Do anti‐tumour necrosis factor‐α biologics affect subclinical measures of atherosclerosis and arteriosclerosis? A systematic review
Aims: Inflammatory cytokines, particularly tumour necrosis factor‐α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to arteriosclerosis and atherosclerosis. We reviewed the existing evidence of the effect of anti‐TNFα treatment on arteriosclerosis and atherosc...
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| Published in: | British journal of clinical pharmacology Vol. 86; no. 5; pp. 837 - 851 |
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| Main Authors: | , , |
| Format: | Journal Article |
| Language: | English |
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England
John Wiley and Sons Inc
01-05-2020
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| Abstract | Aims: Inflammatory cytokines, particularly tumour necrosis factor‐α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to arteriosclerosis and atherosclerosis. We reviewed the existing evidence of the effect of anti‐TNFα treatment on arteriosclerosis and atherosclerosis in chronic inflammatory disease.
Methods: We performed a systematic review of studies examining effects of monoclonal antibodies against TNFα on subclinical measures of arteriosclerosis (arterial pulse wave velocity) and atherosclerosis (endothelial function measured by flow‐mediated dilation or forearm blood flow responses to endothelium‐dependent agonists, and common carotid intima‐media thickness).
Results: We identified 60 studies (of 854 potential studies identified using a systematic search) in which effects of anti‐TNFα biologics on these measures were assessed in patients receiving anti‐TNFα therapy for a clinical indication (usually an inflammatory disease such as an inflammatory arthritis, psoriasis or inflammatory bowel disease). Of these, only 6 were randomised clinical controlled trials. Whilst many observational studies and noncontrolled studies reported positive findings, positive finding were reported in only 1 of 6 randomised clinical controlled trials.
Conclusions: There is no strong evidence for an effect of anti‐TNFα biologics on the subclinical measures of arteriosclerosis or atherosclerosis examined in this review. This does not exclude a positive effect of TNFα biologics on clinical outcomes through alternate pathways including those induced by remission of the primary inflammatory disease. |
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| AbstractList | AIMSInflammatory cytokines, particularly tumour necrosis factor-α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to arteriosclerosis and atherosclerosis. We reviewed the existing evidence of the effect of anti-TNFα treatment on arteriosclerosis and atherosclerosis in chronic inflammatory disease. METHODSWe performed a systematic review of studies examining effects of monoclonal antibodies against TNFα on subclinical measures of arteriosclerosis (arterial pulse wave velocity) and atherosclerosis (endothelial function measured by flow-mediated dilation or forearm blood flow responses to endothelium-dependent agonists, and common carotid intima-media thickness). RESULTSWe identified 60 studies (of 854 potential studies identified using a systematic search) in which effects of anti-TNFα biologics on these measures were assessed in patients receiving anti-TNFα therapy for a clinical indication (usually an inflammatory disease such as an inflammatory arthritis, psoriasis or inflammatory bowel disease). Of these, only 6 were randomised clinical controlled trials. Whilst many observational studies and noncontrolled studies reported positive findings, positive finding were reported in only 1 of 6 randomised clinical controlled trials. CONCLUSIONSThere is no strong evidence for an effect of anti-TNFα biologics on the subclinical measures of arteriosclerosis or atherosclerosis examined in this review. This does not exclude a positive effect of TNFα biologics on clinical outcomes through alternate pathways including those induced by remission of the primary inflammatory disease. Aims: Inflammatory cytokines, particularly tumour necrosis factor‐α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to arteriosclerosis and atherosclerosis. We reviewed the existing evidence of the effect of anti‐TNFα treatment on arteriosclerosis and atherosclerosis in chronic inflammatory disease. Methods: We performed a systematic review of studies examining effects of monoclonal antibodies against TNFα on subclinical measures of arteriosclerosis (arterial pulse wave velocity) and atherosclerosis (endothelial function measured by flow‐mediated dilation or forearm blood flow responses to endothelium‐dependent agonists, and common carotid intima‐media thickness). Results: We identified 60 studies (of 854 potential studies identified using a systematic search) in which effects of anti‐TNFα biologics on these measures were assessed in patients receiving anti‐TNFα therapy for a clinical indication (usually an inflammatory disease such as an inflammatory arthritis, psoriasis or inflammatory bowel disease). Of these, only 6 were randomised clinical controlled trials. Whilst many observational studies and noncontrolled studies reported positive findings, positive finding were reported in only 1 of 6 randomised clinical controlled trials. Conclusions: There is no strong evidence for an effect of anti‐TNFα biologics on the subclinical measures of arteriosclerosis or atherosclerosis examined in this review. This does not exclude a positive effect of TNFα biologics on clinical outcomes through alternate pathways including those induced by remission of the primary inflammatory disease. Aims: Inflammatory cytokines, particularly tumour necrosis factor‐α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to arteriosclerosis and atherosclerosis. We reviewed the existing evidence of the effect of anti‐TNFα treatment on arteriosclerosis and atherosclerosis in chronic inflammatory disease. Methods: We performed a systematic review of studies examining effects of monoclonal antibodies against TNFα on subclinical measures of arteriosclerosis (arterial pulse wave velocity) and atherosclerosis (endothelial function measured by flow‐mediated dilation or forearm blood flow responses to endothelium‐dependent agonists, and common carotid intima‐media thickness). Results: We identified 60 studies (of 854 potential studies identified using a systematic search) in which effects of anti‐TNFα biologics on these measures were assessed in patients receiving anti‐TNFα therapy for a clinical indication (usually an inflammatory disease such as an inflammatory arthritis, psoriasis or inflammatory bowel disease). Of these, only 6 were randomised clinical controlled trials. Whilst many observational studies and noncontrolled studies reported positive findings, positive finding were reported in only 1 of 6 randomised clinical controlled trials. Conclusions: There is no strong evidence for an effect of anti‐TNFα biologics on the subclinical measures of arteriosclerosis or atherosclerosis examined in this review. This does not exclude a positive effect of TNFα biologics on clinical outcomes through alternate pathways including those induced by remission of the primary inflammatory disease. Inflammatory cytokines, particularly tumour necrosis factor-α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to arteriosclerosis and atherosclerosis. We reviewed the existing evidence of the effect of anti-TNFα treatment on arteriosclerosis and atherosclerosis in chronic inflammatory disease. We performed a systematic review of studies examining effects of monoclonal antibodies against TNFα on subclinical measures of arteriosclerosis (arterial pulse wave velocity) and atherosclerosis (endothelial function measured by flow-mediated dilation or forearm blood flow responses to endothelium-dependent agonists, and common carotid intima-media thickness). We identified 60 studies (of 854 potential studies identified using a systematic search) in which effects of anti-TNFα biologics on these measures were assessed in patients receiving anti-TNFα therapy for a clinical indication (usually an inflammatory disease such as an inflammatory arthritis, psoriasis or inflammatory bowel disease). Of these, only 6 were randomised clinical controlled trials. Whilst many observational studies and noncontrolled studies reported positive findings, positive finding were reported in only 1 of 6 randomised clinical controlled trials. There is no strong evidence for an effect of anti-TNFα biologics on the subclinical measures of arteriosclerosis or atherosclerosis examined in this review. This does not exclude a positive effect of TNFα biologics on clinical outcomes through alternate pathways including those induced by remission of the primary inflammatory disease. |
| Author | Knowles, Laurence Chowienczyk, Philip J. Nadeem, Nida |
| AuthorAffiliation | 2 King's College London, British Heart Foundation Centre London UK 1 Guy's and St Thomas's Foundation Trust London UK |
| AuthorAffiliation_xml | – name: 1 Guy's and St Thomas's Foundation Trust London UK – name: 2 King's College London, British Heart Foundation Centre London UK |
| Author_xml | – sequence: 1 givenname: Laurence orcidid: 0000-0003-2316-4676 surname: Knowles fullname: Knowles, Laurence organization: Guy's and St Thomas's Foundation Trust – sequence: 2 givenname: Nida surname: Nadeem fullname: Nadeem, Nida organization: King's College London, British Heart Foundation Centre – sequence: 3 givenname: Philip J. surname: Chowienczyk fullname: Chowienczyk, Philip J. email: phil.chowienczyk@kcl.ac.uk organization: King's College London, British Heart Foundation Centre |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31957052$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_jad_2022_07_024 crossref_primary_10_1016_j_piel_2020_06_009 crossref_primary_10_3390_biomedicines11020318 crossref_primary_10_1161_CIRCRESAHA_121_318061 crossref_primary_10_3390_ph15091101 crossref_primary_10_1111_srt_13302 crossref_primary_10_1007_s00296_022_05226_w crossref_primary_10_1007_s10067_023_06505_y crossref_primary_10_1080_1744666X_2021_1899809 crossref_primary_10_1093_rheumatology_keaa849 crossref_primary_10_1017_S0954422421000378 crossref_primary_10_3389_fphar_2021_774808 crossref_primary_10_2139_ssrn_4104260 crossref_primary_10_3389_fmed_2022_864185 |
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| Snippet | Aims: Inflammatory cytokines, particularly tumour necrosis factor‐α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to... Inflammatory cytokines, particularly tumour necrosis factor-α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to... Aims: Inflammatory cytokines, particularly tumour necrosis factor‐α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to... AIMSInflammatory cytokines, particularly tumour necrosis factor-α (TNFα), are thought to promote arterial disease through a variety of mechanisms leading to... |
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| Title | Do anti‐tumour necrosis factor‐α biologics affect subclinical measures of atherosclerosis and arteriosclerosis? A systematic review |
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