Disorders of the Pleura |

Serositis as a Rare Pulmonary Manifestation of Chronic Graft-Versus-Host Disease FREE TO VIEW

Omar Mohamedaly, MD; Carolyn Mulroney, MD; Samir Makani, MD
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University of California, San Diego, San Diego, CA

Chest. 2013;144(4_MeetingAbstracts):489A. doi:10.1378/chest.1704943
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SESSION TITLE: Pleural Case Report Posters

SESSION TYPE: Affiliate Case Report Poster

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

INTRODUCTION: Pleural effusions are common in the first 100 days after hematopoietic stem cell transplantation (SCT), but are not recognized as a classic manifestation of chronic graft-versus-host disease (cGVHD). Here we describe a patient with persistent pleural and pericardial effusions with no infectious or malignant etiology that improved with immunosuppression.

CASE PRESENTATION: A 69 year-old man with multiple myeloma status post 2 failed autologous SCTs and allogeneic SCT followed by donor lymphocyte infusion presented to the hospital with fevers, malaise and non-productive cough. He had contact with family members with upper respiratory tract infections. Review of systems was notable for loose stools and mild facial erythema. He had a history of COPD with a remote 30 pack-year history of tobacco use. On physical examination, he had mild bibasilar crackles, but no wheezes. Chest CT demonstrated moderate bilateral pleural effusions as well as a moderate pericardial effusion, but no mosaicism to suggest air trapping. Echocardiography showed no tamponade physiology from the pericardial effusion and no evidence of heart failure. Respiratory viral shell culture was positive for parainfluenza 3, bacterial cultures were negative. Diuresis failed to improve his effusions on follow-up 2 months after discharge. Sampling was consistent with exudative, lymphocyte-predominant effusions bilaterally. Microbiological and cytological examination were negative. Flow cytometry showed reduced CD25 expression consistent with the reduced T-regulator cell expression seen in GVHD. Medical thoracoscopy with pleural biopsies was recommended, but declined by the patient. A presumptive diagnosis of cGVHD with a predominant serositis component was made and the patient was started on high-dose prednisone followed by sirolimus. His pleural and pericardial effusions gradually decreased in size, and his skin and gastrointestinal complaints resolved.

DISCUSSION: The main pulmonary manifestation of cGVHD following SCT is bronchiolitis obliterans. Rarely, the predominant manifestation is a serositis that cannot be attributed to other causes. According to National Institutes of Health guidelines, this is neither a distinctive nor diagnostic feature of cGVHD. However, increasing reports of pleural and pericardial effusions suggest serosal involvement may be more common than previously thought. Pleural biopsies, if performed, are expected to show reduced CD25+ T cells.

CONCLUSIONS: Unexplained serositis should prompt consideration of cGVHD in the right clinical context.

Reference #1: Filipiovich AH et al. National Institutes of Health consensus development project on criteria for clinical trials in chronic graft-versus-host disease: I. Diagnosis and staging working group report. Biol Blood Marrow Transplant 2005;11(12):945-956.

Reference #2: Miyauchi M et al. Efficacy of pleural biopsy for diagnosis of pleural effusion due to chronic GVHD after hematopoietic stem cell transplantation. Int J Hematol 2012;96:146-148.

DISCLOSURE: The following authors have nothing to disclose: Omar Mohamedaly, Carolyn Mulroney, Samir Makani

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