• biomarker
• diagnosis
• pentraxin-3 (PTX-3)
• prognosis
• sepsis

• Biomarker
• HFRS
• Hantaan virus

• Humans
• Hantaan virus
• Hemorrhagic Fever with Renal Syndrome/diagnosis
• Acute Kidney Injury/diagnosis
• Blood Coagulation
• Thrombocytopenia

• cell death
• inflammation
• molecular chaperone
• sepsis

• Animals
• Mice
• Histones/metabolism
• Clusterin/metabolism
• Inflammation
• Cell Death
• Antineoplastic Agents
• Sepsis/drug therapy

• CRP
• ESR
• diabetes mellitus
• diabetic foot ulcer
• fibrinogen
• limb amputation
• pentraxin-3
• procalcitonin

• Asymptomatic infection carrier
• HTLV-1-associated myelopathy
• Human T-lymphotropic virus 1
• Pentraxin 3

• Graves' disease
• PTX3
• inflammation
• nodular thyroid disease
• thyroid cancer
• thyroid disorders

• Humans
• Female
• Male
• Immunity, Innate
• Epithelial-Mesenchymal Transition
• Autoimmune Diseases
• Thyroid Neoplasms
• Carcinogenesis

• Humanitas Research Hospital

• Male
• Humans
• Glucose
• Blood Glucose/metabolism
• Healthy Volunteers
• Cross-Over Studies
• Biomarkers
• Scavenger Receptors, Class E
• Blood Glucose Self-Monitoring

• COVID - 19
• SARS – CoV – 2
• inflammation
• mortality
• pentraxin 3 (PTX3)

• Humans
• Hospital Mortality
• COVID-19
• Serum Amyloid P-Component/metabolism
• Thrombosis/etiology
• Intubation, Intratracheal

• Ministry of Health

Sepsis and septic shock are a major public health concern and are still associated with high rates of morbidity and mortality. Whilst there is growing understanding of different phenotypes and endotypes of sepsis, all too often treatment strategies still only employ a “one-size-fits-all” approach. Biomarkers offer a unique opportunity to close this gap to more precise treatment approaches by providing insight into clinically hidden, yet complex, pathophysiology, or by individualizing treatment pathways. Predicting and evaluating systemic inflammation, sepsis or septic shock are essential to improve outcomes for these patients. Besides opportunities to improve patient care, employing biomarkers offers a unique opportunity to improve clinical research in patients with sepsis. The high rate of negative clinical trials in this field may partly be explained by a high degree of heterogeneity in patient cohorts and a lack of understanding of specific endotypes or phenotypes. Moving forward, biomarkers can support the selection of more homogeneous cohorts, thereby potentially improving study conditions of clinical trials. This may finally pave the way to a precision medicine approach to sepsis, septic shock and complication of sepsis in the future.

• Biomarkers
• C-Reactive Protein
• Cytokines
• Humans
• Infant, Newborn
• Interleukin 1 Receptor Antagonist Protein
• Interleukin-1
• Interleukin-10
• Interleukin-18
• Interleukin-6
• Interleukin-8
• Prognosis
• ROC Curve
• Sepsis
• Serum Amyloid P-Component
• Tumor Necrosis Factor-alpha

• AUC
• Meta-analysis
• Mortality
• Pentraxin-3
• Sepsis

Neonatal sepsis is a common cause of neonatal morbidity and mortality. The diagnosis of newborn sepsis is still difficult. Different early objective diagnostic tests or specific signs and symptoms, particularly in preterm infants, make it difficult to diagnose neonatal sepsis. This review article describes biomarkers and their role in the early diagnosis, treatment, and prognosis of neonatal sepsis. It also explores the possible advances and future prospects of these biomarkers. An ideal sepsis biomarker will not only help in the guidance of the use of antibiotics when not needed but also the duration of the course of antibiotics if sepsis is proven. It should also have high sensitivity, specificity, positive predictive value, and negative predictive value. These biomarkers hold a promising position in the management of neonatal sepsis and translate into use in clinical settings. Metabolomics, a diagnostic method based on detecting metabolites found in biological fluids, may open new possibilities in the management of critically ill newborns.

• c-reactive proteins(crp)
• infection
• metabolomics
• neonatal sepsis
• serum biomarkers

• IL‑1β
• cell cycle
• invasion
• pentraxin 3
• preeclampsia
• proliferation
• trophoblasts

• PCSK9
• ST-segment elevation myocardial infarction
• major adverse cardiovascular events
• optical coherence tomography
• pentraxin-3
• plaque morphology characteristics

• biomarker
• intensive care units
• pentraxin-3
• prognosis
• sepsis
• septic shock

• Heart failure
• Hypertension
• Pentraxin 3

• Animals
• Apoptosis/drug effects
• Atrial Natriuretic Factor/blood
• Blood Pressure/drug effects
• C-Reactive Protein/pharmacology
• Cytokines/genetics
• Cytokines/metabolism
• Disease Models, Animal
• Heart Failure/drug therapy
• Heart Failure/metabolism
• Heart Failure/physiopathology
• Hypertension/drug therapy
• Hypertension/metabolism
• Hypertension/physiopathology
• Male
• Myocytes, Cardiac/drug effects
• Myocytes, Cardiac/metabolism
• Myocytes, Cardiac/pathology
• Natriuretic Peptide, Brain/blood
• Rats, Inbred SHR
• Rats, Sprague-Dawley
• Recombinant Proteins/pharmacology
• Serum Amyloid P-Component/pharmacology
• Ventricular Function, Left/drug effects
• Rats

Inflammation and oxidative stress characterize sepsis and determine its severity. In this study, we investigated the relationship between albumin oxidation and sepsis severity in a selected cohort of patients from the Albumin Italian Outcome Study (ALBIOS). A retrospective analysis was conducted on the oxidation forms of human albumin [human mercapto-albumin (HMA), human non-mercapto-albumin form 1 (HNA1) and human non-mercapto-albumin form 2 (HNA2)] in 60 patients with severe sepsis or septic shock and 21 healthy controls. The sepsis patients were randomized (1:1) to treatment with 20% albumin and crystalloid solution or crystalloid solution alone. The albumin oxidation forms were measured at day 1 and day 7. To assess the albumin oxidation forms as a function of oxidative stress, the 60 sepsis patients, regardless of the treatment, were grouped based on baseline sequential organ failure assessment (SOFA) score as surrogate marker of oxidative stress. At day 1, septic patients had significantly lower levels of HMA and higher levels of HNA1 and HNA2 than healthy controls. HMA and HNA1 concentrations were similar in patients treated with albumin or crystalloids at day 1, while HNA2 concentration was significantly greater in albumin-treated patients (p < 0.001). On day 7, HMA was significantly higher in albumin-treated patients, while HNA2 significantly increased only in the crystalloids-treated group, reaching values comparable with the albumin group. When pooling the septic patients regardless of treatment, albumin oxidation was similar across all SOFA groups at day 1, but at day 7 HMA was lower at higher SOFA scores. Mortality rate was independently associated with albumin oxidation levels measured at day 7 (HMA log-rank = 0.027 and HNA2 log-rank = 0.002), irrespective of treatment group. In adjusted regression analyses for 90-day mortality, this effect remained significant for HMA and HNA2. Our data suggest that the oxidation status of albumin is modified according to the time of exposure to oxidative stress (differences between day 1 and day 7). After 7 days of treatment, lower SOFA scores correlate with higher albumin antioxidant capacity. The trend toward a positive effect of albumin treatment, while not statistically significant, warrants further investigation.

• albumin
• oxidation
• oxidative stress
• resuscitation
• sepsis
• shock

• inflammation
• neopterin
• pentraxin 3
• rheumatoid arthritis

• mass spectrometry
• sars-cov-2
• prognostic markers

• Adult
• Animals
• Antibodies, Neutralizing/immunology
• Antigens, Neoplasm/metabolism
• Biomarkers, Tumor/metabolism
• C-Reactive Protein/metabolism
• COVID-19/metabolism
• COVID-19/prevention & control
• COVID-19/virology
• Critical Care/statistics & numerical data
• Female
• HEK293 Cells
• Humans
• Kaplan-Meier Estimate
• Male
• Middle Aged
• Proteomics/methods
• RNA, Viral/blood
• RNA, Viral/genetics
• SARS-CoV-2/genetics
• SARS-CoV-2/metabolism
• SARS-CoV-2/physiology
• Serum Amyloid P-Component/metabolism
• Spike Glycoprotein, Coronavirus/immunology
• Spike Glycoprotein, Coronavirus/metabolism
• Viral Load/immunology

• CS-2016-16-011 Department of Health
• RM/17/3/33381 British Heart Foundation
• RG/16/14/32397 British Heart Foundation
• CH/16/3/32406 British Heart Foundation
• FS/18/60/34181 British Heart Foundation
• RE/18/2/34213 British Heart Foundation
• MR/V040162/1 Medical Research Council
• MC/PC/15068 Medical Research Council
• MC_PC_15068 Medical Research Council
• FC001093 Wellcome Trust
• MR/R017751/1 Medical Research Council
• FS/19/58/34895 British Heart Foundation
• RG/19/11/34633 British Heart Foundation
• PG/17/48/32956 British Heart Foundation
• FS/17/65/33481 British Heart Foundation
• 106292/Z/14/Z Wellcome Trust
• SP/17/10/33219 British Heart Foundation
• Wellcome Trust
• FC001093 Arthritis Research UK
• FC001093 Medical Research Council
• Cancer Research UK
• FC001093 Cancer Research UK
• CH/1999001/11735 British Heart Foundation
• British Heart Foundation (BHF)
• Fondation Leducq

• Disease severity
• Early prediction
• Hemorrhagic fever with renal syndrome
• Pentraxin-3
• Prognosis

Single nucleotide polymorphisms (SNPs) of pentraxin 3 (PTX3) are associated with various outcomes of lung infections. This study aimed to analyze the relationship between PTX3 polymorphisms and the severity of community-acquired pneumonia (CAP).

This is a retrospective case-control study comprising 43 patients with severe CAP (SCAP) and 97 patients with non-severe CAP. Three SNPs in the PTX3 gene (rs2305619, rs3816527, and rs1840680) from peripheral blood samples were genotyped by real-time polymerase chain reaction. The association between each SNP and the CAP severity was analyzed by logistic regression analysis.

We found that the rs1840680 polymorphism was significantly associated with CAP clinical severity. However, no such association was observed for the genotypes and allele frequencies of rs2305619 or rs3816527. The PTX3 rs1840680 AG genotype was an independent factor for a lower risk of SCAP after multivariate logistic regression analysis. Male sex and coronary heart disease were associated with an increased risk of SCAP.

The PTX3 rs1840680 AG genotype was found to be associated with a lower risk of SCAP, and may serve as a potential protective biomarker to help clinical judgment and management.

• Severe community-acquired pneumonia
• genetic variant
• genetics
• pentraxin 3
• rs1840680
• single nucleotide polymorphism

• PCSK9
• mortality
• pentraxin 3
• sepsis
• septic shock

• Aged
• Biomarkers/blood
• C-Reactive Protein/metabolism
• Female
• Humans
• Italy/epidemiology
• Male
• Middle Aged
• Proprotein Convertase 9/blood
• Sepsis/mortality
• Sepsis/therapy
• Serum Amyloid P-Component/metabolism
• Shock, Septic/mortality
• Shock, Septic/therapy

• genetic variants
• pelvic lymph node metastasis
• pentraxin 3
• uterine cervical cancer

To evaluate the usefulness of a new marker, pentraxin, as a prognostic marker in septic shock patients.

Single-centre prospective observational study that included all consecutive patients 18 years or older who were admitted to the intensive care unit (ICU) with septic shock. Serum levels of procalcitonin (PCT), C-reactive protein (CRP) and pentraxin (PTX3) were measured on ICU admission.

Seventy-five septic shock patients were included in the study. The best predictors of in-hospital mortality were the severity scores: SAPS II (AUC = 0.81), SOFA (AUC = 0.79) and APACHE II (AUC = 0.73). The ROC curve for PTX3 (ng/mL) yielded an AUC of 0.70, higher than the AUC for PCT (0.43) and CRP (0.48), but lower than lactate (0.79). Adding PTX3 to the logistic model increased the predictive capacity in relation to SAPS II, SOFA and APACHE II for in-hospital mortality (AUC 0.814, 0.795, and 0.741, respectively). In crude regression models, significant associations were found between in-hospital mortality and PTX3. This positive association increased after adjusting for age, sex and immunosuppression: adjusted OR T3 for PTX3 = 7.83, 95% CI 1.35–45.49, linear P trend = 0.024.

Our results support the prognostic value of a single determination of plasma PTX3 as a predictor of hospital mortality in septic shock patients.

• Aged
• Area Under Curve
• Biomarkers/blood
• C-Reactive Protein/metabolism
• Confidence Intervals
• Female
• Hospital Mortality
• Humans
• Intensive Care Units
• Male
• Middle Aged
• Patient Admission
• Prognosis
• ROC Curve
• Regression Analysis
• Serum Amyloid P-Component/metabolism
• Severity of Illness Index
• Shock, Septic/blood

Sepsis is a systemic response to infection with a high rate of mortality and complex pathophysiology involving inflammation, infection response, hemostasis, endothelium, and platelets. The purpose of this study was to develop an equation incorporating biomarker levels at intensive care unit (ICU) admission to predict mortality in patients with sepsis, based on the hypothesis that a combination of biomarkers representative of multiple physiological systems would provide improved predictive value. Plasma samples and clinical data were collected from 103 adult patients with sepsis at the time of ICU admission. Biomarker levels were measured using commercially available methods. A 28-day mortality was used as the primary end point. Stepwise linear regression modeling was performed to generate a predictive equation for mortality. Differences in biomarker levels between survivors were quantified using the Mann-Whitney test and the area under the receiver operating curve (AUC) was used to describe predictive ability. Significant differences (P < .05) were observed between survivors and nonsurvivors for plasminogen activator inhibitor 1 (AUC = 0.70), procalcitonin (AUC = 0.77), high mobility group box 1 (AUC = 0.67), interleukin (IL) 6 (AUC = 0.70), IL-8 (AUC = 0.70), protein C (AUC = 0.71), angiopoietin-2 (AUC = 0.76), endocan (AUC = 0.58), and platelet factor 4 (AUC = 0.70). A predictive equation for mortality was generated using stepwise linear regression modeling, which incorporated procalcitonin, vascular endothelial growth factor, the IL-6:IL-10 ratio, endocan, and platelet factor 4, and demonstrated a better predictive value for patient outcome than any individual biomarker (AUC = 0.87). The use of mathematical modeling resulted in the development of a predictive equation for sepsis-associated mortality with performance than any individual biomarker or clinical scoring system which incorporated biomarkers representative of multiple systems.

• DIC
• disseminated intravascular coagulation
• mortality prediction
• sepsis

• Diagnosis
• marker
• neonate
• pentraxin 3
• sepsis

• Antimicrobial stewardship
• Biomarkers
• C-reactive protein
• Lactate
• Pneumonia
• Proadrenomedulin
• Procalcitonin
• Sepsis

• C-reactive protein
• biomarkers
• bioscore
• procalcitonin
• sepsis

• Collectin-11
• Complement system
• Ficolins
• Mannose-binding lectin
• PTX3
• Sepsis

This study investigated the clinical value of interleukin-6 (IL-6), pentraxin 3 (PTX3), and procalcitonin (PCT) in patients with sepsis and septic shock diagnosed according to the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).

Serum levels of IL-6, PTX3, and PCT were measured in 142 enrolled subjects (51 with sepsis, 46 with septic shock, and 45 as controls). Follow-up IL-6 and PTX3 levels were measured in patients with initial septic shock within 24 h of hospital discharge. Optimal cut-off values were determined for sepsis and septic shock, and prognostic values were evaluated.

Serum IL-6 levels could discriminate sepsis (area under the curve [AUC], 0.83–0.94, P <  0.001; cut-off value, 52.60 pg/mL, 80.4% sensitivity, 88.9% specificity) from controls and could distinguish septic shock (AUC, 0.71–0.89; cut-off value, 348.92 pg/mL, 76.1% sensitivity, 78.4% specificity) from sepsis. Twenty-eight-day mortality was significantly higher in the group with high IL-6 (≥ 348.92 pg/mL) than in the group with low IL-6 (< 348.92 pg/mL) (P = 0.008). IL-6 was an independent risk factor for 28-day mortality among overall patients (hazard ratio, 1.0004; 95% confidence interval, 1.0003–1.0005; p = 0.024). In septic shock patients, both the initial and follow-up PTX3 levels were consistently significantly higher in patients who died than in those who recovered (initial p = 0.004; follow-up P <  0.001).

The diagnostic and prognostic value of IL-6 was superior to those of PTX3 and PCT for sepsis and septic shock.

• Emergency department
• Interleukin-6
• Pentraxin 3
• Procalcitonin
• Sepsis
• Septic shock

The first line of defense in innate immunity is provided by cellular and humoral mediators. Pentraxins are a superfamily of phylogenetically conserved humoral mediators of innate immunity. PTX3, the first long pentraxin identified, is a soluble pattern recognition molecule rapidly produced by several cell types in response to primary pro-inflammatory signals and microbial recognition. PTX3 acts as an important mediator of innate immunity against pathogens of fungal, bacterial and viral origin, and as a regulator of inflammation, by modulating complement activation and cell extravasation, and facilitating pathogen recognition by myeloid cells. In sepsis, PTX3 plasma levels are associated with severity of the condition, patient survival, and response to therapy. In combination with other established biomarkers, PTX3 could improve stratification of sepsis patients and thus, complement the system of classification and monitoring of this disease.

• inflammation
• innate immunity
• pentraxin
• pentraxin 3 (PTX3)
• sepsis

Biomarkers may facilitate clinical decisions in order to guide antimicrobial treatment and prediction of prognosis in community-acquired pneumonia (CAP). We measured serum C-reactive protein, procalcitonin (PCT) and calprotectin levels, and plasma pentraxin 3 (PTX3) and presepsin levels, along with whole-blood white cell counts, at three time-points, and examined their association with microbial aetiology and adverse clinical outcomes in CAP.

Blood samples were obtained at hospital admission, clinical stabilisation and 6-week follow-up from 267 hospitalised adults with CAP. Adverse short-term outcome was defined as intensive care unit admission and 30-day mortality. Long-term outcome was evaluated as 5-year all-cause mortality.

Peak levels of all biomarkers were seen at hospital admission. Increased admission levels of C-reactive protein, PCT and calprotectin were associated with bacterial aetiology of CAP, while increased admission levels of PCT, PTX3 and presepsin were associated with adverse short-term outcome. In univariate and multivariate regression models, white blood cells and calprotectin at 6-week follow-up were predictors of 5-year all-cause mortality.

Calprotectin emerges as both a potential early marker of bacterial aetiology and a predictor for 5-year all-cause mortality in CAP, whereas PCT, PTX3 and presepsin may predict short-term outcome.

In 267 adults with community-acquired pneumonia, systemic calprotectin emerges as an early marker of bacterial aetiology and a predictor of 5-year mortality, whereas systemic procalcitonin, pentraxin 3 and presepsin are predictors of short-term outcomehttp://ow.ly/dz6S30nAFvn

• community-acquired pneumonia
• etiology
• hospital mortality
• pentraxin-3
• prospective studies

Oxidative stress and uncontrolled inflammation are hallmarks of sepsis, leading to organ failure and death. As demonstrated in animal studies, oxidative stress can be alleviated by antioxidant therapies. Paraoxonase-1 (PON1) is a serum-based antioxidant, anti-inflammatory agent, detoxifier, and quorum-sensing factor found to be a prognostic marker in sepsis. However, its associations with multiple organ dysfunction syndrome (MODS), a complication of sepsis and the leading cause of death in the surgical intensive care units (ICU), as well as with specific organ dysfunction, infection site, and invading pathogen remain unknown. Therefore, we measured arylesterase activity of PON1 in 87 individuals (35 with MODS) and related it to the clinical type, organ failure, infection site, pathogens, and hematological and biochemical indices of inflammation at admission to ICU and during a five-day follow-up. Suitability of PON1 and its indices derived from a follow-up as biomarkers in MODS was evaluated as well. MODS was associated with decreased PON1, more so in patients with septic shock, displaying an excellent accuracy as a marker of MODS (91%) and a fair one as a marker in differentiating septic shock from severe sepsis (76%). Decreased admission PON1 accompanied cardiovascular insufficiency (CVI), and, as its marker, PON1 displayed a good accuracy (82%). It was also associated with the abdomen as a site of infection but not with an invading pathogen. In multivariate analysis, 50% of variability in PON1 activity in patients with MODS was explained by the patients' age, CVI, and abdomen as a site of infection. Patients with septic shock, CVI, and abdominal MODS had distinctly different dynamics of PON1 during a follow-up. Mean PON1 activity during the follow-up reflected the associations observed for admission PON1 but was also significantly associated with metabolic dysfunction. Our results show PON1 potential as a biomarker in MODS, particularly as an indicator of CVI.

Sepsis, which is the leading cause of death in intensive care units (ICU), has been acknowledged as a global health priority by the WHO in 2017. Identification of biomarkers allowing early stratification and recognition of patients at higher risk of death is crucial. One promising biomarker candidate is pentraxin-3 (PTX3); initially elevated and persistently increased plasma concentration in septic patients has been associated with increased mortality. PTX3 is an acute phase protein mainly stored in neutrophil granules. These cells are responsible for rapid and prompt release of PTX3 in inflammatory context, but the cellular origin responsible for successive days' elevation in sepsis remains unknown. Upon inflammatory stimulation, PTX3 can also be produced by other cell types, including endothelial and immune cells. As in septic patients immune alterations have been described, we therefore sought to investigate whether such cells participated in the elevation of PTX3 over the first days after septic shock onset. To address this point, PTX3 was measured in plasma from septic shock patients at day 3 after ICU admission as well as in healthy volunteers (HV), and the capacity of whole blood cells to secrete PTX3 after inflammatory stimulation was evaluated ex vivo. A significantly mean higher (100-fold) concentration of plasma PTX3 was found in patients compared to HV, which was likely due to the inflammation-induced initial release of the pre-existing PTX3 reservoir contained in neutrophils. Strikingly, when whole blood was stimulated ex vivo with LPS no significant difference between patients and HV in PTX3 release was found. This was in contrast with TNFα which decreased production was illustrative of the endotoxin tolerance phenomenon occurring in septic patients. Then, the release of PTX3 protein from a HV neutrophil-free PBMC endotoxin tolerance model was investigated. At the transcriptional level, PTX3 seems to be a weakly tolerizable gene similar to TNFα. Conversely, increased protein levels observed in anergy condition reflects a non-tolerizable phenotype, more likely to an anti-inflammatory marker. Hence, altered immune cells still have the ability to produce PTX3 in response to an inflammatory trigger, and therefore circulating white blood cell subset could be responsible of the sustained PTX3 plasma levels over the first days of sepsis setting.

• endotoxin tolerance
• immune dysfunction
• pentraxin 3
• sepsis
• septic shock

Shigella spp. are pathogenic bacteria that cause bacillary dysentery in humans by invading the colonic and rectal mucosa where they induce dramatic inflammation. Here, we have analyzed the role of the soluble PRR Pentraxin 3 (PTX3), a key component of the humoral arm of innate immunity. Mice that had been intranasally infected with S. flexneri were rescued from death by treatment with recombinant PTX3. In vitro PTX3 exerts the antibacterial activity against Shigella, impairing epithelial cell invasion and contributing to the bactericidal activity of serum.

PTX3 is produced upon LPS-TLR4 stimulation in accordance with the lipid A structure of Shigella. In the plasma of infected patients, the level of PTX3 amount only correlates strongly with symptom severity. These results signal PTX3 as a novel player in Shigella pathogenesis and its potential role in fighting shigellosis. Finally, we suggest that the plasma level of PTX3 in shigellosis patients could act as a biomarker for infection severity.

Soluble pattern recognition molecules, PRMs, are components of the humoral arm of innate immunity. The long pentraxin 3, PTX3, is a prototypic soluble PRM that is produced in response to primary inflammatory signals. Shigella spp. are human entero-pathogens which invade colonic and rectal mucosa where they cause deleterious inflammation. We show that PTX3 acts as an ante-antibody and contributes to the clearance of extracellular Shigella. As a countermeasure, Shigella uses invasiveness and low-inflammatory LPS to control PTX3 release in infected cells. This study highlights that the extracellular phase of the invasion process can be considered the “Achille heels” of Shigella pathogenesis.

• meta-analysis
• mortality
• plasminogen activator inhibitor-1
• sepsis
• systematic review

• Biomarkers
• Humans
• Mortality
• Odds Ratio
• Plasminogen Activator Inhibitor 1/blood
• Prognosis
• Sepsis/blood
• Sepsis/diagnosis
• Sepsis/mortality
• Severity of Illness Index

• acute-phase proteins
• arthroplasty
• complement
• glucocorticoids
• inflammation

• Aged
• Anti-Inflammatory Agents/therapeutic use
• Arthroplasty, Replacement, Knee
• Biomarkers/metabolism
• C-Reactive Protein/metabolism
• Complement System Proteins/metabolism
• Double-Blind Method
• Female
• Humans
• Immunity, Innate
• Inflammation/immunology
• Lectins/metabolism
• Male
• Mannose-Binding Lectin/blood
• Methylprednisolone/therapeutic use
• Middle Aged
• Placebo Effect
• Preoperative Care
• Serum Amyloid P-Component/metabolism
• Ficolins