scholarly journals Differences in Virus Prevalence and Load in the Hearts of Patients with Idiopathic Dilated Cardiomyopathy with and without Immune-Mediated Inflammatory Diseases

2012 ◽  
Vol 19 (8) ◽  
pp. 1182-1187 ◽  
Author(s):  
Robert Dennert ◽  
Pieter van Paassen ◽  
Petra Wolffs ◽  
Catrien Bruggeman ◽  
Sebastiaan Velthuis ◽  
...  

ABSTRACTInfections with cardiotrophic viruses and immune-mediated responses against the heart have been suggested to play a dominant role in the pathogenesis of idiopathic dilated cardiomyopathy (DCM). Furthermore, immune-mediated inflammatory diseases (IMIDs) may result in DCM. It has not previously been assessed whether DCM patients with and without an IMID have different prevalences and quantities of cardiotrophic viruses in the heart. Therefore, we compared the profiles of cardiotrophic viruses in heart tissue of DCM patients with and without an IMID. Serum and myocardial tissue samples were obtained from 159 consecutive patients with DCM and 20 controls. Patients were subdivided into three groups, the first two based on the presence (n= 34) or absence (n= 125) of an IMID and the third being a control group. The parvovirus B19 virus genome was detected in equal quantities in the non-IMID DCM patients (100/125) and the control group (15/20) but in lower quantities in the IMID patients (21/34,P= 0.02). Both the non-IMID and IMID DCM patients demonstrated increased myocardial inflammation compared to controls: 12.5 ± 1.8 and 14.0 ± 3.2 CD45-positive inflammatory cells, respectively, versus 5.1 ± 0.7 for the controls (P< 0.05 for both). Importantly, significantly higher parvovirus B19 copy numbers could be amplified in non-IMID than in IMID patients (561 ± 97 versus 191 ± 92 copies/μg DNA,P< 0.001) and control subjects (103 ± 47 copies/μg DNA,P< 0.001). The present study shows decreased parvovirus B19 prevalence and copy numbers in hearts of DCM patients with an IMID compared to those without an IMID. These findings may suggest that DCM patients with an IMID have a different pathophysiologic mechanism from that which is present in the virus-induced form of DCM.

Author(s):  
Jaqueline de Jesus Pereira ◽  
Renata Nishiyama Ikegami ◽  
Joyce Tiyeko Kawakami ◽  
Shérrira Menezes Garavelo ◽  
Marcia Martins Reis ◽  
...  

BackgroundIdiopathic dilated cardiomyopathy (IDCM) myocardial inflammation may be associated with external triggering factors such as infectious agents. Here, we searched if moderate/severe heart transplantation rejection is related to the presence of myocardial inflammation in IDCM explanted hearts, associated with microbial communities.MethodReceptor myocardial samples from 18 explanted hearts were separated into groups according to post-transplant outcome: persistent moderate rejection (PMR; n = 6), moderate rejection (MR; n = 7) that regressed after pulse therapy, and no rejection (NR; n = 5)/light intensity rejection. Inflammation was quantified through immunohistochemistry (IHC), and infectious agents were evaluated by IHC, molecular biology, in situ hybridization technique, and transmission electron microscopy (TEM).ResultsNR presented lower numbers of macrophages, as well as B cells (p = 0.0001), and higher HLA class II expression (p ≤ 0.0001). PMR and MR showed higher levels of Mycoplasma pneumoniae (p = 0.003) and hepatitis B core (p = 0.0009) antigens. NR presented higher levels of parvovirus B19 (PVB19) and human herpes virus 6 (HHV6) and a positive correlation between Borrelia burgdorferi (Bb) and enterovirus genes. Molecular biology demonstrated the presence of M. pneumoniae, Bb, HHV6, and PVB19 genes in all studied groups. TEM revealed structures compatible with the cited microorganisms.ConclusionsThis initial study investigating on infectious agents and inflammation in the IDCM explanted hearts showed that the association between M. pneumoniae and hepatitis B core was associated with a worse outcome after HT, represented by MR and PMR, suggesting that different IDCM microbial communities may be contributing to post-transplant myocardial rejection.


2004 ◽  
Vol 193 (2-3) ◽  
pp. 75-82 ◽  
Author(s):  
Ulrich Lotze ◽  
Renate Egerer ◽  
Christiane Tresselt ◽  
Brigitte Gl�ck ◽  
Gudrun Dannberg ◽  
...  

2003 ◽  
Vol 50 (4) ◽  
pp. 1187-1194 ◽  
Author(s):  
Lukasz Wicherek ◽  
Magdalena Dutsch ◽  
Pawel Mak ◽  
Marek Klimek ◽  
Jacek Skladzien ◽  
...  

The tumor associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) expressed with high frequency in various cancer and trophoblast cells, inhibits growth of estrogen receptor-expressing cells and induces apoptosis. Because previous reports demonstrated RCAS1 presence only by non-quantitative immunocytochemistry methods, we decided to use a Western blotting with anti-RCAS1 monoclonal antibodies for estimation of the relative content of the tumor-associated antigen. One hundred tissue samples were assayed (neoplasms, chronic inflammatory diseases, healthy tissues, trophoblasts and placentas at term). RCAS1 was present in all neoplastic, placental and trophoblast tissue samples and its level in malignant samples was statistically significantly higher than in benign neoplasms. The amount of RCAS1 in chronic inflammations was also significantly increased in immune mediated diseases, like allergic nasal polyps and sarcoidosis. The RCAS1 protein was not revealed in healthy mucous membrane and in muscle tissues. The presented results suggest that RCAS1 might play an important role in tumor escape from host immunological surveillance and carry weight in the down regulation of the maternal immune response, thereby maintaining pregnancy.


2020 ◽  
Vol 4 (7) ◽  
pp. 394-398
Author(s):  
O.O. Kuznetsova ◽  
◽  
S.Yu. Nikulina ◽  
A.A. Chernova ◽  
V.N. Maximov ◽  
...  

Aim: to identify patterns of development of idiopathic dilated cardiomyopathy (IDC) and ischemic cardiomyopathy (ICM) by studying the rs 1801252 (Ser49Gly) polymorphic variant of the ADRB1 gene.Patients and Methods: a cohort of 221 patients (mean age — 55.30±9.69 years) was examined. All respondents underwent a standard set of laboratory and instrumental examinations, including coronary angiography. The first group included 111 patients with IDC, 99 of them (89.2%) were men, who were excluded from probable factors of dilated cardiomyopathy. The second group included 110 patients with IDC, including 100 (91.5%) men who had reliable signs of CHD. The control group included 221 people (mean age — 53.6±4.8 years) without signs of cardiovascular diseases. A molecular genetic study of the rs 1801252 (Ser49Gly) polymorphism of the ADRB1 gene was performed in all patients and in the control group. Results: among patients with IDC of both gender, 70.3% were carriers of the common homozygous A145A genotype, 27.0% of the heterozygous A145G genotype, and 2.7% of the rare homozygous G145G genotype. In the control group, there was also a predominant number of patients who carried the homozygous genotype for the common A145A allele — 71.9%. Carriers of the heterozygous A145G genotype were 25.3%, and the homozygous G145G genotype for a rare allele — 2.7%. The analysis of the genotypes frequency distribution of the polymorphic locus rs 1801252 (Ser49Gly) of the ADRB1 gene in patients with IDC and in the control group showed no differences. In the group of patients with ICM, the frequency of the common homozygous A145A genotype was 68.2%, there were fewer patients with the heterozygous A145G genotype — 29.1%, and the rare homozygous G145G genotype was detected in 2.7% of cases. There was no association with the ICM 1801252 (Ser49Gly) polymorphism of the ADRB1 gene in the group of patients with ICM, since the results of comparison with the control group data showed no statistically significant differences. At the same time, there were differences in the frequency of alleles of the polymorphic locus rs1801252 (Ser49Gly) of the ADRB1 gene: in male patients with IDC and ICM, the 145A allele was statistically significantly more common (p=0.0001) than in the control group.Conclusion: the data obtained suggest that the carrier of the 145A allele of the ADRB1 gene may serve as an additional risk factor for the development of dilated cardiomyopathy.KEYWORDS: dilated cardiomyopathy, ischemic cardiomyopathy, genetic polymorphism, β-1-adrenergic receptor gene, heart failure, genetic predisposition.FOR CITATION: Kuznetsova O.O., Nikulina S.Yu., Chernova A.A. et al. β-1-adrenoreceptor gene polymorphism role in the development of dilated cardiomyopathy. Russian Medical Inquiry. 2020;4(7):394–398. DOI: 10.32364/2587-6821-2020-4-7-394-398.


2016 ◽  
Vol 89 (1) ◽  
pp. 55-63 ◽  
Author(s):  
Yohan N'Guyen ◽  
François Lesaffre ◽  
Damien Metz ◽  
Sophie Tassan ◽  
Yves Saade ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Stettner-Leonkiewicz ◽  
E Grywalska ◽  
Z.Y Zhang ◽  
J Rolinski ◽  
A Wysokinski

Abstract Introduction Dilated cardiomyopathy is associated with various immunological abnormalities, such as decreases in the activity and subsets of suppressor T cells and in the activity of natural killer cells, suggesting the involvement of immunological mechanisms in the pathogenesis of this disease. However, the role of NKT like cells and NK cells in the pathogenesis of idiopathic dilated cardiomyopathy remains still uncertain. The aim of the study was to compare the frequencies of peripheral NKT like cells and NK cells among patients with IDCM to healthy controls. Methods The frequencies of NKT like cells and NK cells were measured by flow of cytometry among 50 patients with IDCM from Cardiology Clinic in Lublin. The control group consisted of 50 healthy sex- and age- matched volunteers. The diagnosis of IDCM was based on the common known ESC Guidenlines 2018 criteria. Statistical analysis of the results was conducted using IBM program. A value of p less than 0.05 was considered statistically significant. Results The frequency (%) (mean ± SD) of NK cells (CD3+/CD16+CD56+) was significantly lower (p≤0.001) in IDCM group (12.0±4.5) when compared to control group (15.6±3.4). The frequency (%) (mean ± SD) of NK T like cells (CD3+/CD16+CD56+) was significantly elevated (p≤0,04) in IDCM group (4,66±3,4) in comparison to the control group (3,23±1,7). Conclusions Our findings of the abnormalities in immune cells distribution in peripheral blood of IDCM patients suggest that IDCM development and progression is related to the dysregulation of the immune system. The decreases in the activity in the NK cells among patients with IDCM might indicate chronic myocarditis and lymphocyte infiltration in the myocardium. Moreover, the elevation of NKT like cells could be a result of prolonged exposure to pathogen in which TCD3+ cells become involved more than less mature NK cells in engaging specific immunity response. Funding Acknowledgement Type of funding source: Private hospital(s). Main funding source(s): Medical University in Lublin, Grant for Young Reserchers


Author(s):  
Davide Firinu ◽  
Andrea Perra ◽  
Marcello Campagna ◽  
Roberto Littera ◽  
Giuseppe Fenu ◽  
...  

AbstractSARS-CoV-2 vaccination with mRNA product BNT162b2 elicited high immunogenicity in healthy subjects in trials. This study aims to better understand the factors that influence the humoral immune response to vaccination against SARS-CoV-2 in patients with immune-mediated inflammatory diseases (IMIDs). We enrolled patients and healthy healthcare workers control group (HCW) that underwent mRNA BNT162b2 vaccination and measured the serum IgG anti-S-RBD response at booster dose (T1), one month after booster dose (T2) and up to 5 months (T3). Demographic, disease-specific and vaccination data were recorded. Vaccination response of 551 participants naïve to SARS-CoV-2 infection were included in HCW and 102 in the IMID group, analyzing separately those on anti-CD20. At T2 all naïve HCW developed anti-S-RBD-IgG, while 94% of IMID responded (p < 0.001). IMID patients had a significantly different level of IgG than HCW at both T1 (p = 0.031), T2 (p < 0.001), while there was no significant difference at T3. There were no statistically significant differences according to the IMID type or to ongoing treatment with immunosuppressants, corticosteroids or biological drugs other than anti-CD20. The proportion and magnitude of response was significantly lower in IMID treated with anti-CD20 drugs. There was a correlation with age at T1 and at T2 but not at T3, stronger in patients than in HCW. Immune response close after BNT162b2 vaccination is reduced in patients with IMID, but there is no significant difference at 5 months. The measured reduction is related to age and the disease itself rather than treatments, with the exception of anti-CD20 drugs.


2019 ◽  
Author(s):  
Silje Watterdal Syversen ◽  
Guro Løvik Goll ◽  
Kristin Kaasen Jørgensen ◽  
Inge Christoffer Olsen ◽  
Øystein Sandanger ◽  
...  

Abstract Background Infliximab (INX) and other TNF-inhibitors (TNFi) have revolutionised the treatment of several immune mediated inflammatory diseases. Still, many patients do not respond sufficiently to therapy or loose efficacy over time. The large individual variation in serum drug concentrations on standard doses and the development of anti-drug antibodies are thought to be major reasons for treatment failures. Therapeutic drug monitoring (TDM), an individualised treatment strategy based on systematic assessments of serum drug concentrations, has been proposed as a clinical tool to optimise efficacy of INX treatment. TDM seems reasonable both from a clinical and an economical point of view, but the effectiveness of this treatment strategy has not yet been demonstrated in randomised clinical trials. The NORwegian DRUg Monitoring study (NOR-DRUM) aims to assess the effectiveness of TDM, both with regard to achieve remission in patients starting INX treatment (part A) as well as to maintain disease control in patients on INX treatment (part B). Methods The NOR-DRUM study is a randomised, open, controlled, parallel-group, comparative, multi-centre, national, superiority, phase IV study with two separate parts, NOR-DRUM A and NOR-DRUM B. Patients with rheumatoid arthritis, psoriatic arthritis, spondyloarthritis, ulcerative colitis, Crohn’s disease and psoriasis are included. In both study parts participants are randomised 1:1 to either TDM of infliximab (intervention group) or to standard treatment with infliximab without knowledge of drug levels or ADAb status (control group). 400 patients starting INX therapy will be included in NOR-DRUM A. The primary outcome is remission at 30 weeks. In NOR-DRUM B, 450 patients on maintenance treatment with INX will be included. The primary endpoint is occurrence of disease worsening during the 52 weeks study period. Discussion As the first trial to assess the effectiveness, safety and cost-effectiveness of TDM in patients receiving TNFi for a range of immune mediated inflammatory diseases, we hope that the NOR-DRUM study can contribute to the advancement of evidence based personalised treatment with biological medicines.


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