The histologic classification of the lymphoma, as well as the locations and severity of the disease, all influence the clinical presentation of HIV-related lymphomas.[4] HIV-related lymphomas are more likely to present with advanced stage disease, constitutional symptoms (also known as "B" symptoms; fever, weight loss, and night sweats), extranodal involvement, or disease involving unusual locations (such as the body cavity or soft tissue) than lymphomas in the HIV-negative population.[5][6]
Diffuse large B-cell lymphoma is a highly aggressive type of B-cell lymphoma. It is distinguished by the widespread proliferation of large neoplastic B lymphocytes with nuclei that are equal to or larger than normal histiocytic nuclei.[10] The illness manifests with B symptoms at an advanced stage of the illness. It mostly affects patients who are severely immunosuppressed and can occur at nodal or extranodal sites, with the gastrointestinal tract being the most common site.[11][12] It makes up between 45 and 50 percent of all lymphomas seen in this group, making it the most prevalent AIDS-associated lymphoma subtype.[13][14] All ages are affected by DLBCL, which typically manifests as a rapidly growing lymph node mass in the neck or abdomen.[15] Up to 40% of patients have extranodal extramedullary disease, and about 30% of patients exhibit B symptoms.[16]
The second most prevalent NHL subtype that affects HIV-positive individuals with a comparatively high CD4 cell count is Burkitt's lymphoma. Patients typically have elevated lactate dehydrogenase levels and poor performance status.[15] The central nervous system is involved in 8 to 28% of cases, with extranodal involvement occurring more frequently.[11] It usually manifests at a younger age and with CD4 cell counts greater than 200 cells/μL.[17] It develops quickly and is a kind of tumor that starts from B cells. In addition, it is fatal if untreated.[18]Burkitt's lymphoma is linked to a high incidence of oral cavity involvement and makes up 10-15% of AIDS-defining lymphomas.[15] Three clinical subtypes of Burkitt's lymphoma have been identified: endemic, sporadic, and immunodeficiency-related.[19] Thirty to forty percent of AIDS-related NHL cases are Burkitt's lymphoma subtype, which is most prevalent in HIV/AIDS patients.[18]
Plasmablastic lymphoma (PBL) originates from terminally differentiated, activated B-cells at the post-germinal center that are changing from immunoblasts to plasma cells.[15] About 2% of all AIDS-associated lymphomas are PBL-associated lymphomas.[26]HIV infection is closely associated with this uncommon form of lymphoma, which primarily affects the oral cavity.[27][verification needed]
With a widespread proliferation of massive neoplastic cells that resemble B-cell immunoblasts but have the immunophenotype of plasma cells, it is incredibly aggressive.[28]
Hodgkin lymphoma (HL) is one of the most common cancers that do not indicate AIDS, and since highly active antiretroviral therapy was introduced, its incidence has increased. It is a germinal center-derived cell that produces Hodgkin Reed–Sternberg (HRS) cells.[15] It is more common in immunocompromised individuals, especially those with HIV.[29] Compared to mild immune compromise, the incidence of HL is lower in states of extreme immunodeficiency. It's possible that there was insufficient immunological contact between non-neoplastic inflammatory cells and HRS cells.[30]
Mechanism
HIV-positive patients have a higher incidence of malignancies for a variety of reasons. These consist of inflammation, cytokine dysregulation, and persistent antigenic stimulation.[15] Moreover, oncogenic viruses are more likely to infect HIV/AIDS patients.[31] Thus, a variety of factors, such as a compromised immune system, genetic changes, viral infection, and persistent B cell activation, contribute to the pathogenesis of HIV/AIDS-associated lymphoma.[15]
^Rigolet A, Bossi P, Caumes E, et al. (September 2001). "Caractéristiques épidémiologiques et évolution de l'incidence des lymphomes cérébraux primitifs observés chez 80 patients infectés par le VIH entre 1983 et 1999" [Epidemiological features and incidence trends of primary cerebral lymphomas observed in 80 HIV-infected patients from 1983 to 1999]. Pathologie-biologie (in French). 49 (7): 572–5. doi:10.1016/S0369-8114(01)00206-1. PMID11642021.
^"UpToDate". UpToDate. Retrieved February 10, 2024.
^Heise, Walter (2010). "GI-lymphomas in immunosuppressed patients (organ transplantation; HIV)". Best Practice & Research Clinical Gastroenterology. 24 (1). Elsevier BV: 57–69. doi:10.1016/j.bpg.2010.01.001. ISSN1521-6918. PMID20206109.
^Abellán-Martínez, Javier; Guerra-Vales, Juan-Manuel; Fernández-Cotarelo, María-José; González-Alegre, María-Teresa (2009). "Evolution of the incidence and aetiology of fever of unknown origin (FUO), and survival in HIV-infected patients after HAART (Highly Active Antiretroviral Therapy)". European Journal of Internal Medicine. 20 (5). Elsevier BV: 474–477. doi:10.1016/j.ejim.2009.01.004. ISSN0953-6205. PMID19712847.
^Castillo, Jorge J.; Bibas, Michele; Miranda, Roberto N. (April 9, 2015). "The biology and treatment of plasmablastic lymphoma". Blood. 125 (15). American Society of Hematology: 2323–2330. doi:10.1182/blood-2014-10-567479. ISSN0006-4971. PMID25636338.
Levine, Alexandra M. (1991). "Epidemiology, Clinical Characteristics, and Management of AIDS-Related Lymphoma". Hematology/Oncology Clinics of North America. 5 (2). Elsevier BV: 331–342. doi:10.1016/s0889-8588(18)30445-3. ISSN0889-8588. PMID2022597.
