Statins and Candida

Statins Candida infections are the fourth most common cause of nosocomial blood stream infections and are associated with a significant mortality. Delays in antifungal therapy have been associated with increased hospital costs of over US$6,000 per patient and overall mortality. The role of HMG CoA reductase inhibitors (statins) in improving outcomes bacteremic sepsis is currently being debated with recent papers showing significantly improved survival in patients with systemic inflammatory response syndrome in the intensive care unit, in patients with chronic kidney renal disease and patients with community acquired pneumonia and influenza. One explanation of this effect is that statins in animal models have shown to reduce inflammatory markers, in particular the release of cytokines and cytotoxic effects of neutrophils. The reduction in inflammatory cytokines has also been demonstrated in patients in a prospective randomized study comparing simvastatin to placebo where there was a significant reduction in tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in the statin group. Yeasts use the same HMG CoA reductase as humans, however their end-product is ergosterol rather than cholesterol. In vitro studies have demonstrated that simvastatin greatly inhibits the growth of Candida species. This review suggests there is a clinical benefit of statin therapy throughout antifungal therapy in intensive care unit patients with confirmed candidemia.

Statins in Candidemia: clinical outcomes from a matched cohort study. 2010 BMC Infectious Diseases 10: 152 doi:10.1186/1471-2334-10-15210
HMG CoA reductase inhibitors (statins) in patients with bacteremic sepsis have shown significant survival benefits in several studies. There is no data on the effect of statins in candidemic patients, however in-vitro models suggest that statins interfere with ergesterol formation in the wall of yeasts.
This retrospective matched- cohort study from 1/2003 to 12/2006 evaluated the effects of statins on patients with candidemia within intensive care units. Statin-users had candidemia as a cause of their systemic inflammatory response and were on statins throughout their antifungal therapy, while non-statin-users were matched based on age +/- 5 years and co-morbid factors. Primary analysis was 30-day survival or discharge using bivariable comparisons. Multivariable comparisons were completed using conditional logistic regression. All variables with a p-value less than 0.10 in the bivariable comparisons were considered for inclusion in the conditional logistic model.
There were 15 statin-users and 30 non-statin users that met inclusion criteria, all with similar demographics and co-morbid conditions except the statin-users had significantly more coronary artery disease (P<0.01), peripheral vascular disease (P=0.03) and lower median APCAHE II scores (p=0.03). There were no differences in duration of candidemia , antifungal therapy or Candida species between the groups. Statins were associated with lower mortality on bivariable and multivariable analyses compared to controls; although, in the latter the protective effect lacked statistical signficance.
In our small, single-center matched cohort study, statins appear may provide a survival benefit in candidemia, however further studies are warranted to validate and further explore this association.


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