Abstract Introduction Pulmonary lymphoma often shares radiographic findings with interstitial lung disease (ILD) and should be considered in the differential. Concurrent lymphoproliferative malignancy and alcohol associated cirrhosis is rare. There is evidence linking cirrhosis to such malignancies from chronic lymphoid activation. This case highlights the challenges in diagnosis of ILD in a patient with advanced liver disease, also found to have fluid overload- large B cell lymphoma. Case Presentation 66-year-old male with history of decompensated ETOH-associated cirrhosis, previously diagnosed hepatopulmonary syndrome (on 8L and rest, 15L with activity) presents to the hospital with tense ascites. He also had recent CT chest showing bilateral sub-pleural reticulations with associated mild traction bronchiectasis without honeycombing or opacities (Figure A), with pattern indeterminate for UIP. His subsequent CT showed progression in parenchymal disease (Figure B). His serologic workup showed positive ANA and negative for ANCA, MPO, PR3, SS-A, SS-B, SCL 70, and RNP antibody negative. He presented to the ED with complaints of rapidly recurrent tense ascites. Prior SAAG supported portal hypertensive etiology. He undergoes repeat paracentesis with flow cytometry revealing a diagnosis of fluid overloaded-large B cell lymphoma. PET scan did not show disease outside of the peritoneum. His ILD workup was notable for autoimmune features with increasingly positive ANA and positive for PL-7 ab. Given his comorbidities and significant hypoxia, he was not deemed to be a candidate for cancer-directed therapy and comfort care was pursued. Discussion This case highlights the complex interplay between chronic inflammation and systemic disease. Lymphoma can have ILD-like manifestations that poses diagnostic challenges. Rare subtypes of lymphoma can present with infiltrates, ground glass opacities, and organizing pneumonia. Thus, both primary and secondary pulmonary lymphoma should be on the differential for ILD, especially indeterminate patterns. This patient’s presentation was further confounded by strongly positive autoimmune markers. We hypothesize that the patient’s parenchymal disease may have been due to known hepatopulmonary syndrome along with secondary pulmonary lymphoma, with potential autoimmune component as well. The presence of PL-7 myositis AB potentially provides a unifying diagnosis linking both his ILD and fluid overloaded-large B cell lymphoma which has associations with autoimmune syndromes. The interplay between advanced liver disease with severe hepatopulmonary syndrome, ILD, new lymphoma with autoimmune overlap made treatment particularly challenging. There was shared recognitions that patient’s ability to tolerate multiple systemic cancer therapy drugs, transplant, or even high dose steroids carried the risk for life threatening complications. This abstract is funded by: None
Vangala et al. (Fri,) studied this question.