Ординатура / Офтальмология / Английские материалы / Primary Intraocular Lymphoma_Chan, Gonzales_2007

34 Primary Intraocular Lymphoma

increasing since the report by Eby et al. in 1988. For the group with inclusion of never-married males, the incidence rate in patients below 60 years of age was 1.7 per 10 million population, and in those over 60 years of age it was 7.3 per 10 million in population for the period 1973–1975. The period 1991–1993 saw the incidence rate increased to 16.9 in 10 million and 100.9 in 10 million for those under 60 years and those over 60 years, respectively. With the inclusion of never-married men, the incidence rates started at 1.9 and 8.5 in 10 million for those less than 60 years and those greater than 60 years, respectively. By 1993, the incidence rates had increased to 59.6 (for patients less than 60 years of age) and 103.6 (for those over the age of 60 years) in 10 million population. Corn and colleagues showed their findings graphically for PCNSL with non-PCNSL NHLs, gliomas, and glioblastoma. PCNSL certainly showed a lesser incidence rate for all periods of time than the other three tumors analyzed, but the rate of increase in incidence was greater than that for nonPCNSL NHLs. While Fine and Mayer and Eby et al. recognized that advancements in imaging of intracranial lesions and screening had been made that might explain in part the rise in incidence, Corn and colleagues also mentioned that perhaps the incidence of the disease would have been underestimated, at least in AIDS patients. The reason for this is due to a disinclination of surgeons to biopsy AIDS patients with brain masses.92 Since the diagnosis of PCNSL is based on histopathology (i.e. tissue must show evidence of a lymphomatous process), the lack of biopsies in AIDS patients could certainly leave many cases of PCNSL in this population underdiagnosed. In addition, after extrapolation to the year 2000, PCNSL showed no decline or leveling off. The trends for other tumors, including non-PCNSL NHLs, gliomas, and glioblastomas showed a modest increase in incidence. The rate of diagnosis for PCNSL had also increased over the interval of time analyzed.

The Role of Infectious Agents in PCNSL and PIOL. Investigators have suggested a role involving oncogenic viral infections. Though infectious agents could potentially play a role in causing PCNSL in immunocompetent patients, no definitive association has been made. EBV has been associated with Burkitt’s lymphoma and PCNSL.22,93,94 Intriguingly, Corboy et al. found that DNA of the human herpes virus 8 (HHV-8), an infectious agent associated with Kaposi’s sarcoma, primary effusion lymphomas, Castleman’s disease, and multiple myeloma, was detected in the 56% of PCNSLs from 36 patients with and without AIDS.95 Unlike the lymphomatous cells, the surrounding

Epidemiology of Primary Intraocular Lymphoma 35

normal brain tissue was negative for the viral DNA. Others have described findings of infectious agents in PCNSLs, including PIOLs, occurring in nonAIDS patients. Chan and colleagues from the National Eye Institute (NEI) discovered that in four ocular samples of PIOL cells of 13 examined, there was DNA from HHV-8; among these specimens only one from a patient with AIDS contained EBV DNA.96 Later, Shen and colleagues reported that two ocular specimens of 10 PIOL immunocompetent patients contained Toxoplasma gondii DNA.97 Though these findings in immunocompetent patients are captivating, there has been no definitive link of infectious agents causing PCNSLs or PIOLs in this population.

Other infectious agents may be associated with other ocular lymphomatous processes. For example, some extranodal marginal zone lymphomas of mucosa-associated lymphoid tissue (MALT), specifically gastric MALTs (arising from the major causative agent in gastric ulcers) have been found to arise due to infection by the bacterium Helicobacter pylori.98,99 Indeed, Helicobacter pylori DNA is found in conjuncitval MALT lymphoma.100 Currently, 15% of NHLs in patients infected with HIV are PCNSLs, while this malignancy makes up 1% of NHLs in immunocompetent patients. Certainly in AIDS patients, latent EBV infection is associated with the development of PCNSL and PIOL.26 However, as noted previously, the use of HAART may have the potential to affect what genotypic subtype of PCNSL and PIOL develops within the AIDS patients. As HAART decreases the ability of opportunistic infections to cause disease in AIDS patients and as this important therapy is able to maintain a B and T cell milieu that is more similar to an immunocompetent patient, we may find that a shift from ABC DLBCL toward GCB DLBCL type PCNSLs occurs. This is important because as we direct therapy towards PCNSLs and PIOLs, targeting the genes or gene products that are expressed in genotypic subtypes of CNS lymphomas will more specifically eradicate the disease.

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