, MA, Kotyla, PJ
Current pharmaceutical design. 2019;(27):2909-2918
Abstract
BACKGROUND Ferritin is a molecule that plays many roles being the storage for iron, signalling molecule, and modulator of the immune response. METHODS Different electronic databases were searched in a non-systematic way to find out the literature of interest. RESULTS The level of ferritin rises in many inflammatory conditions including autoimmune disorders. However, in four inflammatory diseases (i.e., adult-onset Still's diseases, macrophage activation syndrome, catastrophic antiphospholipid syndrome, and sepsis), high levels of ferritin are observed suggesting it as a remarkable biomarker and pathological involvement in these diseases. Acting as an acute phase reactant, ferritin is also involved in the cytokine-associated modulator of the immune response as well as a regulator of cytokine synthesis and release which are responsible for the inflammatory storm. CONCLUSION This review article presents updated information on the role of ferritin in inflammatory and autoimmune diseases with an emphasis on hyperferritinaemic syndrome.
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Plasma Ferritin and Hepcidin Are Lower at 4 Months Postpartum among Women with Elevated C-Reactive Protein or α1-Acid Glycoprotein.
Jorgensen, JM, Yang, Z, Lönnerdal, B, Chantry, CJ, Dewey, KG
The Journal of nutrition. 2017;(6):1194-1199
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Abstract
Background: Ferritin and hepcidin are markers of iron status that typically increase during inflammation or infection. The postpartum period is a physiologically unique life stage in which the relations between these proteins and other markers of inflammation have not been extensively studied.Objective: We aimed to determine whether 2 markers of inflammation [high-sensitivity C-reactive protein (CRP) and α1-acid glycoprotein (AGP)] were associated with ferritin or hepcidin in postpartum women in California.Methods: This is a secondary analysis of a randomized controlled iron-intervention trial. Plasma CRP, AGP, ferritin, and hepcidin were analyzed at 2 and 17 wk postpartum in 114 lactating women. We examined Pearson correlation coefficients between all biomarkers at both time points and differences in mean values of ferritin and hepcidin between those with and without elevated CRP and/or AGP.Results: At 2 and 17 wk postpartum, 58% and 26% of women had CRP >5 mg/L and 78% and 29% had AGP >1 g/L, respectively. Neither CRP nor AGP was significantly correlated with ferritin (r = 0.07 and -0.06; n = 114 at 2 wk; -0.14 and -0.14; n = 95 at 17 wk) or hepcidin (r = 0.18 and -0.03 at 2 wk; -0.05 and -0.14 at 17 wk; P > 0.05 for all). At 2 wk, geometric mean plasma ferritin and hepcidin concentrations did not differ between women with and without elevated CRP or AGP (P > 0.5), but at 17 wk women with elevated CRP or AGP had lower mean (95% CI) ferritin and hepcidin than did women without either elevated CRP or AGP [ferritin: 30.3 ng/mL (23.4, 39.1 ng/mL) compared with 40.2 ng/mL (32.9, 49.2 ng/mL); P < 0.01; hepcidin: 44.3 ng/mL (32.3, 60.9 ng/mL) compared with 67.6 ng/mL (56.1, 81.5 ng/mL); P = 0.02].Conclusion: Lower ferritin and hepcidin among women with elevated CRP or AGP at 17 wk postpartum suggests that these markers of iron status react differently to physiologic immune activation than to pathologic inflammatory states.