Abstract Post-transplant Kaposi sarcoma (PT-KS) is the most common Human Herpesvirus 8 (HHV-8) related disease in single-organ transplant recipients (SOTR), with SOTRs at 60- to 200-fold elevated risk for KS compared to the general population. There are two proposed methods of infection: an HHV-8 seropositive donor to a seronegative recipient (primary infection) or viral reactivation in a previously infected recipient following immunosuppression. KS is caused by a reactive polyclonal angioproliferative response towards HHV-8 wherein polyclonal cells change to form oligoclonal cell populations that undergo malignant transformation. Typical presentations of pulmonary KS include dyspnea, nonproductive cough, and hypoxemia. Most common CT findings are interstitial thickening, nodules, pleural effusion, and mediastinal adenopathy. A 58-year-old-woman with history of cystic lung disease and bilateral lung transplant seven months prior presented with progressive dyspnea, cough, chest pain, and CT chest imaging demonstrating interlobular septal thickening, nodules, and bilateral pleural effusions. Her post-transplant course was complicated by a recurrent right pleural effusion, and three courses of steroids for suspected acute rejection. Her infectious work up was significant for a positive seasonal coronavirus respiratory PCR. Following a negative BAL and pleural fluid analysis, she underwent pleuroscopy with pleural biopsies and bronchoscopy with parenchymal and lymph node cryobiopsies, which showed spindle cell lesions that were positive for CD34, ERG, and HHV8 on immunohistochemistry, diagnostic for PT-KS. She was later found to have a positive HHV-8 serum PCR. She transitioned from tacrolimus to sirolimus and started paclitaxel. With treatment, her symptoms improved. The patient’s lack of cutaneous and mucosal KS lesions, and the high concern for acute rejection may have contributed to delay in her diagnosis. Her HHV-8 status prior to transplant was unknown. There are no standard guidelines for universal screening for HHV-8, nor the frequency and duration of monitoring for HHV-8 infection post-transplant. This is largely due to the lack of standardized serologic assays for HHV-8 antibodies. In recipients who are seropositive for HHV-8 or receive organs from seropositive donors, monitoring HHV-8 viral loads after transplant may be a strategy to determine risk of developing clinical disease. Avoidance of over-immunosuppression in high-risk individuals and those with detectable HHV-8 viremia is critical for prevention of development of PT-KS. Some cohort studies have found that liver and lung recipients are most susceptible to HHV-8 infection of SOTRs, and a high suspicion for this rare condition is important to prevent diagnostic and treatment delays. This abstract is funded by: None
Loui et al. (Fri,) studied this question.
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