Incidence of new-onset diabetes with 1 mg versus 4 mg pitavastatin in patients at high risk of developing diabetes during a 3-year follow-up.
Adult
Aged
Biomarkers
/ blood
Blood Glucose
/ drug effects
Diabetes Mellitus, Type 2
/ blood
Dyslipidemias
/ blood
Female
Follow-Up Studies
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
/ administration & dosage
Incidence
Lipids
/ blood
Male
Middle Aged
Prospective Studies
Quinolines
/ administration & dosage
Randomized Controlled Trials as Topic
Risk Assessment
Risk Factors
Time Factors
Treatment Outcome
Acute coronary syndrome
Metabolic syndrome
New-onset diabetes
Pitavastatin
Journal
Cardiovascular diabetology
ISSN: 1475-2840
Titre abrégé: Cardiovasc Diabetol
Pays: England
ID NLM: 101147637
Informations de publication
Date de publication:
21 11 2019
21 11 2019
Historique:
received:
16
09
2019
accepted:
13
11
2019
entrez:
23
11
2019
pubmed:
23
11
2019
medline:
19
5
2020
Statut:
epublish
Résumé
Statin therapy reduces the risk of cardiovascular events across a broad spectrum of patients; however, it increases the risk of new-onset diabetes (NOD). Although the highest dose pitavastatin is considered to not be associated with NOD, there are limited data regarding the impact of long-term highest dose pitavastatin use on the development of NOD in patients at high risk of developing diabetes. Therefore, we prospectively compared the differences in the development of NOD between the lowest and the highest dose of pitavastatin in patients at high risk of developing diabetes during a 3-year follow-up. This post hoc analysis of a prospective, single-blinded, randomized study compared the risk of NOD between the highest dose of pitavastatin (4 mg) and the lowest dose of pitavastatin (1 mg) over a 3-year follow-up in patients with acute coronary syndrome. Among 1044 patients of the original study, 667 patients at high risk of developing type 2 diabetes mellitus were in the subgroup analysis. The primary endpoint was a comparison of the differences in the cumulative incidence of NOD in the pitavastatin 1 mg and 4 mg groups during a 3-year follow-up. With propensity score matching, there were no significant differences in baseline demographic characteristics between the 2 groups. Incidence of NOD was similar between the pitavastatin 1 mg and 4 mg groups [12 of 289 patients (4.2%) and 8 of 289 patients (2.8%), respectively; p = 0.36]. In a prespecified analysis, there were no significant differences in NOD events according to sex, age, diagnosis, body mass index, glucose intolerance, or dyslipidemia. Administration of highest-dose pitavastatin did not increase the risk of NOD in patients at high risk of developing diabetes during the 3-year follow-up. Moreover, various risk factors for NOD such as metabolic syndrome components, glucose intolerance, dyslipidemia, obesity, or hypertension did not affect the development of NOD during pitavastatin administration. Thus, the highest dose pitavastatin can be safely used in patients with metabolic syndrome who are at high risk of developing diabetes. Trial registration Clinical Trial registration information. URL: https://clinicaltrials.gov/ct2/show/NCT02545231. Unique identifier: NCT02545231.
Sections du résumé
BACKGROUND
Statin therapy reduces the risk of cardiovascular events across a broad spectrum of patients; however, it increases the risk of new-onset diabetes (NOD). Although the highest dose pitavastatin is considered to not be associated with NOD, there are limited data regarding the impact of long-term highest dose pitavastatin use on the development of NOD in patients at high risk of developing diabetes. Therefore, we prospectively compared the differences in the development of NOD between the lowest and the highest dose of pitavastatin in patients at high risk of developing diabetes during a 3-year follow-up.
METHODS
This post hoc analysis of a prospective, single-blinded, randomized study compared the risk of NOD between the highest dose of pitavastatin (4 mg) and the lowest dose of pitavastatin (1 mg) over a 3-year follow-up in patients with acute coronary syndrome. Among 1044 patients of the original study, 667 patients at high risk of developing type 2 diabetes mellitus were in the subgroup analysis. The primary endpoint was a comparison of the differences in the cumulative incidence of NOD in the pitavastatin 1 mg and 4 mg groups during a 3-year follow-up.
RESULTS
With propensity score matching, there were no significant differences in baseline demographic characteristics between the 2 groups. Incidence of NOD was similar between the pitavastatin 1 mg and 4 mg groups [12 of 289 patients (4.2%) and 8 of 289 patients (2.8%), respectively; p = 0.36]. In a prespecified analysis, there were no significant differences in NOD events according to sex, age, diagnosis, body mass index, glucose intolerance, or dyslipidemia.
CONCLUSIONS
Administration of highest-dose pitavastatin did not increase the risk of NOD in patients at high risk of developing diabetes during the 3-year follow-up. Moreover, various risk factors for NOD such as metabolic syndrome components, glucose intolerance, dyslipidemia, obesity, or hypertension did not affect the development of NOD during pitavastatin administration. Thus, the highest dose pitavastatin can be safely used in patients with metabolic syndrome who are at high risk of developing diabetes. Trial registration Clinical Trial registration information. URL: https://clinicaltrials.gov/ct2/show/NCT02545231. Unique identifier: NCT02545231.
Identifiants
pubmed: 31752850
doi: 10.1186/s12933-019-0969-z
pii: 10.1186/s12933-019-0969-z
pmc: PMC6868797
doi:
Substances chimiques
Biomarkers
0
Blood Glucose
0
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Lipids
0
Quinolines
0
pitavastatin
M5681Q5F9P
Banques de données
ClinicalTrials.gov
['NCT02545231']
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
162Références
Am J Cardiol. 2014 Feb 15;113(4):631-6
pubmed: 24360773
QJM. 2011 Feb;104(2):109-24
pubmed: 20934984
Atherosclerosis. 2015 Aug;241(2):409-18
pubmed: 26074315
Korean Circ J. 2016 May;46(3):275-306
pubmed: 27275165
Diabetes Metab J. 2011 Dec;35(6):561-6
pubmed: 22247896
JAMA. 2011 Jun 22;305(24):2556-64
pubmed: 21693744
Atheroscler Suppl. 2015 Jan;16:1-27
pubmed: 25575403
Curr Med Res Opin. 2011 Aug;27(8):1551-62
pubmed: 21682551
Drugs Aging. 2017 Mar;34(3):203-209
pubmed: 28138911
N Engl J Med. 2008 Nov 20;359(21):2195-207
pubmed: 18997196
J Atheroscler Thromb. 2018 May 1;25(5):422-429
pubmed: 29187694
Cardiovasc Diabetol. 2018 Dec 5;17(1):155
pubmed: 30518364
Arch Intern Med. 2012 Jan 23;172(2):144-52
pubmed: 22231607
Am J Cardiol. 2016 Feb 1;117(3):382-7
pubmed: 26732422
Lancet. 2005 Oct 8;366(9493):1267-78
pubmed: 16214597
BMJ. 2013 May 23;346:f2610
pubmed: 23704171
Metabolism. 2014 Jun;63(6):735-45
pubmed: 24641882
Cardiovasc Diabetol. 2017 Aug 22;16(1):107
pubmed: 28830436
J Am Coll Cardiol. 2011 Apr 5;57(14):1535-45
pubmed: 21453832
J Biol Chem. 2002 Jul 19;277(29):25863-6
pubmed: 12032136
Lancet. 2010 Feb 27;375(9716):735-42
pubmed: 20167359
Clin Endocrinol (Oxf). 2015 May;82(5):670-7
pubmed: 25109606
Lancet. 2002 Jul 6;360(9326):57-8
pubmed: 12114044
Circulation. 2013 Jun 11;127(23):e837
pubmed: 23753849
Circulation. 2012 Oct 30;126(18):e282-4
pubmed: 23109518
Diabetologia. 2006 Aug;49(8):1881-92
pubmed: 16685502
Lancet. 2012 Aug 11;380(9841):565-71
pubmed: 22883507
Cardiovasc Diabetol. 2018 Jan 11;17(1):10
pubmed: 29325562
Health Technol Assess. 2007 Apr;11(14):1-160, iii-iv
pubmed: 17408535
PLoS One. 2013 Aug 12;8(8):e71817
pubmed: 23951249
BMJ. 2014 May 29;348:g3244
pubmed: 24874977
Int Heart J. 2018 Mar 30;59(2):315-320
pubmed: 29503404
Korean J Intern Med. 2017 Jul;32(4):656-667
pubmed: 28618772
Nat Rev Endocrinol. 2012 Jan 24;8(4):237-45
pubmed: 22271188
Atherosclerosis. 2008 Dec;201(2):345-52
pubmed: 18472103
Lancet. 2010 Nov 13;376(9753):1670-81
pubmed: 21067804
Circulation. 2018 May 8;137(19):1997-2009
pubmed: 29735587