This report documents a rare case of COVID-19-associated constrictive pericarditis (CP) in the setting of a recent COVID-19 infection. A 55-year-old man with a history of hypertension and gout presented with acute hypoxic respiratory failure and was diagnosed with COVID-19 pneumonia with progression to acute respiratory distress syndrome. His hospital course was complicated by a large pericardial effusion; an emergent bedside transthoracic echocardiography was concerning for cardiac tamponade, so pericardiocentesis was performed. A workup with cardiac magnetic resonance imaging showed changes consistent with a diagnosis of CP. Viral and idiopathic aetiologies are the most common cause of CP in the developed world, with COVID-19 now a proposed predisposing viral illness. The virus induces systemic inflammation and pericardial changes that can lead to CP physiology. Imaging modalities including echocardiogram and cardiac magnetic resonance play an integral role in confirming the diagnosis.

Multicentric Castleman disease (MCD) is a rare lymphoproliferative disorder typically manifesting with bulky lymphadenopathy in multiple lymph node stations. We describe an atypical presentation of human herpes virus 8 (HHV8)-associated MCD in a middle-aged man with no significant medical history who presented with 1 month of systemic symptoms. He was found to be HIV-1 positive. A physical examination did not reveal palpable lymphadenopathy. A contrast-enhanced CT scan was notable for hepatosplenomegaly and mildly enlarged scattered lymph nodes in the abdomen and pelvis. A positron emission tomography/CT scan demonstrated hypermetabolic cervical chain lymph nodes. Posterior cervical lymph node pathology showed HHV8-positive MCD with concurrent HIV-associated Kaposi sarcoma. The patient was treated with rituximab and liposomal doxorubicin without response. We emphasise the lack of the hallmark of bulky lymphadenopathy in this patient, and the importance of a timely pathological diagnosis in MCD.

e17012 Background: XIAP acts in both the extrinsic and intrinsic apoptotic pathways as an inhibitor of cell death, protecting cells from a range of triggers. Regulation due to apoptosis resistance may represent a targetable factor for therapeutic intervention in prostate cancer. This study focuses on XIAP as a biomarker and its expression in correlation with disease aggression. Methods: Expression levels of XIAP was analyzed by immunohistochemistry (IHC), graded 1 through 3 according to signal intensity, in radical prostatectomy samples from 90 patients with prostate cancer with a range of phenotypes including: indolent (A), locally advanced (B), progressive to metastatic (C) and de novo metastatic (D). Prognostic data was collected and Fisher’s exact statistical analysis was performed. Secondary analyses included a Fisher’s exact test with a pairwise comparison between individual disease grades and Gleason scores. Results: Higher XIAP protein expression levels on IHC correlated with disease grade and with total Gleason score (p = 0.0008 and p = 0.0002 respectively) by Fisher’s exact test analysis, indicating more aggressive disease phenotypes. Secondary results looked at a pairwise Fisher’s exact analysis comparing XIAP expression levels among disease grades (A-D) and Gleason scores. XIAP expression only significantly differed between those with grade A and D as well as between individuals with grades B and D (measured by Bonferroni-adjusted p-value of 0.003 and 0.018 respectively). Statistical significance was also achieved in XIAP expression levels when comparing among Gleason scores 6 and 8 (p = 0.025), 6 and 9 (p = 0.0125), as well as 7 and 9 (p = 0.030). Conclusions: This study demonstrates a correlation between XIAP expression levels by IHC and aggressiveness of disease, demonstrating clinical significance of XIAP as a prostate cancer biomarker. [Table: see text]