Effects of discontinuing or continuing ongoing statin therapy in severe sepsis and septic shock: a retrospective cohort study

Dessap, Armand Mekontso; Ouanes, Islem; Rana, Nerlep Kaur; Borghi, Beatrice; Bazin, Christophe; Katsahian, Sandrine; Hulin, Anne; Brun‐Buisson, Christian

doi:10.1186/cc10317

Cited by 21 publications

(6 citation statements)

References 28 publications

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“…Although not found to be statistically significant, daptomycin patients receiving a concomitant statin had a lower frequency of death versus statin non-recipients. These findings among daptomycin recipients are consistent with other retrospective studies that have shown beneficial effects with statin use in bacteremia, including reduction in all-cause mortality and bacteremia-related death [ 13 , 14 ]. Given the lack of relationship between statin use and CPK elevation and the effect on mortality, the recommendations surrounding the concomitant statin use may warrant further investigation for daptomycin recipients.…”

Section: Discussionsupporting

confidence: 90%

Effect of Concomitant 3-Hydroxy-3-Methyl-Glutaryl-CoA Reductase Inhibitor Therapy on Creatine Phosphokinase Levels and Mortality Among Patients Receiving Daptomycin: Retrospective Cohort Study

et al. 2014

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IntroductionThe prescribing information for daptomycin recommends discontinuing statin therapy during receipt of daptomycin. The literature supporting this recommendation is sparse. The objectives of this study were to examine the impact of 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors (statins) on creatine phosphokinase (CPK) elevations and mortality among patients receiving daptomycin therapy.MethodsA retrospective cohort study was performed among daptomycin recipients in the Upstate New York Veterans’ Healthcare Administration from September 15, 2003 to July 1, 2013. Inclusion criteria were: (1) daptomycin for ≥48 h, (2) availability of baseline CPK value and (3) >1 CPK level measurement taken while on therapy. The following were extracted from medical records: demographics, comorbidities, laboratory data, medication history (daptomycin, statins and concomitant drugs known to increase CPK), Acute Physiology and Chronic Health Evaluation (APACHE)-II score and vital status at 30 days. The exposure of interest was use of statins. The primary outcome was CPK elevation defined as a CPK value ≥3 times the upper limit of normal (ULN) if baseline CPK was normal, and ≥5 times ULN if baseline CPK was elevated. The secondary outcome was death within 30 days of commencing daptomycin.ResultsA total of 233 patients were included in this analysis. Among these patients, 53 received concomitant statin therapy. Most baseline clinical characteristics were similar between statin recipients and non-recipients. Five (2.1%) patients experienced a CPK elevation; 3/53 (5.7%) were statin recipients and 2/180 (1.1%) received daptomycin alone (p = 0.08). All patients with CPK elevations had normal baseline CPK values. No effect modification was observed by use of other concomitant medications known to increase CPK values. Death was observed more frequently among statin non-recipients (17.2%) than recipients (9.4%).ConclusionsAmong patients receiving daptomycin, no significant difference was observed in frequency of CPK elevation between statin recipients and non-recipients.Electronic supplementary materialThe online version of this article (doi:10.1007/s40121-014-0041-y) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 90%

Effect of Concomitant 3-Hydroxy-3-Methyl-Glutaryl-CoA Reductase Inhibitor Therapy on Creatine Phosphokinase Levels and Mortality Among Patients Receiving Daptomycin: Retrospective Cohort Study

et al. 2014

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“…As controversial data are present in the literature concerning the safety of statin therapy in septic patients [ 30 , 31 ], our current data add a cautionary note on the use of lovastatin in septic experimental conditions, both in vitro and in vivo, owing to the potential increase of the pro-inflammatory activity of statins in the presence of high levels of endotoxin. In conclusion, we describe evidences for a dose-dependent pro-inflammatory role of Lova in association with LPS on cellular and animal models.…”

Section: Discussionmentioning

confidence: 81%

Lovastatin Dose-Dependently Potentiates the Pro-inflammatory Activity of Lipopolysaccharide Both In Vitro and In Vivo

Zanin

Marcuzzi

Kleiner

et al. 2013

J. of Cardiovasc. Trans. Res.

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Since contradictory findings have been reported on potential effects of statins in modulating the inflammatory response, we have analysed the biological activity of lovastatin both in vitro using the Raw 264.7 murine macrophagic cell line and in vivo using BALB/c mice. When added to Raw 264.7 cells in combination with lipopolysaccharide, lovastatin significantly potentiated the release of interleukin-1β, interleukin-6 and interleukin-12 with respect to lipopolysaccharide alone and showed an additive effect on the release of nitric oxide. Similarly, when lovastatin was intraperitoneally administrated to BALB/c mice, it did not induce any pro-inflammatory effect when used alone, but it significantly potentiated the pro-inflammatory activity of lipopolysaccharide, in terms of number of intraperitoneal cells and serum levels of serum amyloid A, interleukin-1β, interleukin-6 and interleukin-12. A potential clinical implication of our study is that lovastatin might exert a pro-inflammatory activity in subjects affected by inflammatory processes, with clinically evident or subclinical infections.

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“…In the early postoperative period, 67% of statin takers were restarted on statin therapy. While stopping statins postoperatively could potentially have masked any protective effect of statin therapy, prior studies have shown no clear consequences of statin cessation in critical illness (41,42). Moreover, any protective effect of statins would most plausibly depend on drug concentrations at the time of the inciting event (i.e.…”

Section: Discussionmentioning

confidence: 99%

Preoperative Statin Administration Does Not Protect Against Early Postoperative Acute Respiratory Distress Syndrome

Yadav

Lingineni²,

Slivinski³

et al. 2014

Anesthesia &Amp; Analgesia

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Background Statins have been shown to possess anti-inflammatory and immunomodulatory effects. The objective of this study was to determine if preoperative statin therapy is associated with a reduced frequency of postoperative ARDS in surgical populations at increased risk of developing ARDS. Methods We performed a retrospective cohort evaluation of the association between preoperative statin therapy and early postoperative ARDS in patients undergoing elective high-risk thoracic and aortic vascular surgery. The association between preoperative statin therapy and postoperative ARDS was assessed using propensity-adjusted analyses to control for indication bias and confounding factors. Results Of 1845 patients, 722 were receiving preoperative statin therapy. 120 patients developed postoperative ARDS. Frequencies of ARDS among those receiving statin therapy versus those who were not was 7.2% and 6.1%, respectively (OR = 1.20, 95% CI = 0.83–1.75; p=0.330). Neither the stratified propensity score analysis (pooled OR 0.93; 95% CI = 0.60-1.43) nor matched analysis (OR = 0.78; 95% CI = 0.48-1.27) identified a statistically significant association between preoperative statin administration and postoperative ARDS. When compared to matched controls, patients who developed postoperative ARDS did not differ in mortality (7.7% versus 8.8%, p=0.51), hospital length of stay (21 days versus 15 days, p=0.21) or ventilator free days (24 days versus 25 days, p=0.62). Conclusions In patients undergoing high-risk surgery, preoperative statin therapy was not associated with a statistically significant reduction in postoperative ARDS. These results do not support the use of statins as prophylaxis against ARDS in patients undergoing high-risk surgery.

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Effects of discontinuing or continuing ongoing statin therapy in severe sepsis and septic shock: a retrospective cohort study

Cited by 21 publications

References 28 publications

Effect of Concomitant 3-Hydroxy-3-Methyl-Glutaryl-CoA Reductase Inhibitor Therapy on Creatine Phosphokinase Levels and Mortality Among Patients Receiving Daptomycin: Retrospective Cohort Study

Effect of Concomitant 3-Hydroxy-3-Methyl-Glutaryl-CoA Reductase Inhibitor Therapy on Creatine Phosphokinase Levels and Mortality Among Patients Receiving Daptomycin: Retrospective Cohort Study

Lovastatin Dose-Dependently Potentiates the Pro-inflammatory Activity of Lipopolysaccharide Both In Vitro and In Vivo

Preoperative Statin Administration Does Not Protect Against Early Postoperative Acute Respiratory Distress Syndrome

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