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AIDS-Related Malignancy
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Mark Bower, Elena Gervasi, Alessia Dalla Pria
The clinical management of HIV patients with primary effusion lymphoma and plasmablastic lymphoma remains uncertain because of the relatively low numbers of patients. The prognosis for these patients appears to be significantly inferior to other AIDS-related lymphomas.21,22 These lymphomas are CD20-negative and in view of the poorer prognosis are generally treated with EPOCH rather than CHOP. In these lymphomas as well as DLBCL, prophylaxis against central nervous system relapse is advocated using the same criteria that are applied in the HIV-negative population.23
What happens in Leukemias, Lymphomas, and Myelomas?
Published in Tariq I Mughal, John M Goldman, Sabena T Mughal, Understanding Leukemias, Lymphomas, and Myelomas, 2017
Tariq I Mughal, John M Goldman, Sabena T Mughal
Currently several strains of HTLV have been identified and at least three of these have been causally associated with a variety of cancers arising from the lymphatic system: HTLV-I has been associated with ATLL, as described above; HTLV-II has been implicated in a few cases of prolymphocytic leukemia and CLL, but this finding needs further confirmation. Scientists have also reported a possible causal link between HTLV-V and a unique lymphoma, which affects the skin, called cutaneous T-cell lymphoma. Recently, a causal association between the hepatitis C virus and low-grade lymphomas has been reported; this will require further confirmation. An observation linking a subtype of the human herpes virus (called HHV-8) and a very rare form of lymphoma called primary effusion lymphoma has also been reported.
Cidofovir and Brincidofovir
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Graciela Andrei, Robert Snoeck
Human herpesvirus 8 is the cause of several proliferative diseases of which Kaposi’s sarcoma is probably the most frequent and best known. The limited case studies of CDV therapy of Kaposi’s sarcoma concluded that CDV was inactive, even when injected directly into the cutaneous tumor (Hammoud et al., 1998; Little et al., 2003; Simonart et al., 1998a; Simonart et al., 1998b). In contrast, complete remission has been reported in patients with primary effusion lymphoma (a B-cell malignancy associated with Kaposi’s sarcoma) who were treated with CDV intracavity. This may be explained by the higher amount of cells undergoing lytic replication in primary effusion lymphoma compared to Kaposi’s sarcoma (Halfdanarson et al., 2006; Luppi et al., 2005; Stingaciu et al., 2010).
Daratumumab induces cell-mediated cytotoxicity of primary effusion lymphoma and is active against refractory disease
Published in OncoImmunology, 2023
Prabha Shrestha, Yana Astter, David A. Davis, Ting Zhou, Constance M. Yuan, Ramya Ramaswami, Hao-Wei Wang, Kathryn Lurain, Robert Yarchoan
Primary effusion lymphoma (PEL) is a rare but aggressive non-Hodgkin B-cell lymphoma and occurs primarily in individuals with HIV. It is caused by Kaposi sarcoma-associated herpesvirus (KSHV). KSHV also causes multicentric Castleman disease (MCD), Kaposi sarcoma (KS), and KSHV-associated inflammatory cytokine syndrome (KICS).1–5 Approximately 60–90% of PEL tumors are co-infected with Epstein–Barr virus (EBV).6 PEL is usually treated with combination anthracycline-containing chemotherapy and antiretroviral therapy (ART). Cures are observed in 40% to 50% of patients, but median overall survival is only about 2 years because many patients experience refractory disease or relapse.7,8 Therefore, there is an urgent need to develop new effective therapies for PEL.
Prevention of viral infections in solid organ transplant recipients in the era of COVID-19: a narrative review
Published in Expert Review of Anti-infective Therapy, 2022
Paraskevas Filippidis, Julien Vionnet, Oriol Manuel, Matteo Mombelli
HHV-8 or Kaposi-Sarcoma-associated Herpes Virus belongs to the family of Gammaherpesvirinae. The seroprevalence of HHV-8 is highly variable depending on geographical location, ranging from 3% to 8% in the US [166] up to almost 90% in the sub-Saharan Africa [167,168]. In SOT recipients, the most common clinical manifestation of HHV-8 infection is cutaneous and visceral Kaposi sarcoma, multicentric Castelman disease and primary effusion lymphoma. No established preventive strategy is currently available for HHV-8 in SOT recipients. In endemic regions, determination of HHV-8 serostatus of donor and recipient followed by viral monitoring may identify patients at high risk for HHV-8-associated disease [169]. Modulation of immunosuppression (for example, switch to mTOR inhibitors) and/or administration of valganciclovir may be considered in case of reactivation or donor-related primary infection [165].
Tentative diagnostic criteria and disease severity classification for Castleman disease: A report of the research group on Castleman disease in Japan
Published in Modern Rheumatology, 2018
Shino Fujimoto, Tomohiro Koga, Atsushi Kawakami, Hiroshi Kawabata, Shinichiro Okamoto, Masao Mizuki, Shingo Yano, Makoto Ide, Kazuko Uno, Katsumi Yagi, Toshiyuki Kojima, Minoru Mizutani, Yukihiro Tokumine, Norihiro Nishimoto, Hiroshi Fujiwara, Shin-ichi Nakatsuka, Kazuko Shiozawa, Noriko Iwaki, Yasufumi Masaki, Kazuyuki Yoshizaki
Castleman disease (CD) is a refractory lymphoproliferative disorder of unknown origin [1,2] and is present as two distinct clinical entities: the localized form (unicentric CD (UCD)) and the multicentric form (multicentric CD (MCD)) [3,4]. In addition, this disease is pathologically classified into the hyaline-vascular (HV), plasma cell (PC) and mixed types [5]. Most cases of UCD exhibit the HV type, whereas patients with MCD predominantly have the PC type or mixed type [5]. Depending on the clinical and pathologic subtypes, the clinical manifestations and management strategies of this disease are distinct. Patients with UCD typically have localized lymph nodes and are generally asymptomatic or mildly symptomatic [6,7]. Unlike UCD, MCD is a systemic disease with peripheral lymphadenopathy and systemic symptoms include fever, night sweats, weight loss and fatigue [6,7]. Although the pathogenesis of MCD is poorly understood, these manifestations are essentially resulted from proinflammatory hypercytokinemia including interleukin-6 (IL-6) [8,9]. In addition, a part of MCD is associated with the human immunodeficiency virus (HIV) [10] and human herpesvirus 8 (HHV-8) infection [11]. Some HHV8-positive MCD patients complicate with Kaposi’s sarcoma and rare B cell lymphomas called primary effusion lymphoma occurring in the body cavities [12,13]. Of note, there is also a group of HIV-negative and HHV-8-negative MCD patients with unknown etiology and pathophysiology, referred to as idiopathic MCD (iMCD) [14,15].