Hostname: page-component-78c5997874-xbtfd Total loading time: 0 Render date: 2024-11-14T04:25:39.815Z Has data issue: false hasContentIssue false

Bloodstream Infections in Patients Given Treatment With Intravenous Prostanoids

Published online by Cambridge University Press:  02 January 2015

Alexander J. Kallen*
Affiliation:
Division of Healthcare Quality Promotion, National Center for Preparedness, Detection, and Control of Infectious Diseases, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia Epidemic Intelligence Service, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia
Edith Lederman
Affiliation:
Epidemic Intelligence Service, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia
Alexandra Balaji
Affiliation:
Epidemic Intelligence Service, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia
Ingrid Trevino
Affiliation:
Epidemic Intelligence Service, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia
Emily E. Petersen
Affiliation:
CDC Experience Fellowship, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia
Rivka Shoulson
Affiliation:
Epidemiology Elective Program, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia
Lisa Saiman
Affiliation:
Divisions of Pediatric Infectious Diseases, Department of Pediatrics, Columbia University College of Physicians and Surgeons, New York-Presbyterian Hospital, New York, New York Departments of Epidemiology, New York-Presbyterian Hospital, New York, New York
Evelyn M. Horn
Affiliation:
Medicine, New York-Presbyterian Hospital, New York, New York
Mardi Gomberg-Maitland
Affiliation:
Department of Medicine, Section of Cardiology, University of Chicago, Chicago, Illinois
Robyn J. Barst
Affiliation:
Pediatric Cardiology, Department of Pediatrics, Columbia University College of Physicians and Surgeons, New York-Presbyterian Hospital, New York, New York
Arjun Srinivasan
Affiliation:
Division of Healthcare Quality Promotion, National Center for Preparedness, Detection, and Control of Infectious Diseases, Office of Workforce and Career Development, Centers for Disease Control and Prevention, Atlanta, Georgia
*
1600 Clifton Road NE, MS A-35, Atlanta, GA 30333 (AKallen@cdc.gov)

Abstract

Objective.

In September 2006, the Centers for Disease Control and Prevention was notified of cases of gram-negative bloodstream infection (BSI) occurring among outpatients who received an intravenous formulation of the prostanoid treprostinil. An investigation was conducted to determine rates of prostanoid-associated BSI in this patient population and possible risk factors for infection.

Methods.

We performed a retrospective cohort study of patients who had received intravenous formulations of at least 1 of the 2 approved prostanoids (epoprostenol and treprostinil) from January 1, 2004, through late 2006. Chart reviews were conducted at 2 large centers for pulmonary arterial hypertension, and a survey of infection control practices was conducted at 1 center.

Results.

A total of 224 patients were given intravenous prostanoid treatment, corresponding to 146,093 treatment-days during the study period. Overall, there were 0.55 cases of BSI and 0.18 cases of BSI due to gram-negative organisms per 1,000 treatment-days. BSI rates were higher for patients who received intravenous treprostinil than for patients who received intravenous epoprostenol (1.13 vs. 0.42 BSIs per 1,000 treatment-days; P < .001), as were rates of BSI due to gram-negative organisms (0.81 vs. 0.04 BSIs per 1,000 treatment-days; P < .001). Adjusted hazard ratios for all BSIs and for BSIs due to gram-negative organisms were higher among patients given treatment with intravenous treprostinil. The survey identified no significant differences in medication-related infection control practices.

Conclusion.

At 2 centers, BSI due to gram-negative pathogens was more common than previously reported and was more frequent among patients given treatment with intravenous treprostinil than among patients given treatment with intravenous epoprostenol. Whether similar results would be found at other centers for pulmonary arterial hypertension warrants further investigation. This investigation underscores the importance of surveillance and evaluation of healthcare-related adverse events in patients given treatment primarily as outpatients.

Type
Original Article
Copyright
Copyright © The Society for Healthcare Epidemiology of America 2008

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.McLaughlin, W, Shillington, A, Rich, S. Survival in primary pulmonary hypertension: the impact of epoprostenol therapy. Circulation 2002;106:14771482.Google Scholar
2.Barst, RJ, Rubin, LJ, Long, WA, et al.A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. N Engl J Med 1996;334:296302.Google Scholar
3.Lang, I, Gomez-Sanchez, M, Kneussel, M, et al.Efficacy of long-term subcutaneous treprostinil sodium therapy in pulmonary hypertension. Chest 2006;129:16361643.Google Scholar
4.Gomberg-Maitland, M, Tapson, V, Benza, RL, et al.Transition from intravenous epoprostenol to intravenous treprostinil in pulmonary hypertension. Am J Respir Crit Care Med 2005;172:15861589.CrossRefGoogle ScholarPubMed
5.Sitbon, O, Humbert, M, Nunes, H, et al.Long-term intravenous epoprostenol infusion in primary pulmonary hypertension: prognostic factors and survival. J Am Coll Cardiol 2002;40:780788.Google Scholar
6.Tapson, VF, Gomberg-Maitland, M, McLaughlin, W, et al.Safety and efficacy of IV treprostinil for pulmonary arterial hypertension: a prospective, multicenter, open-label, 12 week trial. Chest 2006;129:683688.CrossRefGoogle ScholarPubMed
7.Roberts, TG Jr, Chabner, BA. Beyond fast track for drug approvals. N Engl J Med 2004;351:501505.Google Scholar
8.Product information: Remodulin (treprostinil sodium) injection. Research Triangle Park, NC: United Therapeutics, 2006. Available at: http://www.fda.gov/cder/foi/label/2006/021272s0051bl.pdf. Accessed February 17, 2008.Google Scholar
9.Laliberte, K, Arneson, C, Jeffs, R, Hunt, T, Wade, M. Pharmacokinetics and steady-state bioequivalence of treprostinil sodium (Remodulin) administered by the intravenous and subcutaneous route to normal volunteers. J Cardiovasc Pharmacol 2004;44:209214.CrossRefGoogle ScholarPubMed
10.Yap, RL, Mermel, LA. Micrococcus infections in patients receiving epoprostenol by continuous infusion. Eur J Clin Microbiol Infect Dis 2003;22:704705.Google Scholar
11.Oudiz, RJ, Widlitz, A, Beckmann, XJ, et al.Micrococcus-associated central venous catheter infections in patients with pulmonary arterial hypertension. Chest 2004;126:9094.Google Scholar
12.Rubenfire, M, Mclaughlin, W, Allen, RP, et al.Transition from intravenous epoprostenol to subcutaneous treprostinil in pulmonary arterial hypertension: a controlled trial. Chest 2007;132:757763.Google Scholar
13.Maki, DG, Kluger, DM, Crnich, CJ. The risk of bloodstream infection in adults with different intravascular devices: a systematic review of 200 published prospective studies. Mayo Clin Proc 2006;81:11591171.Google Scholar
14.Lee, SH, Rubin, LJ. Current treatment strategies for pulmonary arterial hypertension. J Intern Med 2005;258:199215.Google Scholar
15.Prescribing information: Flolan (epoprostenol sodium) for injection. Research Triangle Park, NC: Glaxo Smith Kline, 2008. Available at: http://us.gsk.com/products/assets/us_flolan.pdf. Accessed June 15, 2007.Google Scholar
16.Brannan, DK. Biology of microbes. In: Brannan, DK, ed. Cosmetic microbiology: a practical handbook. Washington, DC: CRC Press, 1997:4849.Google Scholar
17.Aronhoff, DM, Peres, CM, Serezani, CH, et al.Synthetic prostacyclin analogs differentially regulate macrophage function via distinct analog-receptor binding specificities. J Immunol 2007;178:16281634.Google Scholar
18.Lindemann, S, Gierer, C, Darius, H. Prostacyclin inhibits adhesion of polymorphonuclear leukocytes to human vascular endothelial cells due to adhesion molecule independent regulatory mechanisms. Basic Res Cardiol 2003;98:815.Google Scholar
19.Eisenhut, T, Sinha, B, Grottrup-Wolfers, E, et al.Prostacyclin analogs suppress the synthesis of tumor necrosis factor-a in LPS-stimulated human peripheral blood mononuclear cells. Immunopharmacology 1993;26:259264.Google Scholar
20.Czeslick, EG, Simm, A, Grand, S, Silber, RE, Sablotzki, A. Inhibition of intracellular tumor necrosis factor (TNF)-a and interleukin (IL)-6 production in human monocytes by iloprost. Eur J Clin Invest 2003;33:10131017.Google Scholar
21.Dumble, LJ, Gibbons, S, Tejpal, N, et al.15 AU81, a prostacyclin analog, potentiates immunosuppression and mitigates renal injury due to cy-closporine. Transplantation 1993;55:11241128.CrossRefGoogle Scholar
22.Centers for Disease Control and Prevention. Bloodstream infections among patients treated with intravenous epoprostenol and intravenous treprostinil for pulmonary arterial hypertension—seven sites, United States, 2003-2006. MMWR Morb Mortal Wkly Rep 2007;56:170172.Google Scholar
23.Baciu, A, Stratton, K, Burke, SP, eds. The future of drug safety: promoting and protecting the health of the public. Washington, DC: Institute of Medicine, 2006.Google Scholar