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Abstract: Case Reports |

Pulmonary Sarcoidosis as a Complication of Interferon Treatment of Chronic Hepatitis C FREE TO VIEW

Sean Devine, MD; Jeffrey Liu; Rohit Ahuja, MD; Gonzalo Gianella, MD; Daniel Salerno, MD; Ganesan Murali, MD; Kenneth Rothstein, MD; Michael Lippmann, MD
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Albert Einstein Medical Center & Thomas Jefferson University Hospital, Philadelphia, PA


Chest


Chest. 2003;124(4_MeetingAbstracts):246S-247S. doi:10.1378/chest.124.4_MeetingAbstracts.246S
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Abstract

INTRODUCTION:  Two patients with chronic hepatitis C (CHepC) receiving interferon (IFN) and ribavirin (RIB) present with progressive dyspnea and pulmonary infiltrates.CASE PRESENTATIONS: Case(1) A 43-yr old woman with CHepC had a non-productive cough and dyspnea for 6 weeks. There was a remote history of suspected sarcoidosis. She had completed 10 months of intra-muscular injection of Pegylated IFNα-2b every week and RIB 600 mg by mouth twice a day. She was afebrile and anicteric with stable vital signs. Inspiratory crackles were heard at lung bases. Chest xray revealed bilateral infiltrates and chest CT scan revealed diffuse interstitial infiltrates without hilar adenopathy.(Fig:1) Mild restrictive pattern with severe reduction of diffusing capacity was noted on pulmonary function tests. Angiotensin converting enzyme (ACE) level:1400 mmol/L. Cobblestoning of bronchial mucosa was noted on bronchoscopy (Fig:2) and transbronchial lung biopsy(TBB) revealed non-caseating granuloma.(Fig:3). Case (2): A 51 yr-old male smoker with CHepC had dry cough, malaise for 2 months. Prior to the onset of symptoms, he had received IFN and RIB for 4 months. His vital signs were stable. Inspiratory bibasilar crackles were heard. He had a normal ACE level and negative autoimmune workup. A chest xray revealed bilateral interstitial pattern. CT Chest confirmed diffuse reticulonodular disease.TBB revealed noncaseating granulomas. IFN and RIB were discontinued in both patients. Three months later, their cough has improved significantly.DISCUSSION: T helper (Th-1) cells play a major role in the pathogenesis of sarcoidosis. IFN α is known to activate macrophages and T-Cells. This leads to release of IFN-2 and IFN-γ that induce CD4+ cells to differentiate into Th-1 effector cells. Whereas this immune cascade occurs naturally over the course of an infection, exogenous IFN may potentially contribute to the Th-1 response in sarcoidosis.

CONCLUSION:  IFN for hepatitis C is being reported to be associated with either a flare up of underlying indolent sarcoidosis and de novo pulmonary sarcoidosis. This also support an immunomodulatory hypothesis behind the development of sarcoidosis.

DISCLOSURE:  S. Devine, None.

Monday, October 27, 2003

4:15 PM - 5:45 PM


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