scholarly journals Role of Hepcidin in Anemia of Chronic Disease in Rheumatoid Arthritis

Author(s):  
Eleni Nita ◽  
Eleni Bairaktari ◽  
George Kolios ◽  
Michail P. Migkos ◽  
Georgios-Petros Somarakis ◽  
...  

Abstract Objective: Anemia of chronic disease is a frequent consequence in rheumatoid arthritis and is associated with major clinical and patient outcomes. The present cross-sectional study explored the role of hepcidin (HEP) in anemia of chronic disease in rheumatoid arthritis by studying its relationships with markers of anemia, iron metabolism, inflammation, and erythropoiesis. Methods: Blood samples from anemic (n = 43) and nonanemic (n = 43) rheumatoid arthritis patients were analyzed for markers of anemia (hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, red cells distribution width, and reticulocyte hemoglobin), iron metabolism (iron, total iron binding capacity, ferritin, transferrin saturation, soluble transferrin receptor), inflammation (erythrocyte sedimentation rate, C-reactive protein, and interleukin 6), and erythropoiesis (erythropoietin and HEP). Correlation analysis was used to identify relationships between HEP and all other variables. Principal component analysis was used to identify common underlying dimensions representing linear combinations of all variables. Results: HEP had statistically significant mostly moderate-to-large correlations with markers of anemia (0.30–0.70, all p < 0.01), small correlation with markers of iron metabolism and markers of inflammation (r = 0.20–0.40, all p < 0.01), and moderate correlations with markers of erythropoiesis. Principal component analysis revealed two underlying components (factors) capturing approximately 50% of total variability. Factor 1 comprised mainly of markers of anemia, iron metabolism, and erythropoiesis and was related to “erythrocyte health status,” while factor 2 comprised mainly markers of inflammation and iron metabolism and was related to “acute phase reactants.” HEP was the only variable demonstrating substantial loadings on both factors. Conclusions: HEP is related to markers of anemia, iron metabolism, inflammation, and erythropoiesis. In addition, when all variables are “reduced” to a minimum number of two “latent” factors, HEP is loaded on both, thus underlying its pivotal role in the complex interaction of the erythropoietic response in inflammation-induced anemia and/or functional iron deficiency.

1999 ◽  
Vol 92 (2) ◽  
pp. 153-160 ◽  
Author(s):  
P.V. Voulgari ◽  
G. Kolios ◽  
G.K. Papadopoulos ◽  
A. Katsaraki ◽  
K. Seferiadis ◽  
...  

Blood ◽  
2002 ◽  
Vol 100 (2) ◽  
pp. 474-482 ◽  
Author(s):  
Helen A. Papadaki ◽  
Heraklis D. Kritikos ◽  
Vasilis Valatas ◽  
Dimitrios T. Boumpas ◽  
George D. Eliopoulos

Abstract Circumstantial evidence has implicated tumor necrosis factor α (TNF-α) in the pathogenesis of anemia of chronic disease (ACD) in rheumatoid arthritis (RA). We investigated the role of TNF-α in erythropoiesis of patients with active RA (n = 40) and the effect of anti–TNF-α antibody administration (cA2). Patients with RA had lower numbers of CD34+/CD71+ and CD36−/glycophorin A+ (glycoA+) bone marrow (BM) cells and increased proportions of apoptotic cells within the CD34+/CD71+ and CD36+/glycoA+ cell compartments, compared to healthy controls (n = 24). Erythroid burst-forming units (BFU-Es) obtained by BM mononuclear or purified CD34+ cells were significantly lower in RA patients compared to controls. These abnormalities were more pronounced among patients with ACD. Increased TNF-α levels in patient long-term BM culture supernatants inversely correlated with BFU-Es and hemoglobin levels and positively with the percentage of apoptotic CD34+/CD71+ and CD36+/glycoA+ cells. Following cA2 therapy, a normalization was documented in the number of CD34+/CD71+ and CD36−/glycoA+ cells, the number of BFU-Es, and the proportion of apoptotic CD34+/CD71+ and CD36+/glycoA+ cells, which was associated with a significant increase in hemoglobin levels compared to baseline. Recovery from anemia was more prominent in patients with ACD. The exogenous addition of an anti–TNF-α antibody in the cultures increased BFU-E number in patients prior to cA2 treatment but not after treatment, further substantiating the inhibitory role of TNF-α on patients' erythropoiesis. We conclude that TNF-α–mediated apoptotic depletion of BM erythroid cells may account for ACD in RA and that cA2 administration may ameliorate ACD in these patients by down-regulating the apoptotic mechanisms involved in erythropoiesis.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1437.2-1438
Author(s):  
T. Kvlividze ◽  
V. Polyakov ◽  
В. Zavodovsky ◽  
Y. Polyakova ◽  
L. Seewordova ◽  
...  

Background:Interest in highly specialized tissue cytokines contributed to the discovery of new biologically active molecules. Nesfatin-1 (NF) - discovered in 2006 as an anorexigenic factor. NF-1 is believed to be involved in the regulation of energy homeostasis by regulating appetite and water intake. The role of NF-1 in the pathogenesis of inflammatory diseases is poorly understood. Recently, studies have found a relationship between an increased level of NF-1 and inflammatory markers in various pathologies.Objectives:Study of the level of nesfatin-1 in the blood serum of healthy people, determination of the correlation between the level of NF-1 with the severity of clinical symptoms and classic markers of inflammation in patients with RA.Methods:120 persons were examined: 90 patients with RA and 30 healthy people. All patients underwent a complete clinical and laboratory examination. Plasma NF-1 levels were determined using commercial test systems (RaiBiotech, cat # EIA-NESF) according to the manufacturer’s instructions. Patients with various forms of RA were comparable in age to the group of healthy individuals. Statistical processing of clinical examination data was carried out using the “STATISTICA 10.0 for Windows” software package. Quantitative data were processed statistically using the parametric Student’s t-test, qualitative data using the non-parametric chi-square test. The significance of differences between groups was determined using analysis of variance. The results were considered statistically significant at p <0.05.Results:The average level of NF-1 in blood serum in healthy individuals was 31.79 ± 3.21 ng / ml (M ± σ). The level of normal NF-1 values in healthy individuals, defined as M ± 2σ, ranged from 25.3 to 37.83 ng / ml. There was no significant difference in the levels of circulating NF-1 and BMI in healthy individuals and patients with RA (p> 0.05). The inverse relationship of a lower level of NF-1 with an increase in BMI was not significant.Group 1 (66 patients with RA) with increased serum NF-1 levels (> 37.83 ng / ml), and group 2 (44 patients) with normal values (<37.83 ng / ml). A high level of NF-1 was characteristic for patients with high activity according to DAS28, RF seropositive, ACCP-positive, with extra-articular manifestations, who had been ill for 10 years or more. A reliable relationship between the level of NF-1 in the blood serum and laboratory parameters of RA activity - ESR, CRP, was shown, and secondary synovitis was more common. Our data show a direct correlation between the NF-1 level of the pro-inflammatory markers of RA.Conclusion:The positive correlation between the level of NF-1 and classical markers of inflammation, such as CRP and ESR, confirms the involvement of NF-1 in the pathophysiology of inflammation in RA. This is also evidenced by the correlation of a high level of NF-1 in the blood serum with a more severe clinical picture of RA. It is known that NF-1 can promote the release of pro-inflammatory cytokines such as interleukin-8 (IL-8), interleukin-6 (IL-6), and macrophage inflammatory protein-1a (MIP-1a) in the chondrocytes of RA patients.It is necessary to further study the role of NF-1 in the pathogenesis of systemic inflammatory reactions and the possibility of targeting pro-inflammatory cytokines, the possibility of regulating the level of NF-1 by drugs.References:[1]Kvlividze T.Z., Zavodovsky B.V., Akhverdyan Yu.R. Kvlividze T.Z., Zavodovsky B.V., Akhverdyan Yu.R., Polyakova Yu.V., Sivordova L.E., Yakovlev A.T., Zborovskaya I.A. Serum nesfatin -1 as a marker of systemic inflammation in rheumatoid arthritis. Klinicheskaya Laboratornaya Diagnostika (Russian Clinical Laboratory Diagnostics). 2019; 64 (1): 53-56 (in Russ.).Disclosure of Interests:None declared


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sung-Yoon Kang ◽  
Hyojung Kim ◽  
Sungwon Jung ◽  
Sang Min Lee ◽  
Sang Pyo Lee

Abstract Background The microbiota of the lower respiratory tract in patients with non-tuberculous mycobacterial pulmonary disease (NTM-PD) has not been fully evaluated. We explored the role of the lung microbiota in NTM-PD by analyzing protected specimen brushing (PSB) and bronchial washing samples from patients with NTM-PD obtained using a flexible bronchoscope. Results Bronchial washing and PSB samples from the NTM-PD group tended to have fewer OTUs and lower Chao1 richness values compared with those from the control group. In both bronchial washing and PSB samples, beta diversity was significantly lower in the NTM-PD group than in the control group (P = 2.25E-6 and P = 4.13E-4, respectively). Principal component analysis showed that the PSBs and bronchial washings exhibited similar patterns within each group but differed between the two groups. The volcano plots indicated differences in several phyla and genera between the two groups. Conclusions The lower respiratory tract of patients with NTM-PD has a unique microbiota distribution that is low in richness/diversity.


1970 ◽  
Vol 18 (1) ◽  
pp. 60-65
Author(s):  
Md Azizul Haque ◽  
ARM Saifuddin Ekram ◽  
Quazi Tarikul Islam

Rheumatoid arthritis is a chronic disease with the potential to cause substantial joint damage and disability. During the past 10 years, improved understanding of the pathophysiology of rheumatoid arthritis has led to several key changes in the approach to therapy. Most important of that is the development of some biological agents interfering with the activity of several important cytokines. Infliximab, etanarcept, and adalimumab are TNF blockers, anakinra is IL-1 receptor antagonist, and rituximab is anti CD-20 monoclonal antibody. These newer agents proved to be useful for alleviating symptoms and slowing the disease progression in the patients with RA who have failed to respond to conventional DMARDs.   doi: 10.3329/taj.v18i1.3309 TAJ 2005; 18(1): 60-65


2019 ◽  
Vol 34 (6) ◽  
pp. 908-909
Author(s):  
K Hakinson ◽  
J Moses ◽  
J RIvera ◽  
A Guerra ◽  
M Davis ◽  
...  

Abstract Objective Examine the relationship of verbal mediation with visual memory errors and intelligence to understand the role of spoken language on other assessment measures. Method Assessment records were obtained from a Veteran Affairs clinic for veterans (n=100) with diverse neuropsychiatric conditions who completed the Wechsler Adult Intelligence Scale, third edition (WAIS-III), Multilingual Aphasia Examination (MAE), and Benton Visual Retention Test (BVRT). A Principal Component Analysis (PCA) was used to examine the interrelationship among these assessments. The components of spoken language, types of errors on the BVRT, and the four factors of the WAIS-III were factored using the PCA to identify common sources of variance. Results A principal component analysis revealed a six-factor model explaining 68.16% of the shared variance among the WAIS-III factors, MAE components, and BVRT Errors. Omission errors loaded with Processing Speed and Controlled Word Association. Distortions and size errors loaded with Perceptual Organization. Size errors also loaded with Verbal Comprehension and Visual Naming. Misplacements loaded with Working Memory and Sentence Repetition. Misplacements, perseverations, and omissions loaded with the Token Test (a measure associated with auditory comprehension). Rotation errors loaded with Perceptual Organization. Conclusions Results indicated significant shared variance between visual memory errors, spoken language, and intelligence factors. This suggests that spoken language is involved in the process of visual memory, and deficits in spoken language may result in increased errors on visual memory tasks. Therefore, treatment recommendations for visual memory difficulties should take into consideration verbal capabilities and intelligence factors to better individualize treatment.


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