Search

Introduction: Patients with community-acquired pneumonia (CAP) often exhibit a declining hemoglobin (Hb) concentration. During inflammation pro-inflammatory cytokines and cells of the reticuloendothelial system induce disturbances in iron homeostasis. In this study inflammation markers and hepcidin-25 concentrations were monitored together with short-term alterations in reticulocyte hemoglobinization (RET-He)., Methods: A total of 25 patients with CAP participated in the study. The assay for serum hepcidin-25 is based on a combination of weak cation exchange chromatography and time-of-flight mass spectrometry., Results: At hospital admission serum hepcidin-25 concentrations (14.6 ± 6.9 nMol/L, mean ± SD) were established in the upper level of the reference range (0.5-13.9 nMol/L). Results for C-reactive protein (CRP) and Interleukin-6 (IL-6) were obviously increased compared to the reference ranges. From admission until day 14 hepcidin-25, CRP and IL-6 steadily decreased towards the reference ranges. Hb concentrations declined from admission until day 4 from 8.1 ± 1.0 mMol/L to 7.4 ± 0.9 mMol/L. At admission Ret-He results were within the lower region of the reference range (1900-2300aMol) and results demonstrated a decline during admission from 1931 ± 241 aMol until 1845 ± 199 aMol (NS) at day 4. From a minimum Ret-He value at day 4 results increased towards 2129 ± 136 aMol at day14., Conclusion: A transient increase of cytokine-stimulated serum hepcidin-25 in combination with a temporary decrease of Hb and Ret-He is demonstrated in patients with CAP. Our results support the hypothesis that hepcidin-25 induces transient impairment of reticulocyte hemoglobin content (Ret-He).

Bioincompatibility is the total of side effects during hemodialysis (HD) including, amongst others, changes in platelet (PLT) level. Deviations in PLT count, immature PLT count, PLT morphology, CD62p expression, Platelet Factor 4 (PF4), β-Thromboglobulin (β-TG), serotonin, Thrombin-Antithrombin III (TAT) and Prothrombin Fragment 1+2 (F1+2) are monitored before and during treatment with HD in order to elucidate the interaction between modifications in PLT morphology, PLT activation and markers concerning activation of coagulation. Different patterns with time indicate that there is no correlation between an increased amount of depleted PLTs and increased amounts of PLT activation markers such as CD62p, PF4, β-TG and serotonin. A statistically significant correlation between increased PLT activation markers and markers for increased activation of coagulation such as TAT and F1+2 has not been established. Only a weak correlation is demonstrated between the increase of markers for activation of coagulation and the decrease in PLT counts, immature PLT counts and depleted PLTs during HD treatment. The change in the extracorporeal circuit during HD is probably a more critical factor in the mechanism leading to activation of the coagulation pathway than the modifications in PLT morphology.