Immunotherapy and combined assay of serum levels of carcinoembryonic antigen and acute-phase reactants

1998 ◽  
Vol 46 (1) ◽  
pp. 14-20 ◽  
Author(s):  
K. Ogoshi ◽  
Masao Miyaji ◽  
Kenji Nakamura ◽  
Yasumasa Kondoh ◽  
Hiroyasu Makuuchi ◽  
...  
2021 ◽  
Author(s):  
Jahanzeb Malik ◽  
Uzma Ishaq ◽  
Talha Laique ◽  
Amna Ashraf ◽  
Asmara Malik ◽  
...  

Background and Objective Coronavirus disease 2019 (COVID-19) manifests as multiple clinical and pathological organ dysfunctions. It also disrupts metabolic profile due to the release of pro-inflammatory cytokines causing a systemic inflammation reaction. However, the development and correlation of dyslipidemia with acute phase reactants is unknown. This investigation was performed to assess the pathological alterations of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein (HDL), triglycerides, and total cholesterol levels in COVID-19 patients. Methods This was a prospective study performed on real-world patients to assess serum levels of LDL-C, HDL, TG, TC on COVID-19 patients (mild: 319; moderate: 391; critical: 357) hospitalized at our center between April 2020 through January 2021. Age- and gender-matched controls who had their lipid profiles in the same period were included as the control group. Results LDL-C, HDL, TG, and TC levels were significantly lower in COVID-19 patients when compared with the control group (P < 0.001, 0.047, 0.045, < 0.001, respectively). All parameters decreased gradually with COVID-19 disease severity (LDL-C: median (IQR), mild: 98 (91,134); moderate: 97 (81,113); critical: 68 (68,83); HDL: mild: 45 (37,50); moderate: 46 (41,50); critical: 40 (37,46); TG: mild: 186 (150,245); moderate: 156 (109,198); critical: 111 (98,154); TC: mild: 224 (212,238); moderate: 212 (203,213); critical: 154 (125,187)). LDL-C, TC, and TG were inversely correlated with acute phase reactants (interleukin-6 (IL-6), Procalcitonin, C-reactive protein (CRP), and D-dimers). Logistic regression demonstrated lipid profile, thyroid profile, and acute phase reactants as predictors of severity of COVID-19 disease. Conclusion Hypolipidemia develops in increasing frequency with severe COVID-19 disease. It inversely correlates with levels of acute-phase reactants, indicating SARS-COV-2 as the causative agent for alteration in lipid and thyroid levels.


2019 ◽  
Vol 57 (3) ◽  
pp. 274-279 ◽  
Author(s):  
A. S. Avdeeva ◽  
A. M. Satybaldyev ◽  
N. V. Demidova ◽  
N. Yu. Nikishina ◽  
E. V. Gerasimova ◽  
...  

Objective:to analyze therapy with rituximab (RTM) in real clinical practice according to the data available in OREL registry of patients with active rheumatoid arthritis (RA).Subjects and methods. The analysis included 349 patients. All the patients received RTM: 340 – the original drug (MabThera®) and 9 – the biosimilar Acellbia®. 263 patients (75.4%) received RTM in combination with disease-modifying anti-rheumatic drugs (DMARDs) and 86 (24.6%) – RTM as monotherapy.Results and discussion. Of the 349 patients included in the analysis, 272 (77.9%) patients received RTM as the first biologic agent (BA) (263 patients were treated with the original drug and 9 – with the biosimilar) and 77 (22.1%) patients had previously used the BA. The majority of patients (n=205 (58.7%)) received three or more; 109 (31.2%) patients – one, and 35 (10%) – two RTM courses of RTM therapy. RTM caused a significant reduction in disease activity just after the first therapy course and in the levels of acute-phase reactants (C-reactive protein (CRP) and ESR); after the fifth therapy course, median CRP concentration decreased by 1.4 times and amounted to 7 [1.2; 17.9] mg/l and that of ESR reduced by 1.8 times and was 10 [5; 20] mm/hr (p<0.05).Conclusion.The analysis of RTM therapy in RA patients in real clinical practice demonstrated that in most cases RTM was given as the first BA, in combination with DMARDs, the main agent of which was methotrexate. The use of RTM was accompanied by a significant reduction in disease activity and in the serum levels of acute-phase reactants and autoantibodies.


2006 ◽  
Vol 59 (11-12) ◽  
pp. 545-549 ◽  
Author(s):  
Borisav Jankovic ◽  
Dobrila Veljkovic ◽  
Srdjan Pasic ◽  
Zorica Rakonjac ◽  
Dragana Jevtic ◽  
...  

Introduction. Accurate evaluation and correct treatment of neonates for possible sepsis still represent the most challenging clinical tasks. Early diagnosis of neonatal sepsis is largely based on the measurement of serum concentrations of different mediators of systemic inflammation, as well as, on a group of proteins named acute phase reactants. Among acute phase reactants, C-reactive protein (CRP) has been the most extensively used and investigated so far. Synthesis and biological role of CRP. This article reviews current knowledge on the synthesis, structure and biologic roles of CRP. Also, we present our original results in regard to the kinetics of serum CRP concentration during the first 24 hours of systemic infection, as well as different patterns of CRP dynamics associated with the initial choice of antibiotics, complications and the final outcome of systemic infection. Interleukins and procalcitonin in diagnosis of sepsis. Because CRP is specific, but somewhat late marker of neonatal sepsis, possible diagnostic use of other indicators of inflammation, i.e. interleukins 6 and 8, and procalcitonin during neonatal sepsis is also considered. The theoretical advantage of these early indicators is discussed in comparative analysis of the time of their activation after initial infectious stimuli. Conclusion. In conclusion, we point to the diagnostic accuracy of serial measurements of serum CRP levels. As an alternative, simultaneous measurement of CRP and serum levels using a faster marker, such as procalcitonin, is recommended.


1983 ◽  
Vol 61 (9) ◽  
pp. 1041-1048 ◽  
Author(s):  
J. C. Jamieson ◽  
H. A. Kaplan ◽  
B. M. R. N. J. Woloski ◽  
M. Hellman ◽  
K. Ham

Inflammation results in an increase in the levels of a variety of glycoproteins in serum. The glycoproteins that respond in this way are usually referred to as acute-phase reactants. Studies on the acute-phase response of rat α1-acid glycoprotein showed that there was an increase in the liver levels of this glycoprotein at 12 h after turpentine inflammation. This was followed by increased serum levels at 48–72 h after inflammation, suggesting a precursor–product relationship between liver and serum α1-acid glycoprotein. Incorporation studies coupled with measurements of synthesis rates of α1-acid glycoprotein showed that increased synthesis was responsible for the acute-phase response of this protein to inflammation. These studies also showed that albumin was a negative acute-phase reactant. The acute-phase response of α1-acid glycoprotein was accompanied by increased liver pools of UDP–N-acetylglucosamine (UDP–GlcNAc) and UDP–N-acetylgalactosamine (UDP–GalNAc) and increased liver activities of glucosamine-6-phosphate synthase and UDP–GlcNAc 2-epimerase. Activities of galactosyl and sialyl transferases in liver were also elevated and serum sialyl transferase was increased substantially in inflammation, suggesting that it may also be an acute-phase reactant. Liver activities of β-N-acetylhexosaminidase and β-galactosidase declined by about 50% at 24 h after inflammation; there was evidence that serum levels of these enzymes increased at 24–72 h after inflammation, suggesting that the lysosomal glycosidases may be released from liver during inflammation. Inflammation resulted in elevated serum Cortisol, insulin, and adrenocorticotropic hormone and induced increased glycogenosis; liver cAMP levels were also increased during inflammation. Preliminary studies are presented to show that leukocyte-derived factors may be involved in the acute-phase response of α1-acid glycoprotein to inflammation.


2020 ◽  
Vol 33 (6) ◽  
Author(s):  
Hesham A. Nada ◽  
Mohamed M. Elshabrawy ◽  
Doaa M. Aly ◽  
Mohammad Jafferany ◽  
Mohamed L. Elsaie

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1316.2-1317
Author(s):  
L. De Stefano ◽  
S. Bugatti ◽  
S. Rossi ◽  
C. Montecucco ◽  
A. Manzo

Background:Rheumatoid arthritis (RA) and psoriatic arthritis (PsA) are both characterized by significant heterogeneity in terms of clinical presentation and outcomes. Furthermore, RA and PsA may share some overlapping features such as autoantibody-negativity, polyarticular involvement, response to certain therapies and pattern of joint damage. The pathobiological bases underlying the intra-disease heterogeneity and the inter-disease similiarities between RA and PsA are however unkown.Objectives:Aim of the current study was to investigate the relationship between the synovial immune phenotype and different clinical subsets in patients with RA and PsA.Methods:The study population included 96 patients undergoing ultrasound-guided synovial biopsy of the knee and serum sampling on the same day. Patients were recruited according to defined clinical subtypes: anti-citrullinated positive (ACPA) RA (n=26), ACPA-negative RA (n=32), polyarticular (≥5 involved joints) PsA (n=15), and oligoarticular PsA (n=23). Patients were compared for: (i) demographic and clinical features; (ii) synovial histopathological characteristics including CD68-positive infiltrating macrophages, CD3-positive T lymphocytes, CD20-positive B lymphocytes (semi-quantitative scores 0-3); (iii) serum levels of the lymphoid chemokine CXCL13 as a marker of germinal centre activity.Results:Collectively, ACPA-positive RA patients, ACPA-negative RA patients and patients with polyarticular PsA presented comparable demographic and clinical features including gender distribution, age, number of involved joints and levels of acute phase reactants. Patients with oligoarticular PsA were instead younger, more frequently males, and with lower levels of acute phase reactants. The degree of macrophage and T cell infiltration correlated with the erythrocyte sedimentation rate (rho 0.38, p=0.001 and rho 0.24, p=0.04 respectively) and C-reactive protein levels (rho 0.38, p=0.001 and rho 0.28, p=0.01 respectively) irrespective of diagnosis, and was significantly lower in oligoarticular PsA (Figure 1A,B). In contrast, the degree of B cell infiltration showed significant differences in relation to the disease subtype: the lowest levels were found in oligoarticular PsA, the highest levels in ACPA-positive RA, whilst ACPA-negative RA and polyarticular PsA presented with intermediate and comparable levels between the two extremes (Figure 1C). Serum levels of CXCL13 correlated with the synovial B cell score (rho 0.30, p=0.03) and, similarly to synovial B cell infiltration, were differentially increased according to the clinical phenotype, with again similarities between ACPA-negative RA and polyarticular PsA (Figure 1D).Figure 1.Conclusion:In patients with chronic inflammatory arthritis, synovial B cell infiltration and systemic markers of germinal centre activity are heterogeneously increased irrespective of disease diagnosis. ACPA-positive RA and oligoarticular PsA appear located at the extremes of a pathobiological continuum, whilst ACPA-negative RA and polyarticular PsA present with intermediate and comparable degrees of B cell involvement. Collectively, our findings open the interesting perspective of a tailored management of patients with inflammatory arthritis based on the disease pathotype rather than on clinical diagnosis.Disclosure of Interests:Ludovico De Stefano: None declared, Serena Bugatti Speakers bureau: Bristol-Myers Squibb, Sanofi, Lilly, Novartis, Pfizer, Abbvie, Silvia Rossi: None declared, Carlomaurizio Montecucco: None declared, Antonio Manzo Speakers bureau: Bristol-Myers Squibb, Abbvie, Pfizer


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