Disorders of the Pleura: Impact of Pleural Disorders |

A Review of Chronic Graft vs Host Disease-Associated Serositis: What We Know and Don’t FREE TO VIEW

Priyanka Ballal; Patrick Arndt, MD
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University of Minnesota, Minneapolis, MN

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):579A. doi:10.1016/j.chest.2016.08.668
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SESSION TITLE: Impact of Pleural Disorders

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Monday, October 24, 2016 at 07:30 AM - 08:30 AM

PURPOSE: Serositis is an uncommon and poorly described manifestation of chronic graft-versus-host disease (cGVHD) after allogenic hematopoietic stem cell transplant (HSCT). Little is known about cGVHD-associated serositis regarding incidence, risk factors, clinical characteristics or laboratory findings. In addition, no specific therapy is currently available. An improved understanding of cGVHD-associated serositis may allow for earlier detection and identification of novel therapies. We undertook this study to examine our experience of cGVHD-associated serositis at the University of Minnesota.

METHODS: Records of patients with cGVHD after HSCT between 2005 and 2013 were reviewed. Patient characteristics, laboratory data, cultures and results from thoracentesis and pericardiocentesis were examined.

RESULTS: A total of 281 patients developed cGVHD between 2005 and 2013 and 51 of these patients had pleural or pericardial effusions. Of these, 39 were excluded either because effusions occurred before day 100 (not defined as cGVHD) or were due to other etiologies (CHF or infection). Overall, 12 patients met the criteria for cGVHD-associated serositis (incidence 4.2%). Male to female ratio was 1.4 and AML was the most common underlying malignancy (33%). All but one (91.6%) had previously established cGVHD with skin and GI being the most commonly involved organs. Median onset was 158 days after the initial diagnosis of cGVHD and 409 days after HSCT. We found a significant drop in serum albumin at presentation compared to one month prior (median 3.5 vs. 2.8g/dl, P value = 0.038). No significant change was found in the absolute monocyte count. Prior studies have not described analysis of pleural fluid in cGVHD-associated serositis. Six patients underwent thoracentesis (n=14, range=1-3), with 10 out of 14 (71%) being transudates. Two patients underwent pericardiocentesis, with 1 transudate. The mean lymphocyte count in pleural fluid was 55.7% (Range=7-94%). Complete drainage of pleural effusions appeared to be an effective treatment in 2 (14%) patients. Overall, treatment was challenging with patients typically unresponsive to augmentation in immunosuppressives.

CONCLUSIONS: Our data suggests that cGVHD-associated serositis occurs in established as opposed to de novo cGVHD. Effusions were typically transudative and lymphocyte predominate. Overall response to therapy was poor.

CLINICAL IMPLICATIONS: Additional investigation is necessary to improve our understanding of cGVHD associated serositis and its treatment.

DISCLOSURE: The following authors have nothing to disclose: Priyanka Ballal, Patrick Arndt

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