Impact of tocilizumab on N-terminal pro-brain natriuretic peptide levels in patients with active rheumatoid arthritis without cardiac symptoms

Yokoe, Isamu; Kobayashi, Hitomi; Kobayashi, Yasuyuki; Giles, Jon T.; Yoneyama, Kihei; Kitamura, Noboru; Takei, Masami

doi:10.1080/03009742.2017.1418424

Cited by 24 publications

(25 citation statements)

References 31 publications

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“…У больных РА при включении в исследование уровень NT-proBNP в крови оказался выше, чем в группе контроля. Большинство работ свидетельствуют о более высоком содержании данного пептида у больных РА по сравнению со здоровыми донорами [6,7,12,[14][15][16][17][18]. Имеются единичные сообщения об отсутствии различий концентрации NT-proBNP у больных воспалительными артритами и здорового контроля [19,20].…”

Section: Discussionunclassified

“…Более высокий уровень NT-proBNP по сравнению со здоровым контролем продемонстрирован у пациентов с РА, не имеющих ССЗ и ТФР [12,21]. Выявленная в исследовании D. Armstrong и соавт.…”

Section: Discussionunclassified

“…В исследовании I. Yokoe и соавт. [12] у больных РА с высоким содержанием AЦЦП уровень NT-proBNP был выше, чем у пациентов с низкой концентрацией АЦЦП. В экспериментальной работе J. Giles и соавт.…”

Section: Discussionunclassified

“…В исследовании I. Yokoe и соавт. [12] у больных РА, не имеющих ССЗ, через 24 нед после начала терапии ТЦЗ уровень NT-proBNP снизился на 63% (с 109,0 до 39,8 пг/мл, p<0,0001). В работе показана корреляция процентных изменений NT-proBNP с SDAI (r=0,46; p=0,003), а также наблюдались близкие к значимым ассоциации с процентным изменением DAS28 (r=0,23; p=0,05) и уровня СРБ (r=0,24; р=0,06).…”

Section: Discussionunclassified

“…ТЦЗ является эффективным генно-инженерным биологическим препаратом (ГИБП), оказывающим быстрый положительный эффект в отношении широкого спектра клинических проявлений и лабораторных нарушений при РА. В ряде работ на фоне терапии ТЦЗ отмечено снижение уровня NT-proBNP [5,12]. Необходимы дальнейшие исследования для подтверждения гипотезы о том, что терапия ингибитором рецепторов ИЛ6 может улучшать профиль биомаркеров сердца.…”

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Time course of changes in the level of N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis during therapy with an interleukin-6 receptor inhibitor

Gerasimova¹,

Попкова²,

Martynova³

et al. 2019

Naučno-praktičeskaâ revmatologiâ

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Section: Discussionunclassified

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Time course of changes in the level of N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis during therapy with an interleukin-6 receptor inhibitor

Gerasimova¹,

Попкова²,

Martynova³

et al. 2019

Naučno-praktičeskaâ revmatologiâ

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Analysis of Cytokine Profiles in Pediatric Myocarditis Multicenter Study

Nomura,

Suzuki,

Kunida

et al. 2024

Pediatr Cardiol

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Introduction: Acute myocarditis (AM) is an in ammatory disease of the heart muscle that can progress to fulminant myocarditis (FM), a severe and life-threatening condition. The cytokine pro le of myocarditis in children, especially in relation to fulminant myocarditis, is not well understood. This study aims to evaluate the cytokine pro les of acute and fulminant myocarditis in children.Method: Pediatric patients diagnosed with myocarditis were included in the study. Cytokine levels were measured using a multiplexed uorescent bead-based immunoassay. Statistical analysis was performed to compare patient characteristics and cytokine levels between FM, AM, and healthy control (HC) groups. Principal component analysis (PCA) was applied to cytokine groups that were independent among the FM, AM, and HC groups.Result: The study included twenty-two patients with FM and fourteen with AM patients. We identi ed 4 cytokines that were signi cantly higher in the FM group compared to the AM group: IL1-RA (p=0.002), IL-8 (p=0.005), IL-10 (p=0.011), and IL-15 (p=0.005). IL-4 was signi cantly higher in the AM group compared to FM and HC groups (p=0.006, and 0.0015). PDGF-AA, and VEGF-A were signi cantly lower in the FM group than in the AM group (p=0.013, and <0.001). Similar results were obtained in PCA.Conclusion: Cytokine pro les might be used to differentiate pediatric FM from AM, stratify severity, and predict prognosis. The targeted therapy that works individual cytokines might provide a potential treatment for reducing the onset of the FM and calming the condition, and further studies are needed.

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Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

Hanna

Frangogiannis

2020

Cardiovasc Drugs Ther

248

170

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Heart failure exhibits remarkable pathophysiologic heterogeneity. A large body of evidence suggests that regardless of the underlying etiology, heart failure is associated with induction of cytokines and chemokines that may contribute to the pathogenesis of adverse remodeling, and systolic and diastolic dysfunction. The pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6 have been extensively implicated in the pathogenesis of heart failure. Inflammatory cytokines modulate phenotype and function of all myocardial cells, suppressing contractile function in cardiomyocytes, inducing inflammatory activation in macrophages, stimulating microvascular inflammation and dysfunction, and promoting a matrixdegrading phenotype in fibroblasts. Moreover, cytokine-induced growth factor synthesis may exert chronic fibrogenic actions contributing to the pathogenesis of heart failure with preserved ejection fraction (HFpEF). In addition to their role in adverse cardiac remodeling, some inflammatory cytokines may also exert protective actions on cardiomyocytes under conditions of stress. Chemokines, such as CCL2, are also upregulated in failing hearts and may stimulate recruitment of pro-inflammatory leukocytes, promoting myocardial injury, fibrotic remodeling, and dysfunction. Although experimental evidence suggests that cytokine and chemokine targeting may hold therapeutic promise in heart failure, clinical translation remains challenging. This review manuscript summarizes our knowledge on the role of TNF-α, IL-1, IL-6, and CCL2 in the pathogenesis of heart failure, and discusses the promises and challenges of targeted anti-cytokine therapy. Dissection of protective and maladaptive cellular actions of cytokines in the failing heart, and identification of patient subsets with overactive or dysregulated myocardial inflammatory responses are required for design of successful therapeutic approaches.

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Impact of tocilizumab on N-terminal pro-brain natriuretic peptide levels in patients with active rheumatoid arthritis without cardiac symptoms

Abstract: TCZ decreased the NT-proBNP level in patients with RA without preceding cardiovascular disease and CHF. TCZ may have a cardioprotective effect in those with active RA.

Cited by 24 publications

References 31 publications

Time course of changes in the level of N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis during therapy with an interleukin-6 receptor inhibitor

Time course of changes in the level of N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis during therapy with an interleukin-6 receptor inhibitor

Analysis of Cytokine Profiles in Pediatric Myocarditis Multicenter Study

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

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