Drug-Disease Interaction: Effect of Inflammation and Nonsteroidal Anti-Inflammatory Drugs on Cytochrome P450 Metabolites of Arachidonic Acid

Aghazadeh‐Habashi, Ali; Asghar, Waheed; Jamali, Fakhreddin

doi:10.1016/j.xphs.2017.09.020

Cited by 24 publications

(23 citation statements)

References 46 publications

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“…In contrast, CAP reduced EETs and dysregulated the levels of LOX‐derived mediators, which is indicative of the negative impact of NSAIDs on leukocytes’ resolution biology . Our findings are in line with other COX‐2 inhibitors such as rofecoxib, celecoxib, and meloxicam, which were shown to reduce levels of cardioprotective EETs in the plasma, kidney, and heart to facilitate systemic inflammation in drug–disease interaction reports . In contrast, atorvastatin activates COX‐2 S‐nitrosylation during the innate response through neutrophil–endothelial interactions in order to biosynthesize 13(T)‐series resolvins from docosapentaenoic acid to stimulate inflammation resolution .…”

Section: Discussionsupporting

confidence: 83%

Subacute treatment of carprofen facilitate splenocardiac resolution deficit in cardiac injury

Halade

Kain

Wright

et al. 2018

Journal of Leukocyte Biology

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Inflammation-limiting nonsteroidal pain relievers magnify myocardial infarction (MI) incidences and increase re-admission events in heart failure (HF) patients. However, the molecular and cellular mechanism of this provocative adverse effect is unclear. Our goal was to determine whether carprofen (CAP) impedes splenic leukocyte-directed acute inflammation-resolving response in cardiac injury. After subacute CAP treatment, mice were subjected to permanent coronary ligation maintaining MI- and naïve-controls. Spleen and left ventricle (LV) leukocytes were quantitated using flow cytometry pre- and 24 h post-MI. The inflammation resolution mediators were quantified using mass spectrometry while splenocardiac apoptosis and leukocyte phagocytosis were measured by immunofluorescence and ImageStream, respectively. Subacute CAP treatment promoted strain and cardiac dysfunction before MI and coronary occlusion showed signs of acute HF in CAP and MI-controls. Subacute CAP-injected mice had pre-activated splenic neutrophils, an over activated "don't eat me" signal (CD47) with reduced total Mϕs (F4/80 ) and reparative Mϕs (F4/80/Ly6C /CD206) compared with control in LV and spleen. Post-MI, CAP pre-activated neutrophils (Ly6G ) were intensified and reduced reparative neutrophils (Ly6G /CD206 ) and Mϕs (F4/80/Ly6C ) in LV was indicative of non-resolving inflammation compared with MI-control. Subacute CAP treatment deferred neutrophil phagocytosis functions in the spleen and LV and was more evident post-MI compared with MI-control. CAP pre-activated splenic neutrophils that tailored the Mϕ phagocytosis thereby increased splenocardiac leukocyte death. CAP over amplified COX-1 and COX-2 compared with MI-control and failed to limit prostaglandins and thromboxane in post-MI setting. Further, CAP reduced cardiac-protective epoxyeicosatrienoic acids and over amplified pyrogenic inflammatory cytokines and reduced reparative cytokines, thereby non-resolving inflammation.

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Section: Discussionsupporting

confidence: 83%

Subacute treatment of carprofen facilitate splenocardiac resolution deficit in cardiac injury

Halade

Kain

Wright

et al. 2018

Journal of Leukocyte Biology

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“…Examples of potential mechanisms of cardiac injury from COVID-19 include damage to the microvascular structure, ischemia from low oxygen availability, immune response-related inflammatory syndrome, and direct viral infection of the heart (11,(37)(38)(39)(40). From previous non-COVID-19 studies, it is known that inflammation can negatively affect cardiovascular health through actuating the reninangiotensin system (RAS) and thus disturbing the homeostasis of vasodilator and vasoconstrictor angiotensin peptides in the heart (41,42). Since both TnI and CK-MB are structural cardiac proteins, the severity of COVID-19 infection will determine the intensity of changes in these cardiac-specific markers.…”

Section: Discussionmentioning

confidence: 99%

Assessing the Elevation of Cardiac Biomarkers and the Severity of COVID-19 Infection: A Meta-analysis

Walker

Deb²,

Ling³

et al. 2020

J Pharm Pharm Sci

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- Purpose: Since December 2019, coronavirus disease 2019 infection has become a global pandemic. The cases of Coronavirus Disease 2019 (COVID-19)-related acute cardiac injury with unknown pathophysiologic mechanism has become increasingly prevalent. However, it is not yet understood how the extent of cardiac injury differs with the intensity of viral infection. In the current study, we aimed to assess the association between elevated cardiac biomarkers and the severity of COVID-19 infection. Methods: A systematic literature search was performed across PubMed and Embase databases from December 1, 2019 to July 10, 2020, to identify studies that reported cardiac biomarkers of troponin (TnI) and creatine kinase-myocardial band (CK-MB) in patients with COVID-19. These studies compared non-severe patients with severe patients, or survivors with non-survivors or medical patients with critically ill patients. The data were extracted for TnI, CK-MB, N-terminal-brain natriuretic peptide (NT-BNP), D-dimer, and lactate dehydrogenase (LDH), C-reactive protein (CRP), and interleukin 6 (IL-6). Wherever possible, the data were pooled for meta-analysis (Review Manager, RevMan. version 5.3) with standard or weighted mean or median difference and corresponding 95% confidence intervals (95% CI). Results: A total of 25 studies involving 5,626 patients were included in the present analysis. More severe COVID-19 infection was found to be associated with higher mean values of TnI (-0.54 [-0.72, -0.36]) (ng/mL), CK-MB (-1.55 [-2.23, -0.88]) (ng/mL) and (-4.75 [-13.31, 3.82]) (units/L), NT-BNP (-815.7 [-1073.97, -557.42]) (pg/mL), D-dimer (-1.4 [-2.04, -0.77]) (mcg/mL), and LDH (-176.59 [-224.11, -129.06]) (units/L), as well as CRP (-64.03 [-68.88, -59.19]) (mg/L) and IL-6 (-22.59 [-29.39, -15.79]) (pg/mL). Conclusions: There is significant association between elevated cardiac biomarkers and the severity of COVID-19, which underlines the increased risk of acute cardiac injury with more severe viral infection. This highlights the need to understand the cardiac history among the COVID-19 patients during initial assessment and for monitoring.

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“…Ученые пришли к выводу, что кардиоренальная токсичность НПВП с известными тяжелыми побочными сердечно-сосудистыми эффектами может быть связана с измененным метаболизмом ArA, опосредованным цитохромом P450. Профиль метаболизма ArA может быть маркером безопасности и токсичности НПВП [13]. Далее этой же группой авторов показано, что воспаление вызывало значительный дисбаланс сердечного и почечного ангиотензинпревращающего фермента, его биологически активных ангиотензиновых пептидов (AngII и Ang1-7) и белков-мишеней, участвующих в связывании пептид-рецептор (AngII типа 1 и типа 2, и рецептора Ang1-7, Mas) при развитии сердечно-почечной токсичности.…”

Section: Nsaids' Adverse Events and Their Reduction нежелательные реаunclassified

Adverse Reactions of the Cardiovascular System when Taking Nonsteroidal Anti-inflammatory Drugs and Ways to Reduce Them

Пырикова

Антропова

Осипова

2019

Racionalʹnaâ farmakoterapiâ v kardiologii

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The most important issue of modern pharmacotherapy is not only efficacy, but also the safety of medicines. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is one of the main methods of treating acute and chronic pain in a wide range of diseases and pathological conditions. However, the prescription of this group of drugs requires consideration of the potential risks of complications, including from the side of the cardiovascular system. The purpose of the review was to assess the adverse reactions of the cardiovascular system when taking NSAIDs and approaches to their reduction. The article presents data on the mutual potential impact of cardiovascular diseases and musculoskeletal system, presents the results of large-scale studies of Russian and foreign authors and meta-analyzes of the NSAIDs effect on blood pressure profile, development of myocardial infarction, stroke and heart failure. The possible pathogenetic mechanisms of the side effects of NSAIDs are reviewed; the complexity of managing comorbid patients is demonstrated; it is shown that symptomatic treatment of pain and inflammatory syndrome should be carried out considering a personalized approach to the patient and rational choice of drugs.Before the NSAIDs prescription, it is necessary to consider all cardiovascular risk factors with the determination of the total risk of cardiovascular complications. In patients with a very high cardiovascular risk, the use of any NSAIDs should be avoided; with high and moderate risk, the use of NSAIDs with the most favorable cardiovascular safety profile is possible. If the patient belongs to the category of low total coronary risk, the doctor can choose any NSAIDs.

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Drug-Disease Interaction: Effect of Inflammation and Nonsteroidal Anti-Inflammatory Drugs on Cytochrome P450 Metabolites of Arachidonic Acid

Cited by 24 publications

References 46 publications

Subacute treatment of carprofen facilitate splenocardiac resolution deficit in cardiac injury

Subacute treatment of carprofen facilitate splenocardiac resolution deficit in cardiac injury

Assessing the Elevation of Cardiac Biomarkers and the Severity of COVID-19 Infection: A Meta-analysis

Adverse Reactions of the Cardiovascular System when Taking Nonsteroidal Anti-inflammatory Drugs and Ways to Reduce Them

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