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Latent human herpes virus 8 (HHV8) infection has been implicated in malignancies occurring predominantly in HIV+ patients, including Kaposi sarcoma (KS), primary effusion lymphoma (PEL), plasmablastic lymphoma and multicentric Castleman disease (MCD).1 However, the oncogenic mechanisms remain enigmatic. Whether different serotypes of HHV8 have the same oncogenic potential, and in patients with concurrent HHV8-related malignancies whether intrapatient genotype variability exists remains to be studied. Such knowledge will be important in understanding the pathogenesis of HHV8-associated neoplasms. We report a case of an HIV+ male with disseminated KS and PEL who subsequently developed recurrent extracavitary relapse of PEL. HHV8 subtyping revealed that both the KS and extracavitary PEL were caused by HHV8 serotype C.
A Chinese man aged 26 years who had sex with men presented with a non-healing left foot lesion, suspected to be a callus. The lesion did not respond to local therapies and progressed to multiple violaceous papules over both his shins. Skin biopsy confirmed HHV8-positive KS. Blood work revealed HIV positivity with a CD4 of 57/μL and viral load of 1.4 x 105 copies/mL. He was started on combination antiretroviral therapy comprising Kaletra, Saquinavir and Truvada. Three months later, an increase in CD4 to 318/μL and drop in viral load to 270 copies/mL heralded progression of KS, consistent with immune reconstitution inflammatory syndrome. While awaiting chemotherapy, the patient was admitted with progressive shortness of breath, increasing bilateral leg oedema, fatigue and night sweats. His performance status declined and he remained bedbound. On examination, extensive mucosal and skin lesions of KS were noted. Bilateral enlarged inguinal lymph nodes were palpable. Bilateral breath sounds were diminished in the middle and lower zones of the lungs. Whole body CT showed multiple enlarged lymph nodes in the neck, mediastinum, axillae and inguinal regions with a conglomerate nodal soft tissue mass along …
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