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Diffuse Lung Disease |

Interferon-Beta-Induced Pulmonary Sarcoidosis in a 30 Year-Old Male With Multiple Sclerosis: A Case Report

Helen King, MD; John King, MD
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Mercer University, Macon, GA


Chest. 2013;144(4_MeetingAbstracts):452A. doi:10.1378/chest.1685574
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Abstract

SESSION TITLE: Interstitial Lung Disease Student/Resident Case Report Posters II

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 29, 2013 at 01:30 PM - 02:30 PM

INTRODUCTION: Interferons (IFNs) are commonly used in the treatment of chronic viral hepatitis, multiple sclerosis (MS) and several forms of cancer due to their ability to modulate both antiviral and anti-proliferative responses of the immune system [1]. The first case of interferon-induced sarcoidosis was reported in 1987[2]. With increasing use of IFNs, several cases of IFN-induced sarcoidosis have since been reported, mostly in association with IFN-alpha during treatment of chronic hepatitis C [1]. To our knowledge, we present the fifth case of IFN-beta-induced pulmonary sarcoidosis with only 4 other reported cases [2,3].

CASE PRESENTATION: A 27 year old African-American male with a 6-year history of multiple sclerosis treated with interferon-beta presented for pulmonary consult with persistent patchy bilateral lung infiltrates on chest imaging that failed to resolve after treatment for community acquired pneumonia. Computed tomography of thorax revealed hilar lymphadenopathy, patchy alveolar infiltrates and nodular interstitial changes (figure 2). Past medical history was notable for multiple sclerosis diagnosed 6 years prior based on classic clinical presentation, MRI findings, and the presence of oligoclonal bands in the CSF. The patient had been treated for 6 years with interferon-beta. Labs were notable for an elevated angiotensin converting enzyme. Bronchoscopy was performed with transbronchial biopsy demonstrating noncaseating granulomas (figure 2). AFB and fungal cultures were negative. Pulmonary function testing demonstrated a decrease in diffusing capacity. The diagnosis of interferon-beta induced sarcoidosis was made. Interferon treatment was discontinued, and he was not treated with steroids. Within three months repeat chest radiographs revealed clearing of infiltrates. Repeat pulmonary function testing revealed improvement of diffusing capacity and increase in total lung capacity supporting the diagnosis.

DISCUSSION: Our case demonstrates a clear link between inferferon-beta treatment and the development of sarcoidosis. This diagnosis is supported by similar case-reports in the literature.

CONCLUSIONS: Awareness of the relationship between IFNs and sarcoidosis is important because patients may potentially be misdiagnosed with primary sarcoidosis and continued on a treatment that may potentiate the underlying process.

Reference #1: Alazemi S, Campos MA. Interferon-induced sarcoidosis. Int J Clin Pract. 2006 Feb;60(2):201-11. Review.

Reference #2: Chakravarty SD, Harris ME, Schreiner AM, Crow MK. Sarcoidosis triggered by interferon-Beta treatment of multiple sclerosis: a case report and focused literature review. Semin Arthritis Rheum. 2012 Oct;42(2):206-12.

Reference #3: Petousi N, et al. “Interferon-beta-induced pulmonary sarcoidosis in a 30-year old woman treated for multiple sclerosis: a case report.” J Med Case Rep. 2012 Oct 8;6(1):344.

DISCLOSURE: The following authors have nothing to disclose: Helen King, John King

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