A 31 years old Chinese male with acquired immunodeficiency syndrome (AIDS) presented with concurrent mycobacterial infection and a synchronous non-Hodgkin's lymphoma of the nose. The diagnoses were made over a period of two months. Treatment for the mycobacterial infection was administered but he succumbed to the disease shortly after the diagnosis of NHL was established. This was an unusual case where two pathologies occurred in the same site in a patient with AIDS.
OBJECTIVE: To assess the role of fine needle aspiration cytology (FNAC) in lymphadenopathy in human immunodeficiency virus-infected individuals (HIVII).
STUDY DESIGN: Thirty-nine HIVII presenting with lymphadenopathy at University Hospital, Kuala Lumpur, were subjected to FNAC. Cytologic smears were routinely stained with May-Grünwald-Giemsa stain. Special stains and immunostains were used when necessary.
RESULTS: In nine cases, the cytologic appearance was compatible with HIV type A and in one case with HIV type C lymphadenopathy. In 21 cases, acid-fast bacilli (AFB) were demonstrated in the cytologic smears, enabling a diagnosis of mycobacterial lymphadenitis. In one of these cases there was a concomitant infection with Penicillium marneffei that was overlooked on initial cytologic examination. The cause of granulomatous lymphadenitis could not be ascertained in one case, where neither AFB nor any other organisms were demonstrable. Two cases of histoplasma and one of cryptococcal lymphadenitis were diagnosed, as was one high grade non-Hodgkin's lymphoma that could be immunophenotyped on cytologic material. In three cases the aspirates were inadequate for a cytologic diagnosis.
CONCLUSION: Lymph node FNAC is a valuable investigative modality in HIVII. Most opportunistic infections (bacterial and fungal) can be correctly identified, and high grade lymphoma can be diagnosed and phenotyped.
Two children with non-Hodgkin's lymphoma (NHL) as the presenting illness of acquired immunodeficiency syndrome (AIDS) are described. There was a delay in diagnosing the underlying AIDS in both cases. In the first case, an 18-month-old boy with stage IV, high-grade,T-cell NHL, the diagnosis of underlying AIDS was suspected only when he developed recurrent and profound opportunistic infection during chemotherapy. The second case, an eight-month-old female infant presented initially with hepatosplenomegaly and thrombocytopenia of undetermined cause. She had progressive abdominal distension and swelling of her right eye one year later due to high grade B-cell NHL. She was later found to be sero-positive for HIV during pre-chemotherapy screening. As the prevalence of HIV infection continues to increase, HIV infection should be considered in the differential diagnoses of childhood hepatosplenomegaly and thrombocytopenia, and as a possible underlying cause of childhood cancer, especially NHL.
We present a case of a 45-year-old female who presented with blurring of right vision associated with constitutional symptoms. Examinations revealed right optic disc swelling with inferior exudative retinal detachment and hepatomegaly. Gynaecological examination showed a fungating cervical mass. Histopathological reports of cone biopsy confirmed the presence of large B cell non-Hodgkin lymphoma. HIV screening was positive. A diagnosis of HIV related lymphoma was made. Chemotherapy and antiretroviral treatment were instituted. The ocular signs resolved. However, the patient could not tolerate the side effects of medical therapy and opted for palliative treatment.
LMP-1, an Epstein-Barr viral (EBV) latency protein, is considered a viral oncogene because of its ability to transform rodent fibroblasts in vivo and render them tumorigenic in nude mice. In human B cells, EBV LMP-1 induces DNA synthesis and abrogates apoptosis. LMP-1 is expressed in EBV-transformed lymphoblastoid cell lines, nasopharyngeal carcinoma (NPC), a subset of Hodgkin's disease (HD), and in EBV-associated lymphoproliferative disorders (EBV-LPDs). Recently, focused deletions near the 3' end of the LMP-1 gene (del-LMP-1, amino acids 346-355), in a region functionally related to the half-life to the LMP-1 protein, have been reported frequently in human immunodeficiency virus (HIV)-associated HD (100%) and EBV+ Malaysian and Danish peripheral T-cell lymphomas (100%, 61% respectively), but less frequently in cases of HD not associated with HIV (28%, 33%) and infectious mononucleosis (33%). To further investigate the potential relationship of del-LMP-1 to EBV-LPDs associated with immunosuppression or immunodeficiency, we studied 39 EBV-associated lymphoproliferations (10 benign, 29 malignant) from four distinct clinical settings: posttransplant (4 malignant, 1 reactive); HIV+ (18 malignant, 2 reactive); nonimmunodeficiency malignant lymphoma (ML) (7 cases); and sporadic EBV infection with lymphoid hyperplasia (7 cases). The presence of EBV within lymphoid cells was confirmed by EBV EBER1 RNA in situ hybridization or by polymerase chain reaction (PCR) analysis. EBV strain type and LMP-1 deletion status were determined by PCR. EBV strain types segregated into two distinct distributions: HIV+ (9 A; 11 B) and non-HIV (19 A, 0 B), consistent with previous reports. Overall, del-LMP-1 were found in 1 of 5 (20%) Burkitt lymphomas (BL); 17 of 24 (71%) aggressive non-Hodgkin's lymphoma (agg-NHL), and 2 of 10 (20%) reactive lymphoid proliferations. Of the agg-NHLs, del-LMP-1 were present in 4 of 4 PT-ML (100%); 10 of 15 HIV+ ML (67%); and 3 of 5 nonimmunodeficiency malignant lymphoma (ML, 60%). A total of 2 of 7 (28%) sporadic EBV-associated lymphoid hyperplasias contained a del-LMP-1. All del-LMP-1 were identical by DNA sequence analysis. No correlation was identified between the presence of del-LMP-1 and the EBV strain type observed. The high incidence of del-LMP-1 observed in agg-NHLs (71%), in contrast to the relatively low incidence observed in reactive lymphoid proliferations (28%), suggests that the deleted form may be preferentially selected in lymphomatous processes. All posttransplant agg-NHLs contained a del-LMP-1, and a similar frequency of del-LMP-1 was observed in both HIV-associated ML (66%) and nonimmunodeficiency ML (60%), suggesting that impairment of immune function alone is not a requirement for the expansion of malignant cells infected by EBV stains containing the deleted LMP-1 gene.