scholarly journals Acute recurrent pericarditis: from pathophysiology towards new treatment strategy

Heart ◽  
2020 ◽  
Vol 106 (14) ◽  
pp. 1046-1051 ◽  
Author(s):  
Patrice Cacoub ◽  
Cindy Marques
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Interleukin 1 ◽  
Treatment Algorithm ◽  
Real Life ◽  
Adaptive Immune System ◽  
Immunosuppressive Drugs ◽  
Controlled Study ◽  
Recurrent Pericarditis ◽  
Receptor Antagonists

Acute idiopathic or so-called viral pericarditis is a frequent and usually benign disease, although recurrences are frequent. Data strongly suggest the presence of underlying autoinflammatory and/or autoimmune disorders. It has been reported that there is an inflammatory response of the innate immune system typical of ‘autoinflammatory diseases’, predominantly mediated by interleukin-1 (IL-1). This may result from the activation of the inflammasome by a cardiotropic virus or a non-specific agent. The inflammatory response of the adaptive immune system, typical of ‘autoimmune diseases’—mainly mediated by autoantibodies or autoreactive T lymphocytes—seems also involved as anti-heart or anti-intercalated disk autoantibodies were associated with a higher number of recurrences and hospitalisations. Current guidelines recommend that aspirin/non-steroidal anti-inflammatory drugs for a few weeks should be associated to colchicine for 6 months in recurrent pericarditis. In refractory cases, low-dose corticosteroids or immunosuppressive drugs have been proposed with limited efficacy. Growing evidences suggest a place of IL-1 receptor antagonists in the treatment of recurrent pericarditis. Many retrospective studies, one recent randomised placebo-controlled study and data of a real-life large international registry showed the good efficacy of anakinra with a good safety profile. Other IL-1 receptor antagonists showed promising results (canakinumab, rilonacept). However, IL-1 receptor antagonists’ position in the treatment algorithm of recurrent pericarditis needs further evaluation in larger prospective clinical trials to replicate initial findings as well as to assess safety, cost-effectiveness and long-term efficacy.

scholarly journals COVID-19 Disease and Dermatomyositis: A Mini-Review

2022 ◽  
Vol 12 ◽  
Author(s):  
Jie Qian ◽  
Hui Xu
Keyword(s):  
Immune System ◽  
Interstitial Lung Disease ◽  
Inflammatory Response ◽  
Lung Disease ◽  
Inflammatory Cytokines ◽  
Early Identification ◽  
Poor Prognosis ◽  
Clinical Manifestations ◽  
Immunosuppressive Drugs ◽  
Interstitial Pulmonary Disease

The pandemic of coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 has caused a large number of deaths, and there is still no effective treatment. COVID-19 can induce a systemic inflammatory response, and its clinical manifestations are diverse. Recently, it has been reported that COVID-19 patients may develop myositis and interstitial pulmonary disease similar to dermatomyositis (DM). This condition is similar to the rapidly progressive interstitial lung disease associated with MDA5+ DM that has a poor prognosis and high mortality, and this poses a challenge for an early identification. Suppression of the immune system can protect COVID-19 patients by preventing the production of inflammatory cytokines. This article attempts to explore the possibility of a relationship between COVID-19 and DM in terms of the potential pathogenesis and clinical features and to analyze the therapeutic effect of the immunosuppressive drugs that are commonly used for the treatment of both DM and COVID-19.

scholarly journals Interleukin-1 blockade with RPH-104 in patients with acute ST-elevation myocardial infarction: study design and rationale

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
M. Samsonov ◽  
V. Bogin ◽  
B. W. Van Tassell ◽  
A. Abbate
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Response ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Interleukin 1 ◽  
Controlled Study ◽  
Risk Of Death ◽  
Increased Risk ◽  
Echocardiographic Parameters

Abstract Background Myocardial injury of ST-segment elevation myocardial infarction (STEMI) initiates an intense inflammatory response that contributes to further damage and is a predictor of increased risk of death or heart failure (HF). Interleukin-1 (IL-1) is a key mediator of local and systemic inflammatory response to myocardial damage. We postulate that the use of the drug RPH-104, which selectively binds and inactivates both α and β isoforms of IL-1 will lead to a decrease in the severity of the inflammatory response which will be reflected by decrease in the concentration of hsCRP, as well as the rate of fatal outcomes, frequency of new cases of HF, changes in levels of brain natriuretic peptide (BNP) and changes in structural and functional echocardiographic parameters. Methods This is a double blind, randomized, placebo-controlled study in which 102 patients with STEMI will receive a single administration of RPH-104 80 mg, RPH-104 160 mg or placebo (1:1:1). The primary endpoint will be hsCRP area under curve (AUC) from day 1 until day 14. Secondary endpoints will include hsCRP AUC from day 1 until day 28, rate of fatal outcomes, hospitalizations due to HF and other cardiac and non-cardiac reasons during 12-month follow-up period, frequency of new cases of HF, changes in levels of brain natriuretic peptide (BNP, NT-pro-BNP), changes in structural and functional echocardiographic parameters during 12-month follow-up period compared to baseline. The study started in October 2020 and is anticipated to end in 2Q 2022. Trial registration: ClinicalTrials.gov, NCT04463251. Registered on July 9, 2020

scholarly journals Fisiopatologia del rigetto acuto e cronico

2019 ◽  
Vol 31 (2) ◽  
pp. 128-132
Author(s):  
Aris Tsalouchos ◽  
Maurizio Salvadori
Keyword(s):  
Immune System ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Graft Loss ◽  
Graft Function ◽  
Adaptive Immune System ◽  
Immunosuppressive Drugs ◽  
Antibody Mediated Rejection ◽  
Pathologic Features ◽  
Activation Antigen

Allograft rejection is defined as tissue injury produced by the effector mechanisms of the alloimmune response, leading to deterioration of graft function. There are two types of rejection: T-cell-mediated rejection (TCMR) and antibody-mediated rejection (AMR). Both types of rejection can be early or late, fulminant or indolent, as well as isolated or concomitant and can share pathologic features on biopsy. The immune response to an allograft is an ongoing dialogue between the innate and adaptive immune system, which if unresolved will lead to rejection of the transplanted cells, tissues, or organs. Activation of elements of the innate immune system, triggered by tissue injury sustained during cell isolation or organ retrieval and ischemia reperfusion, will initiate and amplify the adaptive response. T cells require a minimum of two signals for activation: antigen recognition and co-stimulation. Antibody-mediated rejection triggered by alloantibody binding and complement activation is increasingly recognized as a significant contribution to graft loss. Even though one component of the immune system may dominate and lead to rejection, this is usually multifactorial, resulting from the integration of multiple mechanisms. Identifying the molecular pathways that trigger rejection facilitates the identification of targets for the development of immunosuppressive drugs.

scholarly journals Interleukin-1 Blockade With RPH-104 in Patients With Acute ST-Elevation Myocardial Infarction: Study Design and Rationale.

2021 ◽  
Author(s):  
Mikhail Samsonov ◽  
Vlad Bogin ◽  
Benjamin Van Tassel ◽  
Antonio Abbate
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Response ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Interleukin 1 ◽  
Controlled Study ◽  
Risk Of Death ◽  
Increased Risk ◽  
Echocardiographic Parameters

Abstract BackgroundMyocardial injury of ST-segment elevation myocardial infarction (STEMI) initiates an intense inflammatory response that contributes to further damage and is a predictor of increased risk of death or heart failure (HF). Interleukin-1 (IL-1) is a key mediator of local and systemic inflammatory response to myocardial damage. We postulate that the use of the drug RPH-104, which selectively binds and inactivates both α and β isoforms of IL-1 will lead to a decrease in the severity of the inflammatory response which will be reflected by decrease in the concentration of hsCRP, as well as the rate of fatal outcomes, frequency of new cases of HF, changes in levels of brain natriuretic peptide (BNP) and changes in structural and functional echocardiographic parameters. MethodsThis is a double blind, randomized, placebo-controlled study in which 102 patients with STEMI will receive a single administration of RPH-104 80 mg, RPH-104 160 mg or placebo (1:1:1). The primary endpoint will be hsCRP area under curve (AUC) from Day 1 until Day 14. Secondary endpoints will include hsCRP AUC from Day 1 until Day 28, rate of fatal outcomes, hospitalizations due to HF and other cardiac and non-cardiac reasons during 12-month follow-up period, frequency of new cases of HF, changes in levels of brain natriuretic peptide (BNP, NT-pro-BNP), changes in structural and functional echocardiographic parameters during 12-month follow-up period compared to baseline. The study started in October 2020 and is anticipated to end in 2Q 2022.Trial registrationClinicalTrials.gov, NCT04463251. Registered on July 9, 2020.

scholarly journals Idiopathic recurrent pericarditis – a new orphan autoinflammatory disease? A retrospective analysis of cases of idiopathic recurrent pericarditis and a design of а double-blind, randomized, placebo-controlled study to evaluate the efficacy and safety of RPH-104 treatment in patients with idiopathic recurrent pericarditis

Kardiologiia ◽  
2021 ◽  
Vol 61 (1) ◽  
pp. 72-77
Author(s):  
V.  Yu. Myachikova ◽  
A. L. Maslyanskiy ◽  
O. M. Moiseeva
Keyword(s):  
Retrospective Analysis ◽  
Autoinflammatory Disease ◽  
Current Knowledge ◽  
Interleukin 1 ◽  
Controlled Study ◽  
Recurrent Pericarditis ◽  
Double Blind ◽  
Postpericardiotomy Syndrome ◽  
Randomized Clinical Study ◽  
Pericardial Diseases

Aim To analyze cases of idiopathic recurrent pericarditis (IRP) in the structure of pericardial diseases of various origins from patient visits to the Multidisciplinary Federal Center.Material and methods A retrospective analysis of case records was performed for patients admitted to the V.A. Almazov National Medical Research Center from January 1, 2015 through January 1, 2020 for pericardial effusion of different etiologies.Results For the study period, 4 981 new cases of pericardial damage of different etiologies were found. Among these cases, postpericardiotomy syndrome accounted for 4 360 cases and pericarditis for 621 cases. IRP was detected in 34 cases, which amounted to 5.4 %. Based on the study data, the estimated IRP prevalence in the Russian Federation can be 1.1 cases per 100 thousand population.Conclusion IRP should be regarded as a new autoinflammatory disease, the prevalence of which borders on that of adult Still disease and should be addressed within the concept of orphan diseases. Current knowledge of the pathogenesis and data from recent studies demonstrated a great importance of interleukin-1 blockade as a leading mechanism for achieving remission. This has justified conduction of a randomized clinical study at the Center.

Effect of 8 wk of bicycle training on the immune system of patients with rheumatoid arthritis

1993 ◽  
Vol 75 (4) ◽  
pp. 1691-1695 ◽  
Author(s):  
B. Baslund ◽  
K. Lyngberg ◽  
V. Andersen ◽  
J. Halkjaer Kristensen ◽  
M. Hansen ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune System ◽  
Perceived Exertion ◽  
Natural Killer Cell Activity ◽  
Interleukin 1 ◽  
Killer Cell ◽  
Plasma Concentrations ◽  
Cell Activity ◽  
Training Group ◽  
Controlled Study

The effect of 8 wk of progressive bicycle training on the immune system was evaluated in a controlled study on 18 patients with rheumatoid arthritis and moderate disease activity. Maximal O2 uptake increased significantly, whereas heart rate at stage 2 and rate of perceived exertion decreased significantly, in the training group compared with the controls. Resting levels of a number of immune parameters were measured before and after 4 and 8 wk of training. Training did not induce changes in blood mononuclear cell subpopulations, proliferative response, or natural killer cell activity. Furthermore the plasma concentrations of interleukin-1 alpha, interleukin-1 beta, and interleukin-6 did not change in response to training. It is concluded that 8 wk of bicycle training does not influence the immune system of patients with rheumatoid arthritis.

Usefulness of Interleukin-1 Receptor Antagonists in Patients With Recurrent Pericarditis

2020 ◽  
Vol 127 ◽  
pp. 184-190 ◽  
Author(s):  
Mohamed Khayata ◽  
Nishant P. Shah ◽  
Beni R. Verma ◽  
Aldo S. Giugni ◽  
Saqer Alkharabsheh ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Recurrent Pericarditis ◽  
Receptor Antagonists

Defences against infection

2018 ◽  
Author(s):  
Ajit Lalvani ◽  
Katrina Pollock
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Innate Immune System ◽  
Adaptive Immune System ◽  
The Body ◽  
Innate Immune ◽  
Acute Inflammatory Response ◽  
Adaptive Immune ◽  
Immune Deficiencies ◽  
Prolonged Response

The immune system is classified into a series of component parts, each specialized to defend the host against infection. Cells of the innate immune system are distributed throughout the body, in the tissues, and in the circulation, to defend against the first signs of danger, combining the acute inflammatory response with the ability to kill and remove invading pathogens. Monocytes, macrophages, and neutrophils phagocytose and kill exogenous and endogenous targets, using both oxygen-dependent and oxygen-independent mechanisms. The adaptive immune system creates a structurally specific and prolonged response, mediated by lymphocytes to clear infection and generate immunological memory. In this chapter, the functions of the innate and adaptive immune system are reviewed, together with the clinical features and investigation of acquired and inherited immune deficiencies.

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