Nodular lymphocyte predominance Hodgkin's disease. A distinct clinicopathological entity

This article reviews the evidence that the nodular form of lymphocyte predominance Hodgkin's disease ("nodular paragranuloma") should be recognised as a distinct clinico-pathological entity. The disease is characterised histologically by very large primary lymphoid follicles, containing polytypic small B lymphocytes and extensive meshworks of follicular dendritic cells. The "L and H" or "popcorn" cells scattered within the nodules show clear differences from classical Reed-Sternberg cells, both in their cytological appearance and in their marker profile, being frequently negative for CD15 and for the EBV genome, but often positive for B cell antigens, CD45 (leucocyte common antigen), CDw75 (LN1), epithelial membrane antigen (EMA) and J chain. These findings suggest that L and H cells may be Ig-synthesising monoclonal B cells. Nodular lymphocyte predominance Hodgkin's disease pursues a much more indolent courses that classical Hodgkin's disease, and long term survival is common. It has other distinctive clinical features, e.g. a unimodal age distribution, a predilection to involve single lymph nodes, and a very low incidence of thymic involvement. There is a tendency for diffuse large cell non-Hodgkin's lymphoma, usually of B cell type, to develop during the course of the disease. This type of Hodgkin's disease thus has many features that distinguish it from the nodular sclerosis and mixed cellularity varieties, and it is hoped that future studies will gather more information on its clinical behavior and on the nature of the putative neoplastic cells, as well as exploring different protocols for its treatment.     

The effect of antibiotic therapy on recovery of intracellular bacteria from bronchoalveolar lavage in suspected ventilator-associated nosocomial pneumonia

Several recent reports have suggested that nodular lymphocyte predominance Hodgkin's disease (NLPHD) may be distinct from other forms of Hodgkin's disease and may be more closely related to B-cell non-Hodgkin's lymphoma. This is primarily based on immunophenotypic studies that have shown that the L & H cells in NLPHD demonstrate a B-cell phenotype. In 1989, Poppema reported that the T cells in NLPHD differ from T cells in other forms of Hodgkin's disease in that they demonstrate reactivity for Leu 7 (CD57). In this study we tested the hypothesis that Leu 7 (CD57) reactivity of small lymphocytes in NLPHD is an immunophenotypic feature that distinguishes NLPHD from nodular sclerosing Hodgkin's disease and from certain B-cell lymphomas that may histologically simulate NLPHD, namely T-cell-rich B-cell lymphoma and follicular lymphoma. Using an image analysis method, we found Leu 7 (CD57) reactivity in an average of 18.9% of the small lymphocytes in the nodules of NLPHD compared with 3.9% in nodular sclerosing Hodgkin's disease, 4.3% in T-cell-rich B-cell lymphoma, and 2.1% in follicular lymphoma. Moreover, Leu 7 (CD57)-reactive small lymphocytes often showed a distinctive pattern in NLPHD, forming a ring of cells around the large L & H cells. While scattered Leu 7 (CD57)-reactive lymphocytes were found in the other disorders, the percentage of reactive cells and the pattern of reactivity were significantly different in NLPHD. These results suggest that Leu 7 (CD57) reactivity may be used as an additional immunophenotypic criterion in distinguishing NLPHD from nodular sclerosing Hodgkin's disease, T-cell-rich B-cell lymphoma, and follicular lymphoma. The clinical and biological significance of Leu 7 (CD57) reactivity of small lymphocytes in NLPHD merits further investigation.     

Differential diagnosis between classic Hodgkin's lymphoma, T-cell-rich B-cell lymphoma, and paragranuloma by paraffin immunohistochemistry

There are significant difficulties in the differential diagnosis of lymphomas at the interface between classic Hodgkin's lymphoma and both paragranuloma and T-cell-rich B-cell lymphoma as well as at the interface between T-cell-rich B-cell lymphoma and paragranuloma. We therefore investigated 197 cases (155 classic Hodgkin's lymphomas, 32 T-cell-rich B-cell lymphomas, and 10 paragranulomas) by paraffin immunohistochemistry. Special interest was given to cases with a B-cell phenotype of tumor cells. The reactive inflammatory infiltrate in both classic Hodgkin's lymphoma and T-cell-rich B-cell lymphoma was rich in TIA-1-positive cytolytic lymphocytes, and CD57-positive cells were rarely encountered. In contrast, in paragranuloma CD57-positive cells and small B-lymphocytes predominated the background infiltrate. The tumor cells in cases of classic Hodgkin's lymphoma were positive for CD30 in 95%, for CD15 in 75%, and for CD20 in 22%. Apart from this, vimentin was expressed in >95% of the cases. All cases of T-cell-rich B-cell lymphoma were negative for vimentin, CD30, and CD15. The reactivity of the tumor cells for CD30, CD15, CD20, and vimentin together with the background reactivity for CD57 and TIA-1 seem to reliably discriminate between the entities and should therefore help to increase the interobserver reproducibility of diagnoses in the gray zone around Hodgkin's lymphoma.     

Early intrinsic deflection--a marker for successful radiofrequency ablation of overt accessory pathways

Striking morphological similarities exist between T-cell-rich B-cell lymphoma and lymphocyte-predominant Hodgkin's disease (Hodgkin's paragranuloma), making the distinction between them extremely difficult. Immunohistochemistry provides a means of overcoming this difficulty. Immunostaining with UCHL1, L26, MB1, and 4KB5 was performed on five T-cell-rich B-cell lymphomas and 11 Hodgkin's paragranulomas (7/11 nodular, 4/11 diffuse). L26 stained the tumour cells not only of T-cell-rich B-cell lymphomas, but also of L+H Hodgkin's disease. In contrast, MB1 as well as 4KB5 identified all of the neoplastic cells in 3/5 T-cell-rich B-cell lymphomas, but did not react with the L+H cells in 8/11 Hodgkin's paragranulomas. Some overlap of staining patterns became apparent in the remaining cases, with 2/5 T-cell-rich B-cell lymphomas showing the MB1+/4KB5+ phenotype in a tumor cell subset only. Similarly, in 3/11 Hodgkin's paragranulomas, some MB1/4KB5-positive L+H cells occurred in addition to MB1/4KB5-negative L+H cells. These cases, nevertheless, could be distinguished from one another by the numbers of MB1/4KB5-positive background lymphocytes, which were scanty or absent in T-cell-rich B-cell lymphomas and more numerous in Hodgkin's paragranulomas.     

Roles of COX-1 and COX-2 in gastrointestinal pathophysiology

We studied 40 cases of Hodgkin's disease (HD) from Costa Rica for evidence of Epstein-Barr virus (EBV) in the Reed-Sternberg and Hodgkin (RS-H) cells. We also compared the epidemiologic features of these patients with previous reports of HD in industrialized and developing nations. Because Costa Ricans enjoy a relatively higher standard of living than the residents of other developing Central American nations yet live in the same general geographic region and are genetically similar, we believed that this comparison might shed additional light on the hypothesis that the prevalence of EBV in HD and the epidemiologic factors of HD are influenced by socioeconomic factors. In 16 (40%) of 40 cases, immunohistochemical studies demonstrated that the RS-H cells were positive for EBV latent membrane protein (LMP), including 1 case of lymphocytic depletion analyzed, 12 (86%) of 14 cases of mixed cellularity, and 3 (15%) of 20 cases of nodular sclerosis. All five cases of lymphocytic predominance were negative. In the 16 EBV LMP-positive cases, polymerase chain reaction studies revealed that the virus was type A in 12 cases and type B in 4 cases. Nodular sclerosis was the most common type of HD, accounting for 20 cases (50%), followed by mixed cellularity, with 14 cases (35%). The relatively low prevalence of EBV in the RS-H cells of HD and the high incidence of nodular sclerosis in Costa Rica are similar to industrialized nations and are unlike HD in neighboring Central American countries. These findings further support the hypothesis that the prevalence of EBV in HD and the epidemiologic features of HD are most closely linked with socioeconomic conditions, and geographic location or ethnic heritage are of relatively less importance.     

Explorers. Christopher Columbus and Leonardo da Vinci

Epstein-Barr virus (EBV) recently has been associated with Hodgkin's disease (HD) and the EBV genome was found in CD30-positive Reed-Sternberg cells. Therefore, tissue sections from 25 cases of HD, 35 cases of CD30-positive non-Hodgkin's lymphoma (NHL) (seven CD30-positive anaplastic large cell lymphomas [ALCLs] and 28 CD30-positive non-ALCLs), and 12 cases of CD30-negative NHL that previously had been screened for the presence of EBV by polymerase chain reaction and DNA in situ hybridization were studied by immunohistochemistry for the expression of the latent EBV proteins, latent membrane protein (LMP), and Epstein-Barr nuclear antigen-2 (EBNA-2). We also analyzed the expression of the B-cell activation molecule CD23 and the adhesion molecules LFA-1/CD11a and ICAM-1/CD54 because the upregulation of these molecules by LMP and/or EBNA-2 in vitro has been related to the EBV-induced lymphocyte growth. Latent membrane protein expression was found in Reed-Sternberg cells in nine of 25 cases (36%) of HD and in large, occasionally Reed-Sternberg-like tumor cells in six of 47 cases (12%) of NHL; these six tumors were CD30-positive, histologically high-grade NHL (one CD30-positive ALCL and five CD30-positive non-ALCLs). All the LMP-positive cases were also polymerase chain reaction EBV positive while LMP expression was not found in polymerase chain reaction EBV-negative HD and NHL. No staining for EBNA-2 was detected in our series. In view of the transforming potential of the LMP, these findings suggest that EBV may be associated with the development of some cases of HD and CD30-positive NHL. These findings also suggest a correlation between the expression of LMP and the detection of CD30 in tumor cells of HD and NHL. In contrast, no correlation was found between the expression of LMP and the detection of CD23, LFA-1/CD11a, and ICAM-1/CD54 in tumor cells of HD and NHL.     

Relation of follicular dendritic reticulum cells to Reed-Sternberg cells of Hodgkin's disease with emphasis on the expression of CD21 antigen

Based on observations of 66 cases, in which tissues were specially processed to optimize the simultaneous preservation of cell membrane antigens and morphology, we provide evidence in favor of a relationship between follicular dendritic reticulum cells (FDRC) and Reed-Sternberg (RS) cells of Hodgkin's disease (HD) other than the lymphocyte predominance subtype. RS cells were intimately related to the FDRC network (75% of cases), and the expression of CD21 antigen was frequent (41% of cases). Exclusive expression of CD21 antigen was found in 11 cases of HD, while the expression of other B-cell-associated markers (CD19, CD20, CD22) was both variable and inconsistent. The expression of T-cell antigens (CD3, CD4, CD8) was rare. Null phenotype of RS cells was observed in 27 of 66 cases (41%). Epstein-Barr virus (EBV) nucleic acids were found in 34 of 66 (51.5%) cases. Double labeling techniques showed the presence of EBV-positive RS cells within the FDRC network. A non-B-cell origin of RS cells was supported by the differential expression of EBV latent antigens in HD (latent membrane protein+, EB nuclear antigen 2-), which is unusual in EBV-driven lymphoblastoid cell lines and EBV-positive B-cell lymphomas. FDRC and RS cells are known to share morphological traits (binucleated cells), and both cell types possess Fc receptor for IgG. The hypothesis is further backed by the findings of CD15 antigen expression by occasional RS-like dysplastic FDRC in Castleman's disease (five cases), which is characterized by hyperplasia of FDRC. Whether FDRC might be the only cells involved in the conversion to RS cells by the loss or gain of antigens remains to be determined.     

CD30 antigen expression in florid immunoblastic proliferations. A clinicopathologic study of 14 cases

Reactive immunoblastic proliferations may be confused with certain types of non-Hodgkin's lymphoma and Hodgkin's disease on morphologic grounds. In addition, a characteristic antigen, CD30 (Ki-1; BerH2) on these neoplastic entities may be observed in morphologically atypical yet reactive florid immunoblastic proliferations such as those associated with acute infectious mononucleosis. Although it has been documented, a large series determining the frequency and extent of CD30 antigen expression on a variety of nonneoplastic immunoblastic proliferations is lacking. The authors studied 14 florid immunoblastic proliferations (9 in lymph nodes and 5 in tonsils) for CD30 antigen expression and for B- and T-cell paraffin markers. In situ hybridization to determine the presence of Epstein-Barr virus (EBV) genomes also was performed. Cases were classified into monospot-positive acute infectious mononucleosis (4 cases), EBV-related lymphoproliferative disorder suggestive of acute infectious mononucleosis (5 cases), and other etiologies (5 cases). CD30 Antigen expression was found on the immunoblasts in cases from all three categories and overall in 9 (64%) of 14 specimens. CD30 reactivity in the positive cases varied from occasional to numerous positive cells; 4 samples (3 EBV-related lymphoid proliferations and 1 vaccine-related lymphadenopathy) had numerous CD30-reactive immunoblasts. Expression of CD30 antigen on B or T cells and prominence of B or T cells within a proliferation were variable. Significant "atypia" of immunoblasts was found only in EBV-related disorders and correlated with B-cell prominence of the infiltrate. Appropriate clinical correlation and ancillary laboratory data are necessary to assist in differentiating these CD30(+)-reactive disorders from similar-appearing malignant lymphomas. Most important, a fresh tissue sample should be procured and adequately processed to allow for comprehensive determination of clonality and cellular lineage.     

DNA content and expression of PCNA and p53 in Hodgkin's disease and Hodgkin's-like B-cell lymphoma

DNA ploidy (by image cytometry) and expression of proliferating cell nuclear antigen (PCNA) and p53 tumor suppressor gene product (by immunohistochemistry) were investigated in 15 cases of Hodgkin's disease (HD) and 12 cases of HD-like B-cell lymphoma (HD-like NHL). Reed-Sternberg (RS) cells and their variants were DNA aneuploid in all cases. However, the fraction of hyperoctaploid tumor cells was higher in HD than in HD-like NHL. PCNA expression was high in neoplastic cells (> 50%) and variable (5-40%) in reactive lymphocytes in both HD and HD-like NHL. p53 positivity was found in RS cells and their variants in 64% of HD cases, but only in 25% of cases of HD-like NHL. Our results support the suggestion that HD-like B-cell lymphomas should be considered as highly malignant non-Hodgkin's lymphomas rather than Hodgkin's disease.     

Radiolabelled antimicrobial peptides for imaging of infections: a review

Risk factors suggestive of relatively late exposure to EBV have been consistently associated with Hodgkin's disease (HD) in younger adults. In addition, evidence of EBV infection has been found in the Reed-Sternberg cells themselves in about one-third to one-half of all HD cases. However, no study yet published has correlated these childhood social environment risk factors with the presence of EBV in Hodgkin's tumor cells. We examined whether EBV-positive HD occurs in those patients whose childhood environment would predispose them to relatively late exposure to EBV. The study population consisted of 102 cases of mixed cellularity (MC; n = 25) or nodular sclerosing (n = 77) HD. Samples that tested positive for either EBV-encoded RNA or latent membrane protein or both were considered EBV-positive. Of the 102 cases, 83 completed a questionnaire regarding childhood social environment. The association with EBV-positivity was estimated by the odds ratio (OR) with 95% confidence intervals (CI). Twenty-two percent of the cases were EBV-positive. These cases were more likely to be MC (OR, 6.2; CI, 2.3-16.3) and male (OR, 3.4; CI, 1.3-9.0). History of infectious mononucleosis (IM) was not predictive of EBV-positivity, with only 3 of 14 such patients being EBV-positive (P = 0.82). Contrary to our hypothesis, no association between EBV and childhood environment risk factors was identified. The association of EBV with MC histology and male gender agrees with previous reports. The most intriguing finding was the dissociation between IM history and EBV-positivity, in that almost all of the cases with a history of IM were EBV-negative.     

The B7/BB1 antigen is expressed by Reed-Sternberg cells of Hodgkin's disease and contributes to the stimulating capacity of Hodgkin's disease-derived cell lines

The B7/BB1 molecule has recently been found to be expressed on professional antigen-presenting cells and to be the natural ligand for CD28 and CTLA-4 on T cells. On binding of B7/BB1, CD28 transduces a signal that synergizes with triggering of the T-cell antigen receptor, resulting in enhanced cytokine secretion. In view of the data supporting an antigen-presenting function of Reed-Sternberg cells, we evaluated the expression of B7/BB1 in lymph nodes affected by Hodgkin's disease. B7/BB1 was found to be strongly expressed by the Reed-Sternberg cells in all 47 cases of Hodgkin's disease studied. Moreover, Reed-Sternberg cells were frequently surrounded by CD28-expressing T cells. Evidence for a functional role of B7/BB1 on Reed-Sternberg cells was obtained by our findings that T-cell proliferation and interleukin-2 (IL-2) production in the primary allogenic mixed lymphocyte reaction (MLR), using the B7/BB1-expressing Hodgkin's disease-derived cell lines L428 and KM-H2 as stimulators, could be partially blocked by adding anti-B7 monoclonal antibody. B7/BB1 expression was also evaluated in a group of non-Hodgkin's lymphomas (n = 46). Whereas B7/BB1 was not expressed by the neoplastic cells of most non-Hodgkin's lymphomas, including T-cell-rich B-cell lymphoma (n = 11), it was present on the neoplastic cells of anaplastic large-cell lymphoma (Ki-1 lymphoma) (n = 5) and follicular lymphoma (n = 4). Our data provide further evidence for an accessory cell function of Reed-Sternberg cells. The accessory cell function of Reed-Sternberg cells might lead to pronounced T-cell activation in vivo, which might contribute to the Hodgkin's syndrome. In addition, our study indicates that B7/BB1 may be a useful marker for differentiating Hodgkin's disease from morphologically similar conditions such as T-cell-rich B-cell lymphoma.     

Intravascular large B-cell lymphoma: the CD5 antigen is expressed by a subset of cases

The CD5 antigen is a T-cell associated marker that is also usually expressed by two B-cell neoplasms, chronic lymphocytic leukemia/small lymphocytic lymphoma and mantle cell lymphoma. We observed CD5 antigen expression in a subset of cases of intravascular large B-cell lymphoma (IVLBL), and we report here five cases. The patients, two men and three women, ranged in age from 59 to 81 years. Biopsy specimens were obtained from kidney, lung, bone marrow, abdominal wall, and neck, the latter involving a lymphangioma. All of the cases had histologic features typical of IVLBL, with large and atypical lymphoid cells located predominantly within blood vessels. Immunohistochemical studies performed using routinely fixed, paraffin-embedded tissue sections showed that the neoplastic cells were B cells, positive for the CD20 antigen and negative for the CD3 or CD43 antigens. All cases were also positive for the CD5 antigen. One case had an immunoglobulin heavy chain gene rearrangement shown by using a polymerase chain reaction method. The finding of CD5 antigen expression in a subset of IVLBL cases adds to other evidence in the literature suggesting that IVLBL is a heterogeneous entity. We considered the possibility that these cases were related to or represented unusual histologic forms of transformation from either chronic lymphocytic leukemia/small lymphocytic lymphoma or mantle cell lymphoma. All of the cases, however, were negative for the CD23 antigen and cyclin D1 (bcl-1) protein, which is evidence against this interpretation. The biologic significance of CD5 antigen expression in cases of IVLBL is uncertain. These neoplasms might arise from a separate lineage of CD5-positive B cells or from a specific, early stage of B-cell differentiation. Alternatively, some investigators have suggested that CD5 antigen expression by B cells is a marker of activation.     

Hodgkin's disease: a clinicopathologic study

One hundred and four cases of Hodgkin's disease diagnosed between July 1981 and June 1991 have been analysed. There was a definite male preponderance. Majority of the patients (82.7%) were below the age of 50 years. Mixed cellularity was the most common type (57.7%). It was followed by both nodular sclerosis and lymphocyte predominant types (16.3% each). Lymphocyte depletion Hodgkin's disease, the most aggressive variant, was the least common (9.7%). The detailed observations, as compared to the previous studies in this region as well as in other parts of the world have been presented and discussed.     

中国人经典霍奇金淋巴瘤中人类白细胞共同抗原表达的研究

目的 既往的研究发现在高加索人中,经典霍奇金淋巴瘤肿瘤细胞人类白细胞共同抗原(HLA)的表达与EB病毒感染密切相关,研究在亚洲人中两者的相关性.方法 随机选取北京大学医学部病理学系常规外检及会诊病例中确诊为经典霍奇金淋巴瘤的145例,所有病例均有石蜡包埋组织蜡块.常规HE染色、形态学观察,根据WHO分类标准对所有病例进行重新分类.原位杂交方法检测EB病毒编码的小RNA(EBER)以提示肿瘤与EB病毒的相关性.HLA-Ⅰ类抗原的表达使用HC-10和β 2-微球蛋白抗体检测,而HLA-Ⅱ类抗原的表达使用CR3/43抗体检测.结果 145例中,40%(58例)的病例为EB病毒相关性.EB病毒阳性病例中,混合细胞型较结节硬化型更为常见(71%比16%,P＜0.001).HLA-Ⅰ类抗原在EB病毒阳性病例中的表达率明显高于EB病毒阴性的病例(79%比30%,P＜0.001).而HLA-Ⅱ类抗原的阳性率在EB病毒阳性和阴性病例中差异无统计学意义(52%比43%,P=0.277).结论 中国人经典霍奇金淋巴瘤HLA-Ⅰ类抗原的表达与EB病毒感染密切相关,与高加索人一样,但HLA-Ⅱ类抗原的表达与EB病毒感染无显著相关性.     

Maternal and fetal plasma concentrations of endothelin, lipidhydroperoxides, glutathione peroxidase and fibronectin in relation to abnormal umbilical artery velocimetry

The topoisomerase II alpha (topo II alpha) enzyme is the target for several chemotherapeutic agents, including etoposide, teniposide, mitoxantrone, and doxorubicin (topo II poisons). The enzyme also is a marker of cell proliferation. Most cases of Hodgkin's disease (HD) are responsive to combination chemotherapy regimes that include topo II poisons such as doxorubicin. Immunoperoxidase methods for detection of the topo II alpha isoenzyme are now available for use in formalin-fixed, paraffin-embedded tissues, which may provide information about the proliferative capacity and possible sensitivity of tumors to drugs that target topo II. We used a specific antibody to analyze subsets of HD for topo II alpha staining patterns. Formalin-fixed blocks from 49 cases of HD, including 20 nodular sclerosis (NS), 14 mixed-cellularity (MC), and 15 lymphocyte-predominant (LP) subtypes, were analyzed by dual staining for topo II in combination with monoclonal antibodies against Reed-Sternberg (RS) cells consisting of CD15 for the NS and MC subtypes and CD20 for LP lymphocytic and histiocytic (L & H) cells. The number of morphologically appropriate cells coexpressing the RS or L & H marker and topo II alpha was quantitated. Positive nuclear staining for topo II alpha in RS or L & H cells was seen in 100% of cases, irrespective of subtype. Coexpression of CD15 and topo II alpha was seen in 58.4% of the RS cells or mononuclear variants in NSHD cases and 68.4% in MCHD cases. No significant difference in the percentage of neoplastic cells expressing topo II alpha was found between NS and MC subtypes. Cases of LPHD showed coexpression of CD20 and topo II alpha in 84.4% of the L & H cells, a significant increase over the level of tumor cell coexpression seen in NSHD and MCHD (P < .001). Only one case was found to have a low (< 25% of tumor cell coexpression) level of topo II alpha expression. Immunohistochemical detection of a high level of topo II alpha expression in HD, irrespective of subtype, suggests a molecular explanation for the excellent response of most HD to standard combination chemotherapy, which can include topo II poisons. The LP subtype has a higher expression of topo II alpha in the neoplastic cell population than do NS or MC subtypes, perhaps indicating increased sensitivity of these tumors to topo II poisons. It may be possible to identify subsets of HD that are more or less sensitive to conventional chemotherapeutic regimes, which would help in the selection of appropriate treatment.     

Epstein-Barr virus in primary gastrointestinal T cell lymphomas. Association with gluten-sensitive enteropathy, pathological features, and immunophenotype

Forty-three primary gastrointestinal T cell lymphomas were investigated for the presence of Epstein-Barr virus (EBV) by polymerase chain reaction, RNA in situ hybridization, and immunohistochemistry. In addition, the association between EBV and clinicopathological characteristics of these lymphomas was investigated. Five of the thirty-eight cases that could be evaluated expressed EBV-encoded nonpolyadenylated RNA-1 in most tumor cells. Two of these five cases were EBV latent membrane protein-1 positive. All five cases were CD30 positive. In three of these five EBV-associated T cell lymphomas, the tumor cells were considered to be the neoplastic counterparts of activated cytotoxic T cells as shown by the expression of granzyme B. There was no association with histological characteristics of gluten-sensitive enteropathy, angioinvasion, necrosis, eosinophilia, or epitheliotropism of the tumor cells. The substantial percentage (58%) of EBV DNA polymerase chain reaction-positive cases was largely the result of the presence of EBV-encoded RNA-1-positive reactive cells. In conclusion, EBV might have an important etiological role in only 13% of the primary gastrointestinal T cell lymphomas. This percentage is similar to the findings in primary lymph node and lung T cell lymphomas.     

Relationships between lymphography and the histologic nodal and splenic types in Hodgkin''s disease. Considerations on clinical evolution

Trying to establish the eventual interrelations of the initial histologic nodal type and the splenic one, the general lymphographic picture, the histologic nodal type and spleen involvement, lymphographic and histologic examinations were carried out in 151 patients with Hodgkin's disease. Lympographies were performed in 139 cases, and splenectomy (followed by splenic, hepatic and abdominal lymph node biopsies) in 32. Lymphocyte depletion was found in 72.7% of the patients with lymph node obstruction diagnosed lymphographically. Splenic involvement was more frequent in cases with pathologic lymphographic picture and histologic aspects of lymphocyte predominance or nodular sclerosis. In patients with initial nodal histologic types of nodular sclerosis or lymphocyte depletion, the splenic histopathologic types were the same, but they got more severe in cases with lymphocyte predominance or mixed cellularity. Splenic biopsy might be unconclusive after protracted cytostatic treatment or splenic X-ray therapy. In the authors' opinion, early routine splenectomy is rather more advisable than differentiated splenectomy.     

Polymerase chain reaction amplification of Trichomonas vaginalis DNA from Papanicolaou-stained smears

We describe 3 cases of Hodgkin's disease (HD) of unusual suppurative type, which were diagnosed on fine-needle aspirates. The smears were dominated by neutrophils, macrophages, and cellular debris. Only a few large, atypical cells of Hodgkin and Reed-Sternberg type were observed. The differential diagnoses of such smears include infectious mononucleosis, tuberculosis, metastatic lymph node involvement, non-Hodgkin's large-cell anaplastic Ki-1-positive lymphomas, T-cell-rich B-cell lymphomas, and peripheral T-cell lymphomas of mixed type. Immunocytochemistry identified the large atypical cells as CD 30 (BerH2)-positive and negative for CD 45 (LCA) in cytospin material from 2 patients, which allowed a conclusive diagnosis of HD.