Disorders of the Pleura |

Utility of Pleural Fluid ADA in Malignant Pleural Effusions Secondary to Renal Cell Carcinoma on Sunitinib FREE TO VIEW

Mohammed Malik, MD
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The University of Oklahoma, Oklahoma City, OK

Chest. 2014;146(4_MeetingAbstracts):484A. doi:10.1378/chest.1994764
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SESSION TITLE: Pleural Student/Resident Case Report Posters

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: The concordance between parapneumonic and malignant pleural effusions can lead to a false diagnosis amongst patients with known metastatic pulmonary disease, specifically in an immigrant population. We describe a case of a near misdiagnosis of a parapneumonic effusion for a malignant effusion in the setting of metastatic renal cell carcinoma (RCC).

CASE PRESENTATION: A 49 year-old Hispanic male with stage IV RCC with multiple pulmonary metastases presented with a one-day history of progressively worsening dyspnea. He initially presented in October 2013 with vague abdominal pain and hypercalcemia. At that time, a pleural biopsy demonstrated pathology consistent with metastatic RCC. A subsequent PET CT demonstrated a left-sided renal mass concerning for primary renal cell carcinoma. Initially, we planned for a nephrectomy. However, this was cancelled due to the patient’s worsening hypoxia, with large and rapidly expanding tumor burden. He underwent 8 weeks of chemotherapy with temsirolus and was transitioned to oral sunitinib. A chest CT done in the ER showed a multi-loculated left-sided pleural effusion. A diagnostic thoracentesis was done in interventional radiology. Pleural fluid revealed total protein of 4, LDH of 129, pH of 8.0, and ADA of 4.3 U/L. Serum studies showed total protein of 6.4 and LDH of 198. Based on Light’s Criteria his effusion was classified as an exudate. Due to his immigrant status and recent chemotherapy, fluid was sent for microbiology, including an acid fast stain. On the day of his expected discharge, cultures demonstrated acid fast bacilli. Infectious Disease was contacted and the patient was started on therapy for mycobacterium tuberculosis, pending final cultures.

DISCUSSION: Initial diagnostic evaluation of pleural fluid often consists of classification based on Light’s Criteria. The role of Light’s Criteria in differentiating malignant from paraneumonic effusions is non-specific. Further, diagnostic testing of pleural fluid including glucose, ADA, and pH warrant attention. In our patient, the ADA was not as high as expected. ADA in tuberculous effusions is produced by monocytes and macrophages. Tyrosine kinase inhibitors, such as sunitinib, block the proliferation of these cell lines.

CONCLUSIONS: Tyrosine Kinase inhibitors such as sunitinib should be avoided or used with great caution in patients native to areas where tuberculosis is endemic. This can lead not only to misdiagnosed parapneumonic effusions but undiagnosed tuberculosis as well.

Reference #1: Light, RW, Macgregor, MI, Luchsinger, PC, et al. Pleural effusions: the diagnostic separation of transudates and exudates. Ann Intern Med1972;77,507-513.

Reference #2: Chow CW, Grinstein S, Rotstein OD. Signaling events in monocytes and macrophages. New Horiz. 1995 May;3(2):342-51.

Reference #3: Valdes L, et al. Adenosine deaminase (ADA) isoenzyme analysis in pleural effusions: diagnostic role, and relevance to the origin of increased ADA in tuberculous pleurisy. Eur Respir J 2009; 33: 816-820

DISCLOSURE: The following authors have nothing to disclose: Mohammed Malik

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