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Ku JH, Winthrop KL, Varley CD, et al. Implications for Biologic Therapy: Staphylococcus aureus Decolonization of Individuals With a History of Recurrent Skin and Soft-Tissue Infections. JAMA Dermatol. 2013;149(8):986–989. doi:10.1001/jamadermatol.2013.4405
Copyright 2013 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
Patients with immune-mediated inflammatory diseases (IMIDs) are at an increased risk for skin and soft-tissue infections (SSTIs),1 presumably owing to colonizing organisms like Staphylococcus aureus.1 Although few organism-level data are available by which to judge whether these agents increase the risk of S aureus infection specifically, biologic therapies widely used to treat IMIDs have been shown to increase the risk of SSTIs and other serious infections, complicating therapeutic management of IMIDs.2,3 Although staphylococcal decolonization therapy has been used in various health care settings, no description of such therapy exists for patients with IMIDs with recurrent SSTIs on biologic therapies. For those patients with recurrent infections thought to be due to S aureus, decolonization could theoretically provide protection against subsequent infection.
We retrospectively reviewed our experience within our infectious disease (ID) referral clinic at Oregon Health & Science University (OHSU) in Portland. We identified patients with psoriasis, psoriatic arthritis, or rheumatoid arthritis (RA) being treated with, or considering, biologic therapy, who were referred to the ID clinic from June 2007 through February 2011 owing to prior SSTIs. Following systematic assessment, those found to be colonized were offered decolonization therapy with rifampin, 300 mg twice daily; doxycycline, 100 mg twice daily; mupirocin, 2%, ointment thrice daily to the nares and perineal region for 1 week; and daily chlorhexidine gluconate showers for 7 days (thrice weekly recommended indefinitely thereafter). Patients without cultures that were positive for S aureus were offered the same decolonization therapy if clinical suspicion for colonization was high based on the patient’s medical history (ie, recurrent boils or folliculitis). For patients treated with decolonization therapy, we collected demographic, clinical, and laboratory data in the 12 months prior to consultation and after decolonization.
This study was reviewed by the OHSU institutional review board and was approved with a waiver of informed consent and Health Insurance Portability and Accountability Act research authorization.
We identified 19 patients referred to the ID clinic by our rheumatology or dermatology clinics for SSTIs in the context of prior or planned immunosuppressive therapy. At the time of consult, 16 patients (84%) were colonized with S aureus and 15 (79%) were actively receiving immunosuppressive therapy (Table 1). Nine (53%) reported household pet contacts in the 12 months prior to decolonization. Seventeen (90%) were prescribed decolonization therapy (Table 1). All patients reported adherence to their regimen without adverse events. Sixteen (90%) initiated or resumed immunosuppressive therapy after decolonization (Table 2) and had ongoing follow-up within referring specialty clinics for a mean of 17 months (range, 1-47 months) after decolonization. Four patients (24%) had recurrent SSTI postdecolonization (incidence rate, 1.6 per 100 person-years).
We report our clinical experience in providing S aureus decolonization therapy for patients with SSTI in whom biologic therapy was either interrupted or planned. All patients successfully completed decolonization, and most subsequently remained infection-free for long time periods despite resuming or initiating biologic or other immunosuppressive therapy. Our results suggest that decolonization therapy could be useful in preventing SSTIs in such patients, potentially affording them less infection-related treatment interruptions in their immunosuppressive therapies.
The decolonization regimen used in this study has been previously reported to be effective, although 50% of such patients in prior studies are known to become recolonized at 6 months after therapy, likely owing to contact with colonized household members or other close contacts.4 Several methods to eradicate S aureus colonization have been published, although most patients experience a high rate of recolonization or a lack of long-term follow-up. A recent open-label trial5 evaluating hygiene education, intranasal mupirocin, and bleach baths observed a 71% success rate in decolonization at 4 months after therapy.
Given the retrospective nature of our cases series and lack of a comparator group, we are limited in drawing firm conclusions regarding the effectiveness of S aureus decolonization in this setting. However, nearly all patients in our series were followed subsequently in their referring clinics and systematically reevaluated for SSTI recurrence. The incidence rate of recurrent SSTI in this small group of decolonized individuals was low, at least compared with that observed in other population-based studies of patients with RA.1,6
While it seems plausible, it is unclear if biologic therapy increases SSTI risk in patients colonized with S aureus and whether such patients benefit from decolonization. However, for those with recurrent SSTIs causing interruption in biologic therapy decolonization therapy might facilitate continued use of biologic therapy.
Accepted for Publication: March 16, 2013.
Correspondence: Jennifer H. Ku, MPH, Department of Ophthalmology, Oregon Health & Science University, 3375 Terwilliger Blvd SW, Portland, OR 97239 (email@example.com).
Published Online: June 19, 2013. doi:10.1001/jamadermatol.2013.4405.
Author Contributions: Ms Ku and Dr Winthrop had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Ku, Winthrop, Varley, Sullivan, Deodhar.
Acquisition of data: Ku, Winthrop, Varley, Blauvelt, Deodhar.
Analysis and interpretation of data: Ku, Winthrop, Sullivan, Ehst, Blauvelt.
Drafting of the manuscript: Ku, Winthrop, Varley, Sullivan.
Critical revision of the manuscript for important intellectual content: Ku, Winthrop, Varley, Ehst, Blauvelt, Deodhar.
Statistical analysis: Ku, Winthrop, Varley.
Administrative, technical, and material support: Ku, Winthrop, Varley, Sullivan, Blauvelt, Deodhar.
Study supervision: Winthrop, Ehst, Blauvelt, Deodhar.
Conflict of Interest Disclosures: Dr Winthrop has received a research grant from Pfizer and scientific advisory board or consultant fees from Amgen, Abbott, Genentech, and Pfizer. Dr Blauvelt has received scientific advisory board and consulting fees from Janssen, Abbott, Amgen, Novartis, Pfizer, Anacor, Takeda, and Boehringer Ingelheim. Dr Deodhar has received research grants from Amgen, Genentech, Janssen, Abbott, Novartis, and UCB pharmaceuticals; and consulting fees and speaking honoraria from Abbott, Pfizer, and UCB.
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