Anti-Inflammatory Therapy With Canakinumab for the Prevention and Management of Diabetes
Subclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion. The authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes. The authors randomized 10,061 patients with prio...
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| Published in | Journal of the American College of Cardiology Vol. 71; no. 21; pp. 2392 - 2401 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
29.05.2018
Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0735-1097 1558-3597 1558-3597 |
| DOI | 10.1016/j.jacc.2018.03.002 |
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| Abstract | Subclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion.
The authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes.
The authors randomized 10,061 patients with prior myocardial infarction and high-sensitivity C-reactive protein (hsCRP) ≥2 mg/l to placebo or canakinumab at doses of 50 mg, 150 mg, or 300 mg subcutaneously once every 3 months. The authors tested the effects of canakinumab on major cardiovascular events in patients with and without diabetes at baseline, and evaluated as a pre-specified analysis whether canakinumab would reduce the risk of adjudicated cases of new-onset type 2 diabetes among those with protocol-defined pre-diabetes at trial entry. The authors also evaluated the effect of canakinumab on fasting plasma glucose and glycosylated hemoglobin (HbA1c) in patients with and without established diabetes.
Of the participants, 4,057 (40.3%) had baseline diabetes, 4,960 (49.3%) had pre-diabetes, and 1,044 (10.4%) had normal glucose levels. Among those without diabetes, increasing tertiles of hsCRP at baseline associated with an increased risk of developing diabetes during the median follow-up period of 3.7 years (incidence rates 3.2, 4.1, and 4.4 per 100 person-years; p = 0.003). Canakinumab 150 mg as compared with placebo had similar magnitude effects on major cardiovascular event rates among those with diabetes (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.70 to 1.03), pre-diabetes (HR: 0.86; 95% CI: 0.70 to 1.06), and normoglycemia (HR: 0.81; 95% CI: 0.49 to 1.35). Despite large reductions in hsCRP and IL-6, canakinumab did not reduce the incidence of new-onset diabetes, with rates per 100 person-years in the placebo, 50 mg, 150 mg, and 300 mg canakinumab groups of 4.2, 4.2, 4.4, and 4.1, respectively (log-rank p = 0.84). The HR comparing all canakinumab doses to placebo was 1.02 (95% CI: 0.87 to 1.19; p = 0.82). Canakinumab reduced HbA1c during the first 6 to 9 months of treatment, but no consistent long-term benefits on HbA1c or fasting plasma glucose were observed.
Although IL-1β inhibition with canakinumab had similar effects on major cardiovascular events among those with and without diabetes, treatment over a median period of 3.7 years did not reduce incident diabetes. (Canakinumab Anti-inflammatory Thrombosis Outcomes Study [CANTOS]; NCT01327846)
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| AbstractList | AbstractBackgroundSubclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion. ObjectivesThe authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes. MethodsThe authors randomized 10,061 patients with prior myocardial infarction and high-sensitivity C-reactive protein (hsCRP) ≥2 mg/l to placebo or canakinumab at doses of 50 mg, 150 mg, or 300 mg subcutaneously once every 3 months. The authors tested the effects of canakinumab on major cardiovascular events in patients with and without diabetes at baseline, and evaluated as a pre-specified analysis whether canakinumab would reduce the risk of adjudicated cases of new-onset type 2 diabetes among those with protocol-defined pre-diabetes at trial entry. The authors also evaluated the effect of canakinumab on fasting plasma glucose and glycosylated hemoglobin (HbA 1c) in patients with and without established diabetes. ResultsOf the participants, 4,057 (40.3%) had baseline diabetes, 4,960 (49.3%) had pre-diabetes, and 1,044 (10.4%) had normal glucose levels. Among those without diabetes, increasing tertiles of hsCRP at baseline associated with an increased risk of developing diabetes during the median follow-up period of 3.7 years (incidence rates 3.2, 4.1, and 4.4 per 100 person-years; p = 0.003). Canakinumab 150 mg as compared with placebo had similar magnitude effects on major cardiovascular event rates among those with diabetes (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.70 to 1.03), pre-diabetes (HR: 0.86; 95% CI: 0.70 to 1.06), and normoglycemia (HR: 0.81; 95% CI: 0.49 to 1.35). Despite large reductions in hsCRP and IL-6, canakinumab did not reduce the incidence of new-onset diabetes, with rates per 100 person-years in the placebo, 50 mg, 150 mg, and 300 mg canakinumab groups of 4.2, 4.2, 4.4, and 4.1, respectively (log-rank p = 0.84). The HR comparing all canakinumab doses to placebo was 1.02 (95% CI: 0.87 to 1.19; p = 0.82). Canakinumab reduced HbA 1c during the first 6 to 9 months of treatment, but no consistent long-term benefits on HbA 1c or fasting plasma glucose were observed. ConclusionsAlthough IL-1β inhibition with canakinumab had similar effects on major cardiovascular events among those with and without diabetes, treatment over a median period of 3.7 years did not reduce incident diabetes. (Canakinumab Anti-inflammatory Thrombosis Outcomes Study [CANTOS]; NCT01327846) Subclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion. The authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes. The authors randomized 10,061 patients with prior myocardial infarction and high-sensitivity C-reactive protein (hsCRP) ≥2 mg/l to placebo or canakinumab at doses of 50 mg, 150 mg, or 300 mg subcutaneously once every 3 months. The authors tested the effects of canakinumab on major cardiovascular events in patients with and without diabetes at baseline, and evaluated as a pre-specified analysis whether canakinumab would reduce the risk of adjudicated cases of new-onset type 2 diabetes among those with protocol-defined pre-diabetes at trial entry. The authors also evaluated the effect of canakinumab on fasting plasma glucose and glycosylated hemoglobin (HbA1c) in patients with and without established diabetes. Of the participants, 4,057 (40.3%) had baseline diabetes, 4,960 (49.3%) had pre-diabetes, and 1,044 (10.4%) had normal glucose levels. Among those without diabetes, increasing tertiles of hsCRP at baseline associated with an increased risk of developing diabetes during the median follow-up period of 3.7 years (incidence rates 3.2, 4.1, and 4.4 per 100 person-years; p = 0.003). Canakinumab 150 mg as compared with placebo had similar magnitude effects on major cardiovascular event rates among those with diabetes (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.70 to 1.03), pre-diabetes (HR: 0.86; 95% CI: 0.70 to 1.06), and normoglycemia (HR: 0.81; 95% CI: 0.49 to 1.35). Despite large reductions in hsCRP and IL-6, canakinumab did not reduce the incidence of new-onset diabetes, with rates per 100 person-years in the placebo, 50 mg, 150 mg, and 300 mg canakinumab groups of 4.2, 4.2, 4.4, and 4.1, respectively (log-rank p = 0.84). The HR comparing all canakinumab doses to placebo was 1.02 (95% CI: 0.87 to 1.19; p = 0.82). Canakinumab reduced HbA1c during the first 6 to 9 months of treatment, but no consistent long-term benefits on HbA1c or fasting plasma glucose were observed. Although IL-1β inhibition with canakinumab had similar effects on major cardiovascular events among those with and without diabetes, treatment over a median period of 3.7 years did not reduce incident diabetes. (Canakinumab Anti-inflammatory Thrombosis Outcomes Study [CANTOS]; NCT01327846) [Display omitted] Subclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion. The authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes. The authors randomized 10,061 patients with prior myocardial infarction and high-sensitivity C-reactive protein (hsCRP) ≥2 mg/l to placebo or canakinumab at doses of 50 mg, 150 mg, or 300 mg subcutaneously once every 3 months. The authors tested the effects of canakinumab on major cardiovascular events in patients with and without diabetes at baseline, and evaluated as a pre-specified analysis whether canakinumab would reduce the risk of adjudicated cases of new-onset type 2 diabetes among those with protocol-defined pre-diabetes at trial entry. The authors also evaluated the effect of canakinumab on fasting plasma glucose and glycosylated hemoglobin (HbA ) in patients with and without established diabetes. Of the participants, 4,057 (40.3%) had baseline diabetes, 4,960 (49.3%) had pre-diabetes, and 1,044 (10.4%) had normal glucose levels. Among those without diabetes, increasing tertiles of hsCRP at baseline associated with an increased risk of developing diabetes during the median follow-up period of 3.7 years (incidence rates 3.2, 4.1, and 4.4 per 100 person-years; p = 0.003). Canakinumab 150 mg as compared with placebo had similar magnitude effects on major cardiovascular event rates among those with diabetes (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.70 to 1.03), pre-diabetes (HR: 0.86; 95% CI: 0.70 to 1.06), and normoglycemia (HR: 0.81; 95% CI: 0.49 to 1.35). Despite large reductions in hsCRP and IL-6, canakinumab did not reduce the incidence of new-onset diabetes, with rates per 100 person-years in the placebo, 50 mg, 150 mg, and 300 mg canakinumab groups of 4.2, 4.2, 4.4, and 4.1, respectively (log-rank p = 0.84). The HR comparing all canakinumab doses to placebo was 1.02 (95% CI: 0.87 to 1.19; p = 0.82). Canakinumab reduced HbA during the first 6 to 9 months of treatment, but no consistent long-term benefits on HbA or fasting plasma glucose were observed. Although IL-1β inhibition with canakinumab had similar effects on major cardiovascular events among those with and without diabetes, treatment over a median period of 3.7 years did not reduce incident diabetes. (Canakinumab Anti-inflammatory Thrombosis Outcomes Study [CANTOS]; NCT01327846). Subclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion.BACKGROUNDSubclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion.The authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes.OBJECTIVESThe authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes.The authors randomized 10,061 patients with prior myocardial infarction and high-sensitivity C-reactive protein (hsCRP) ≥2 mg/l to placebo or canakinumab at doses of 50 mg, 150 mg, or 300 mg subcutaneously once every 3 months. The authors tested the effects of canakinumab on major cardiovascular events in patients with and without diabetes at baseline, and evaluated as a pre-specified analysis whether canakinumab would reduce the risk of adjudicated cases of new-onset type 2 diabetes among those with protocol-defined pre-diabetes at trial entry. The authors also evaluated the effect of canakinumab on fasting plasma glucose and glycosylated hemoglobin (HbA1c) in patients with and without established diabetes.METHODSThe authors randomized 10,061 patients with prior myocardial infarction and high-sensitivity C-reactive protein (hsCRP) ≥2 mg/l to placebo or canakinumab at doses of 50 mg, 150 mg, or 300 mg subcutaneously once every 3 months. The authors tested the effects of canakinumab on major cardiovascular events in patients with and without diabetes at baseline, and evaluated as a pre-specified analysis whether canakinumab would reduce the risk of adjudicated cases of new-onset type 2 diabetes among those with protocol-defined pre-diabetes at trial entry. The authors also evaluated the effect of canakinumab on fasting plasma glucose and glycosylated hemoglobin (HbA1c) in patients with and without established diabetes.Of the participants, 4,057 (40.3%) had baseline diabetes, 4,960 (49.3%) had pre-diabetes, and 1,044 (10.4%) had normal glucose levels. Among those without diabetes, increasing tertiles of hsCRP at baseline associated with an increased risk of developing diabetes during the median follow-up period of 3.7 years (incidence rates 3.2, 4.1, and 4.4 per 100 person-years; p = 0.003). Canakinumab 150 mg as compared with placebo had similar magnitude effects on major cardiovascular event rates among those with diabetes (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.70 to 1.03), pre-diabetes (HR: 0.86; 95% CI: 0.70 to 1.06), and normoglycemia (HR: 0.81; 95% CI: 0.49 to 1.35). Despite large reductions in hsCRP and IL-6, canakinumab did not reduce the incidence of new-onset diabetes, with rates per 100 person-years in the placebo, 50 mg, 150 mg, and 300 mg canakinumab groups of 4.2, 4.2, 4.4, and 4.1, respectively (log-rank p = 0.84). The HR comparing all canakinumab doses to placebo was 1.02 (95% CI: 0.87 to 1.19; p = 0.82). Canakinumab reduced HbA1c during the first 6 to 9 months of treatment, but no consistent long-term benefits on HbA1c or fasting plasma glucose were observed.RESULTSOf the participants, 4,057 (40.3%) had baseline diabetes, 4,960 (49.3%) had pre-diabetes, and 1,044 (10.4%) had normal glucose levels. Among those without diabetes, increasing tertiles of hsCRP at baseline associated with an increased risk of developing diabetes during the median follow-up period of 3.7 years (incidence rates 3.2, 4.1, and 4.4 per 100 person-years; p = 0.003). Canakinumab 150 mg as compared with placebo had similar magnitude effects on major cardiovascular event rates among those with diabetes (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.70 to 1.03), pre-diabetes (HR: 0.86; 95% CI: 0.70 to 1.06), and normoglycemia (HR: 0.81; 95% CI: 0.49 to 1.35). Despite large reductions in hsCRP and IL-6, canakinumab did not reduce the incidence of new-onset diabetes, with rates per 100 person-years in the placebo, 50 mg, 150 mg, and 300 mg canakinumab groups of 4.2, 4.2, 4.4, and 4.1, respectively (log-rank p = 0.84). The HR comparing all canakinumab doses to placebo was 1.02 (95% CI: 0.87 to 1.19; p = 0.82). Canakinumab reduced HbA1c during the first 6 to 9 months of treatment, but no consistent long-term benefits on HbA1c or fasting plasma glucose were observed.Although IL-1β inhibition with canakinumab had similar effects on major cardiovascular events among those with and without diabetes, treatment over a median period of 3.7 years did not reduce incident diabetes. (Canakinumab Anti-inflammatory Thrombosis Outcomes Study [CANTOS]; NCT01327846).CONCLUSIONSAlthough IL-1β inhibition with canakinumab had similar effects on major cardiovascular events among those with and without diabetes, treatment over a median period of 3.7 years did not reduce incident diabetes. (Canakinumab Anti-inflammatory Thrombosis Outcomes Study [CANTOS]; NCT01327846). BackgroundSubclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion.ObjectivesThe authors tested the hypothesis that the IL-1β inhibitor canakinumab reduces incident diabetes.MethodsThe authors randomized 10,061 patients with prior myocardial infarction and high-sensitivity C-reactive protein (hsCRP) ≥2 mg/l to placebo or canakinumab at doses of 50 mg, 150 mg, or 300 mg subcutaneously once every 3 months. The authors tested the effects of canakinumab on major cardiovascular events in patients with and without diabetes at baseline, and evaluated as a pre-specified analysis whether canakinumab would reduce the risk of adjudicated cases of new-onset type 2 diabetes among those with protocol-defined pre-diabetes at trial entry. The authors also evaluated the effect of canakinumab on fasting plasma glucose and glycosylated hemoglobin (HbA1c) in patients with and without established diabetes.ResultsOf the participants, 4,057 (40.3%) had baseline diabetes, 4,960 (49.3%) had pre-diabetes, and 1,044 (10.4%) had normal glucose levels. Among those without diabetes, increasing tertiles of hsCRP at baseline associated with an increased risk of developing diabetes during the median follow-up period of 3.7 years (incidence rates 3.2, 4.1, and 4.4 per 100 person-years; p = 0.003). Canakinumab 150 mg as compared with placebo had similar magnitude effects on major cardiovascular event rates among those with diabetes (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.70 to 1.03), pre-diabetes (HR: 0.86; 95% CI: 0.70 to 1.06), and normoglycemia (HR: 0.81; 95% CI: 0.49 to 1.35). Despite large reductions in hsCRP and IL-6, canakinumab did not reduce the incidence of new-onset diabetes, with rates per 100 person-years in the placebo, 50 mg, 150 mg, and 300 mg canakinumab groups of 4.2, 4.2, 4.4, and 4.1, respectively (log-rank p = 0.84). The HR comparing all canakinumab doses to placebo was 1.02 (95% CI: 0.87 to 1.19; p = 0.82). Canakinumab reduced HbA1c during the first 6 to 9 months of treatment, but no consistent long-term benefits on HbA1c or fasting plasma glucose were observed.ConclusionsAlthough IL-1β inhibition with canakinumab had similar effects on major cardiovascular events among those with and without diabetes, treatment over a median period of 3.7 years did not reduce incident diabetes. (Canakinumab Anti-inflammatory Thrombosis Outcomes Study [CANTOS]; NCT01327846) |
| Author | Libby, Peter Donath, Marc Y. Glynn, Robert J. Pradhan, Aruna D. Nicolau, Jose C. Thuren, Tom Ridker, Paul M Everett, Brendan M. Pais, Prem |
| Author_xml | – sequence: 1 givenname: Brendan M. surname: Everett fullname: Everett, Brendan M. email: beverett@bwh.harvard.edu organization: Center for Cardiovascular Disease Prevention, Harvard Medical School, Boston, Massachusetts – sequence: 2 givenname: Marc Y. surname: Donath fullname: Donath, Marc Y. organization: Endocrinology, Diabetes & Metabolism, University Hospital Basel, Basel, Switzerland – sequence: 3 givenname: Aruna D. surname: Pradhan fullname: Pradhan, Aruna D. organization: Center for Cardiovascular Disease Prevention, Harvard Medical School, Boston, Massachusetts – sequence: 4 givenname: Tom surname: Thuren fullname: Thuren, Tom organization: Novartis Pharmaceutical Corporation, East Hanover, New Jersey, and Basel, Switzerland – sequence: 5 givenname: Prem surname: Pais fullname: Pais, Prem organization: St. John’s Research Institute, Bangalore, India – sequence: 6 givenname: Jose C. surname: Nicolau fullname: Nicolau, Jose C. organization: Instituto do Coracao (InCor), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil – sequence: 7 givenname: Robert J. surname: Glynn fullname: Glynn, Robert J. organization: Center for Cardiovascular Disease Prevention, Harvard Medical School, Boston, Massachusetts – sequence: 8 givenname: Peter surname: Libby fullname: Libby, Peter organization: Division of Cardiovascular Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts – sequence: 9 givenname: Paul M surname: Ridker fullname: Ridker, Paul M organization: Center for Cardiovascular Disease Prevention, Harvard Medical School, Boston, Massachusetts |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29544870$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1001/jama.286.3.327 10.1038/nrd4275 10.7326/0003-4819-159-1-201307020-00003 10.2337/dc09-0533 10.1056/NEJMoa1501352 10.1001/archinte.166.8.902 10.1038/ni.1935 10.1016/j.ahj.2013.03.018 10.2337/dc12-1835 10.1159/000088261 10.1001/jama.2016.3609 10.2337/dc11-2219 10.1172/JCI29069 10.2337/diab.44.4.369 10.1172/JCI200215318 10.2337/diabetes.50.8.1683 10.1210/jc.2008-0396 10.1161/CIRCULATIONAHA.112.122556 10.1172/JCI88884 10.1056/NEJMoa1707914 10.1016/S0140-6736(12)61190-8 10.1056/NEJMoa1315878 10.1161/01.CIR.0000132467.45278.59 10.1056/NEJMoa065213 10.1126/science.7678183 10.1016/S0140-6736(17)32814-3 10.1056/NEJMoa1504720 10.1016/S0140-6736(17)32247-X 10.2337/diab.45.7.881 |
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| References | Green, Bethel, Armstrong (bib18) 2015; 373 O'Donoghue, Glaser, Cavender (bib28) 2016; 315 Boni-Schnetzler, Thorne, Parnaud (bib5) 2008; 93 Pradhan, Manson, Rifai, Buring, Ridker (bib1) 2001; 286 Ridker, MacFadyen, Thuren (bib14) 2017; 390 Ridker, MacFadyen, Everett (bib15) 2018; 391 Bernstein, Berry, Kim, Canavan, Grinspoon (bib23) 2006; 166 Ridker, Pradhan, MacFadyen, Libby, Glynn (bib16) 2012; 380 Ridker, Howard, Walter (bib17) 2012; 126 Everett, Pradhan, Solomon (bib26) 2013; 166 Stern (bib29) 1995; 44 Larsen, Faulenbach, Vaag (bib8) 2007; 356 Masters, Dunne, Subramanian (bib6) 2010; 11 Shoelson, Lee, Goldfine (bib25) 2006; 116 Maedler, Spinas, Lehmann (bib7) 2001; 50 Cavelti-Weder, Babians-Brunner, Keller (bib10) 2012; 35 Zinman, Wanner, Lachin (bib19) 2015; 373 Larsen, Faulenbach, Vaag, Ehses, Donath, Mandrup-Poulsen (bib9) 2009; 32 Ofei, Hurel, Newkirk, Sopwith, Taylor (bib21) 1996; 45 Goldfine, Shoelson (bib3) 2017; 127 White, Held, Stewart (bib27) 2014; 370 Dominguez, Storgaard, Rask-Madsen (bib22) 2005; 42 Ridker, Wilson, Grundy (bib30) 2004; 109 (bib13) 2014; 37 Suppl 1 Ridker, Everett, Thuren (bib12) 2017; 377 Goldfine, Fonseca, Jablonski (bib24) 2013; 159 Sloan-Lancaster, Abu-Raddad, Polzer (bib11) 2013; 36 Hotamisligil, Shargill, Spiegelman (bib20) 1993; 259 Maedler, Sergeev, Ris (bib4) 2002; 110 Donath (bib2) 2014; 13 Goldfine (10.1016/j.jacc.2018.03.002_bib3) 2017; 127 Maedler (10.1016/j.jacc.2018.03.002_bib4) 2002; 110 Larsen (10.1016/j.jacc.2018.03.002_bib9) 2009; 32 Everett (10.1016/j.jacc.2018.03.002_bib26) 2013; 166 Maedler (10.1016/j.jacc.2018.03.002_bib7) 2001; 50 Dominguez (10.1016/j.jacc.2018.03.002_bib22) 2005; 42 Ridker (10.1016/j.jacc.2018.03.002_bib15) 2018; 391 Ridker (10.1016/j.jacc.2018.03.002_bib30) 2004; 109 Green (10.1016/j.jacc.2018.03.002_bib18) 2015; 373 Pradhan (10.1016/j.jacc.2018.03.002_bib1) 2001; 286 Donath (10.1016/j.jacc.2018.03.002_bib2) 2014; 13 Bernstein (10.1016/j.jacc.2018.03.002_bib23) 2006; 166 Stern (10.1016/j.jacc.2018.03.002_bib29) 1995; 44 Ridker (10.1016/j.jacc.2018.03.002_bib16) 2012; 380 Masters (10.1016/j.jacc.2018.03.002_bib6) 2010; 11 Ridker (10.1016/j.jacc.2018.03.002_bib12) 2017; 377 Zinman (10.1016/j.jacc.2018.03.002_bib19) 2015; 373 Hotamisligil (10.1016/j.jacc.2018.03.002_bib20) 1993; 259 White (10.1016/j.jacc.2018.03.002_bib27) 2014; 370 Sloan-Lancaster (10.1016/j.jacc.2018.03.002_bib11) 2013; 36 (10.1016/j.jacc.2018.03.002_bib13) 2014; 37 Suppl 1 Goldfine (10.1016/j.jacc.2018.03.002_bib24) 2013; 159 Shoelson (10.1016/j.jacc.2018.03.002_bib25) 2006; 116 Boni-Schnetzler (10.1016/j.jacc.2018.03.002_bib5) 2008; 93 O'Donoghue (10.1016/j.jacc.2018.03.002_bib28) 2016; 315 Cavelti-Weder (10.1016/j.jacc.2018.03.002_bib10) 2012; 35 Ofei (10.1016/j.jacc.2018.03.002_bib21) 1996; 45 Larsen (10.1016/j.jacc.2018.03.002_bib8) 2007; 356 Ridker (10.1016/j.jacc.2018.03.002_bib14) 2017; 390 Ridker (10.1016/j.jacc.2018.03.002_bib17) 2012; 126 29793628 - J Am Coll Cardiol. 2018 May 29;71(21):2402-2404 30213342 - J Am Coll Cardiol. 2018 Sep 18;72(12):1432-1433 30213341 - J Am Coll Cardiol. 2018 Sep 18;72(12):1432 |
| References_xml | – volume: 373 start-page: 2117 year: 2015 end-page: 2128 ident: bib19 article-title: Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes publication-title: N Engl J Med – volume: 370 start-page: 1702 year: 2014 end-page: 1711 ident: bib27 article-title: Darapladib for preventing ischemic events in stable coronary heart disease publication-title: N Engl J Med – volume: 50 start-page: 1683 year: 2001 end-page: 1690 ident: bib7 article-title: Glucose induces beta-cell apoptosis via upregulation of the Fas receptor in human islets publication-title: Diabetes – volume: 390 start-page: 1833 year: 2017 end-page: 1842 ident: bib14 article-title: Effect of interleukin-1beta inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial publication-title: Lancet – volume: 259 start-page: 87 year: 1993 end-page: 91 ident: bib20 article-title: Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance publication-title: Science – volume: 116 start-page: 1793 year: 2006 end-page: 1801 ident: bib25 article-title: Inflammation and insulin resistance publication-title: J Clin Invest – volume: 286 start-page: 327 year: 2001 end-page: 334 ident: bib1 article-title: C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus publication-title: JAMA – volume: 13 start-page: 465 year: 2014 end-page: 476 ident: bib2 article-title: Targeting inflammation in the treatment of type 2 diabetes: time to start publication-title: Nat Rev Drug Discov – volume: 166 start-page: 199 year: 2013 end-page: 207.e15 ident: bib26 article-title: Rationale and design of the Cardiovascular Inflammation Reduction Trial: a test of the inflammatory hypothesis of atherothrombosis publication-title: Am Heart J – volume: 93 start-page: 4065 year: 2008 end-page: 4074 ident: bib5 article-title: Increased interleukin (IL)-1beta messenger ribonucleic acid expression in beta -cells of individuals with type 2 diabetes and regulation of IL-1beta in human islets by glucose and autostimulation publication-title: J Clin Endocrinol Metab – volume: 32 start-page: 1663 year: 2009 end-page: 1668 ident: bib9 article-title: Sustained effects of interleukin-1 receptor antagonist treatment in type 2 diabetes publication-title: Diabetes Care – volume: 315 start-page: 1591 year: 2016 end-page: 1599 ident: bib28 article-title: Effect of losmapimod on cardiovascular outcomes in patients hospitalized with acute myocardial infarction: a randomized clinical trial publication-title: JAMA – volume: 159 start-page: 1 year: 2013 end-page: 12 ident: bib24 article-title: Salicylate (salsalate) in patients with type 2 diabetes: a randomized trial publication-title: Ann Intern Med – volume: 391 start-page: 319 year: 2018 end-page: 328 ident: bib15 article-title: Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomised controlled trial publication-title: Lancet – volume: 44 start-page: 369 year: 1995 end-page: 374 ident: bib29 article-title: Diabetes and cardiovascular disease. The “common soil” hypothesis publication-title: Diabetes – volume: 36 start-page: 2239 year: 2013 end-page: 2246 ident: bib11 article-title: Double-blind, randomized study evaluating the glycemic and anti-inflammatory effects of subcutaneous LY2189102, a neutralizing IL-1beta antibody, in patients with type 2 diabetes publication-title: Diabetes Care – volume: 373 start-page: 232 year: 2015 end-page: 242 ident: bib18 article-title: Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes publication-title: N Engl J Med – volume: 37 Suppl 1 start-page: S81 year: 2014 end-page: S90 ident: bib13 article-title: Diagnosis and classification of diabetes mellitus publication-title: Diabetes Care – volume: 166 start-page: 902 year: 2006 end-page: 908 ident: bib23 article-title: Effects of etanercept in patients with the metabolic syndrome publication-title: Arch Intern Med – volume: 377 start-page: 1119 year: 2017 end-page: 1131 ident: bib12 article-title: Antiinflammatory therapy with canakinumab for atherosclerotic disease publication-title: N Engl J Med – volume: 35 start-page: 1654 year: 2012 end-page: 1662 ident: bib10 article-title: Effects of gevokizumab on glycemia and inflammatory markers in type 2 diabetes publication-title: Diabetes Care – volume: 110 start-page: 851 year: 2002 end-page: 860 ident: bib4 article-title: Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets publication-title: J Clin Invest – volume: 126 start-page: 2739 year: 2012 end-page: 2748 ident: bib17 article-title: Effects of interleukin-1beta inhibition with canakinumab on hemoglobin A1c, lipids, C-reactive protein, interleukin-6, and fibrinogen: a phase IIb randomized, placebo-controlled trial publication-title: Circulation – volume: 11 start-page: 897 year: 2010 end-page: 904 ident: bib6 article-title: Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1beta in type 2 diabetes publication-title: Nat Immunol – volume: 45 start-page: 881 year: 1996 end-page: 885 ident: bib21 article-title: Effects of an engineered human anti-TNF-alpha antibody (CDP571) on insulin sensitivity and glycemic control in patients with NIDDM publication-title: Diabetes – volume: 42 start-page: 517 year: 2005 end-page: 525 ident: bib22 article-title: Metabolic and vascular effects of tumor necrosis factor-alpha blockade with etanercept in obese patients with type 2 diabetes publication-title: J Vasc Res – volume: 356 start-page: 1517 year: 2007 end-page: 1526 ident: bib8 article-title: Interleukin-1-receptor antagonist in type 2 diabetes mellitus publication-title: N Engl J Med – volume: 380 start-page: 565 year: 2012 end-page: 571 ident: bib16 article-title: Cardiovascular benefits and diabetes risks of statin therapy in primary prevention: an analysis from the JUPITER trial publication-title: Lancet – volume: 127 start-page: 83 year: 2017 end-page: 93 ident: bib3 article-title: Therapeutic approaches targeting inflammation for diabetes and associated cardiovascular risk publication-title: J Clin Invest – volume: 109 start-page: 2818 year: 2004 end-page: 2825 ident: bib30 article-title: Should C-reactive protein be added to metabolic syndrome and to assessment of global cardiovascular risk? publication-title: Circulation – volume: 286 start-page: 327 year: 2001 ident: 10.1016/j.jacc.2018.03.002_bib1 article-title: C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus publication-title: JAMA doi: 10.1001/jama.286.3.327 – volume: 13 start-page: 465 year: 2014 ident: 10.1016/j.jacc.2018.03.002_bib2 article-title: Targeting inflammation in the treatment of type 2 diabetes: time to start publication-title: Nat Rev Drug Discov doi: 10.1038/nrd4275 – volume: 159 start-page: 1 year: 2013 ident: 10.1016/j.jacc.2018.03.002_bib24 article-title: Salicylate (salsalate) in patients with type 2 diabetes: a randomized trial publication-title: Ann Intern Med doi: 10.7326/0003-4819-159-1-201307020-00003 – volume: 32 start-page: 1663 year: 2009 ident: 10.1016/j.jacc.2018.03.002_bib9 article-title: Sustained effects of interleukin-1 receptor antagonist treatment in type 2 diabetes publication-title: Diabetes Care doi: 10.2337/dc09-0533 – volume: 373 start-page: 232 year: 2015 ident: 10.1016/j.jacc.2018.03.002_bib18 article-title: Effect of sitagliptin on cardiovascular outcomes in type 2 diabetes publication-title: N Engl J Med doi: 10.1056/NEJMoa1501352 – volume: 166 start-page: 902 year: 2006 ident: 10.1016/j.jacc.2018.03.002_bib23 article-title: Effects of etanercept in patients with the metabolic syndrome publication-title: Arch Intern Med doi: 10.1001/archinte.166.8.902 – volume: 11 start-page: 897 year: 2010 ident: 10.1016/j.jacc.2018.03.002_bib6 article-title: Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1beta in type 2 diabetes publication-title: Nat Immunol doi: 10.1038/ni.1935 – volume: 166 start-page: 199 year: 2013 ident: 10.1016/j.jacc.2018.03.002_bib26 article-title: Rationale and design of the Cardiovascular Inflammation Reduction Trial: a test of the inflammatory hypothesis of atherothrombosis publication-title: Am Heart J doi: 10.1016/j.ahj.2013.03.018 – volume: 36 start-page: 2239 year: 2013 ident: 10.1016/j.jacc.2018.03.002_bib11 article-title: Double-blind, randomized study evaluating the glycemic and anti-inflammatory effects of subcutaneous LY2189102, a neutralizing IL-1beta antibody, in patients with type 2 diabetes publication-title: Diabetes Care doi: 10.2337/dc12-1835 – volume: 42 start-page: 517 year: 2005 ident: 10.1016/j.jacc.2018.03.002_bib22 article-title: Metabolic and vascular effects of tumor necrosis factor-alpha blockade with etanercept in obese patients with type 2 diabetes publication-title: J Vasc Res doi: 10.1159/000088261 – volume: 315 start-page: 1591 year: 2016 ident: 10.1016/j.jacc.2018.03.002_bib28 article-title: Effect of losmapimod on cardiovascular outcomes in patients hospitalized with acute myocardial infarction: a randomized clinical trial publication-title: JAMA doi: 10.1001/jama.2016.3609 – volume: 35 start-page: 1654 year: 2012 ident: 10.1016/j.jacc.2018.03.002_bib10 article-title: Effects of gevokizumab on glycemia and inflammatory markers in type 2 diabetes publication-title: Diabetes Care doi: 10.2337/dc11-2219 – volume: 37 Suppl 1 start-page: S81 year: 2014 ident: 10.1016/j.jacc.2018.03.002_bib13 article-title: Diagnosis and classification of diabetes mellitus publication-title: Diabetes Care – volume: 116 start-page: 1793 year: 2006 ident: 10.1016/j.jacc.2018.03.002_bib25 article-title: Inflammation and insulin resistance publication-title: J Clin Invest doi: 10.1172/JCI29069 – volume: 44 start-page: 369 year: 1995 ident: 10.1016/j.jacc.2018.03.002_bib29 article-title: Diabetes and cardiovascular disease. The “common soil” hypothesis publication-title: Diabetes doi: 10.2337/diab.44.4.369 – volume: 110 start-page: 851 year: 2002 ident: 10.1016/j.jacc.2018.03.002_bib4 article-title: Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets publication-title: J Clin Invest doi: 10.1172/JCI200215318 – volume: 50 start-page: 1683 year: 2001 ident: 10.1016/j.jacc.2018.03.002_bib7 article-title: Glucose induces beta-cell apoptosis via upregulation of the Fas receptor in human islets publication-title: Diabetes doi: 10.2337/diabetes.50.8.1683 – volume: 93 start-page: 4065 year: 2008 ident: 10.1016/j.jacc.2018.03.002_bib5 article-title: Increased interleukin (IL)-1beta messenger ribonucleic acid expression in beta -cells of individuals with type 2 diabetes and regulation of IL-1beta in human islets by glucose and autostimulation publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2008-0396 – volume: 126 start-page: 2739 year: 2012 ident: 10.1016/j.jacc.2018.03.002_bib17 article-title: Effects of interleukin-1beta inhibition with canakinumab on hemoglobin A1c, lipids, C-reactive protein, interleukin-6, and fibrinogen: a phase IIb randomized, placebo-controlled trial publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.112.122556 – volume: 127 start-page: 83 year: 2017 ident: 10.1016/j.jacc.2018.03.002_bib3 article-title: Therapeutic approaches targeting inflammation for diabetes and associated cardiovascular risk publication-title: J Clin Invest doi: 10.1172/JCI88884 – volume: 377 start-page: 1119 year: 2017 ident: 10.1016/j.jacc.2018.03.002_bib12 article-title: Antiinflammatory therapy with canakinumab for atherosclerotic disease publication-title: N Engl J Med doi: 10.1056/NEJMoa1707914 – volume: 380 start-page: 565 year: 2012 ident: 10.1016/j.jacc.2018.03.002_bib16 article-title: Cardiovascular benefits and diabetes risks of statin therapy in primary prevention: an analysis from the JUPITER trial publication-title: Lancet doi: 10.1016/S0140-6736(12)61190-8 – volume: 370 start-page: 1702 year: 2014 ident: 10.1016/j.jacc.2018.03.002_bib27 article-title: Darapladib for preventing ischemic events in stable coronary heart disease publication-title: N Engl J Med doi: 10.1056/NEJMoa1315878 – volume: 109 start-page: 2818 year: 2004 ident: 10.1016/j.jacc.2018.03.002_bib30 article-title: Should C-reactive protein be added to metabolic syndrome and to assessment of global cardiovascular risk? publication-title: Circulation doi: 10.1161/01.CIR.0000132467.45278.59 – volume: 356 start-page: 1517 year: 2007 ident: 10.1016/j.jacc.2018.03.002_bib8 article-title: Interleukin-1-receptor antagonist in type 2 diabetes mellitus publication-title: N Engl J Med doi: 10.1056/NEJMoa065213 – volume: 259 start-page: 87 year: 1993 ident: 10.1016/j.jacc.2018.03.002_bib20 article-title: Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance publication-title: Science doi: 10.1126/science.7678183 – volume: 391 start-page: 319 year: 2018 ident: 10.1016/j.jacc.2018.03.002_bib15 article-title: Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomised controlled trial publication-title: Lancet doi: 10.1016/S0140-6736(17)32814-3 – volume: 373 start-page: 2117 year: 2015 ident: 10.1016/j.jacc.2018.03.002_bib19 article-title: Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes publication-title: N Engl J Med doi: 10.1056/NEJMoa1504720 – volume: 390 start-page: 1833 year: 2017 ident: 10.1016/j.jacc.2018.03.002_bib14 article-title: Effect of interleukin-1beta inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial publication-title: Lancet doi: 10.1016/S0140-6736(17)32247-X – volume: 45 start-page: 881 year: 1996 ident: 10.1016/j.jacc.2018.03.002_bib21 article-title: Effects of an engineered human anti-TNF-alpha antibody (CDP571) on insulin sensitivity and glycemic control in patients with NIDDM publication-title: Diabetes doi: 10.2337/diab.45.7.881 – reference: 29793628 - J Am Coll Cardiol. 2018 May 29;71(21):2402-2404 – reference: 30213342 - J Am Coll Cardiol. 2018 Sep 18;72(12):1432-1433 – reference: 30213341 - J Am Coll Cardiol. 2018 Sep 18;72(12):1432 |
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| Snippet | Subclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin secretion.
The... AbstractBackgroundSubclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic... BackgroundSubclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin... Subclinical inflammation mediated in part by interleukin (IL)-1β participates in peripheral insulin resistance and impaired pancreatic insulin... |
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| SubjectTerms | Aged Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Antibodies, Monoclonal - pharmacology Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized Blood Glucose - drug effects Blood Glucose - metabolism C-reactive protein Cardiology Cardiovascular cardiovascular disease Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - diagnosis Diabetes Mellitus, Type 2 - drug therapy Disease Management Dose-Response Relationship, Drug Double-Blind Method Drug dosages Fasting Female Glucose Heart attacks Hemoglobin Humans Inflammation Insulin Insulin resistance Interleukin 6 Interleukin-1beta - antagonists & inhibitors Laboratory testing Male Middle Aged Monoclonal antibodies Myocardial infarction Pancreas Patients Prediabetic State - blood Prediabetic State - diagnosis Prediabetic State - drug therapy randomized trial Thrombosis |
| Title | Anti-Inflammatory Therapy With Canakinumab for the Prevention and Management of Diabetes |
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