Reticulocytes and reticulocyte enumeration.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J M Ben-Ezra.
Explore the source record for details and available documents.
BACKGROUND: Liver involvement by non Hodgkin's lymphoma usually represents systemic progression of a low grade lymphoma. Sixteen patients without palpable lymphadenopathy who presented with features suggesting hepatic inflammation were found to have non Hodgkin's lymphoma involving the liver. METHODS: Tissue sections stained with hematoxylin and eosin were examined by light microscopy. Immunohistochemical studies were performed on formalin-fixed paraffin embedded tissue to determine phenotype. Patients' medical records were reviewed for clinical details. RESULTS: Clinical presentation included fever, jaundice, and elevated liver enzymes. Peripheral lymphadenopathy was absent. Hepatomegaly and splenomegaly were common. Imaging studies revealed a homogeneous pattern of liver involvement without a discrete mass. Histologically, infiltration of the liver was predominantly portal consisting of large, atypical cells scattered within a background of small lymphoid cells. By immunohistochemistry, it was determined that eight were T-cell and eight were B-cell lymphomas. Of the eight patients who had lymph node sampling, three showed involvement by diffuse mixed, small cleaved, and large cell lymphomas. Each of these three involved lymph nodes was located near the liver. Bone marrow infiltration was demonstrated in 10 of the 11 patients in whom it was sampled. Eleven of the 16 patients died 2 days to 31 months after diagnosis, and at last follow-up, 5 patients were alive 2 weeks to 13 months after diagnosis. CONCLUSIONS: Patients with non-Hodgkin's lymphoma can present with hepatic dysfunction and without peripheral lymphadenopathy. This presentation of lymphoma is associated with extensive disease and an aggressive course.
We compared the effect of different immunosuppressive drug regimens on both mean and long-term allograft survival and the histologic appearance of donor/recipient chimeras in the ACI to Lewis rat heterotopic cardiac transplant model. Intraabdominal cardiac transplantation was performed in standard fashion and microchimerism was assessed using immunohistochemical staining of cut sections of recipient spleen and lymph nodes. All of the drug regimens studied resulted in excellent mean allograft survival. Furthermore, long-term (> 120 day) allograft survival was consistently observed in each group. In fact, many of the recipients continue to have functioning heterotopic grafts even as they approach the end of the natural life span of a Lewis rat. Mixed allogeneic chimerism, however, was not observed with 100% frequency despite the consistent induction of graft tolerance. This finding may be related to the immunosuppressive agents used or the sensitivity of the immunohistochemical assay. Therefore, the exact role, if any, of chimerism in the induction of graft tolerance remains unanswered.
Many low grade B-cell lymphomas, and most T-cells lymphomas, express CD5 on their surface. This expression has been demonstrated in fresh cells or frozen sections. Recently, a new monoclonal antibody to CD5, NCL-CD5, has been introduced that detects CD5 in paraffin-embedded tissues. Paraffin-embedded tissues from five patients with small lymphocytic lymphoma (SL), four patients with chronic lymphocytic leukemia (CLL), and one patient each with large granular lymphocytic leukemia, diffuse large cell lymphoma (T cell), and mycosis fungoides were stained with the NCL-CD5 antibody after unmasking the antibody with the steam/citrate technique. All these cases had CD5 positivity demonstrated by flow cytometry or on cytospin or frozen section preparations. In addition, one case of angiofollicular lymph node hyperplasia (CD5+), two cases of SL/CLL (CD5-), and one case CD5- T-cell lymphoma were also investigated. Of the 12 CD5+ malignancies, only 1, an SL, was positive with the NCL-CD5 antibody. In seven of these cases, both B-5 and formalin-fixed tissues were tested; the one positive case was positive only in the formalin tissue. The three CD5- malignancies were also negative in paraffin sections (P = .001; McNemar test). However, reactive T cells did stain in these biopsy sections. The case of Castleman's disease showed many CD5+ cells with the NCL-CD5 antibody. Although NCL-CD5 does indeed stain reactive T cells in paraffin sections, it does not appear to stain neoplastic CD5+ cells.
The ability to amplify DNA by the polymerase chain reaction (PCR) technique has revolutionized our ability to test for genetic mutations. Many different assay systems are available for analyzing the amplified DNA and RNA. These techniques can be performed easily on material from adults, children, fetuses, and even single cells from blastomeres and polar bodies. The detection rate of the screening test, as well as the frequency of the mutation in the study population and the technical limitations of the procedure, will determine the usefulness of a positive or negative result. Preimplantation testing provides a paradigm for the ease of use of PCR-based testing, yet also underscores the problems encountered with genetic screening because of the multitude of possible mutations and the possible misinterpretation of results.
A previously healthy young child presented with a large pericardial effusion and cardiac tamponade. The chest radiography was key to the recognition of the pericardial effusion. Cytologic examination of the pericardial fluid ultimately established the diagnosis of acute monoblastic leukemia in the absence of associated clinical or laboratory findings. The pericardial fluid was vital for leukemic cell classification because the bone marrow has hypocellular and non-diagnostic. This presentation of acute monoblastic leukemia is very rare, and in the three previously reported pediatric cases has been associated either with peripheral blasts or a history of preleukemia. When the cardiac configuration suggests pericardial effusion in a previously healthy young child, the diagnosis of new onset leukemia should be considered.
Lymphoid nodules in a bone marrow biopsy may be either benign or malignant. Morphological clues may help to differentiate the benign from the malignant nodules. However, it is sometimes difficult, if not impossible, to make this distinction, especially in patients with a known low-grade lymphocytic malignancy. This study was undertaken to determine whether staining bone marrow biopsies with an antibody to the bcl-2 protein might aid in making this differentiation. Using a monoclonal antibody to bcl-2, we stained 26 bone marrows with benign lymphoid aggregates, 19 with a follicular lymphoma, 10 with small lymphocytic lymphoma/chronic lymphocytic leukemia, three with other non-Hodgkin's lymphomas, and three with other miscellaneous hematopoietic lesions. Only one of the 26 benign lymphoid aggregates had moderate to intense staining with this antibody; in contrast, 79% of the follicular lymphomas stained positively. Eight of the 10 small lymphocytic lymphoma/chronic lymphocytic leukemia cases stained with moderate to intense intensity; the other two cases had weak staining. No consistent pattern was seen with the other six lesions. Based on this data, we conclude that lack of staining of small lymphoid aggregates within the bone marrow with the antibody to the bcl-2 protein is suggestive of a benign aggregate, whereas moderate to strong staining intensity is most consistent with a malignant process.
In our laboratory, we observed that a case of small cell carcinoma of the lung (SCLC) stained with a monoclonal antibody (Dako Corp., Bcl-2-124) against the Bcl-2 protein. To determine how common this reaction was, and whether it was specific for SCLC, we stained formalin-fixed, paraffin-embedded tissues from 23 cases of SCLC and 20 cases of squamous cell carcinoma of the lung for Bcl-2. Fifteen of the 23 SCLC cases stained positively for the Bcl-2 oncogene protein. In contrast, weak staining was observed in only three of the squamous cell carcinomas (chi 2-test; P = 0.001). In addition, four small cell carcinoma cell lines (H69, H146, H209, and WB) were tested by immunohistochemistry and flow cytometry for expression of this protein; all four were positive. In these and three other (H128, H432, and H510) SCLC lines, Northern blots of polyadenylated RNA revealed expression of the 6-kb Bcl-2 mRNA. Moreover, Western blots of extracts from these cell lines revealed the characteristic 26-kd band for Bcl-2 protein. In a single cell line, H82, which has previously been characterized as a variant SCLC, we failed to detect expression of the Bcl-2-specific mRNA and protein. We therefore conclude that most cases of SCLC of the lung express the Bcl-2 oncoprotein, which could play a role in the pathogenesis of this disease.
Explore the source record for details and available documents.
When graft-versus-host (GVH) disease affects the liver, it is characteristically the bile ducts which are involved, infiltrated by lymphocytes. To characterize this process further, and to determine whether there were any antigenic changes in the bile ducts, we stained 9 liver biopsies involved by GVH disease, 10 non-GVH biopsies that had a prominent portal lymphocytic component, and 8 biopsies taken incidentally at surgery for noninflammatory liver disease with epithelial membrane antigen, AE-3, AE-1, a keratin cocktail, keratin 19, CD45RO (UCHL-1), CD43 (Leu-22), CD20 (L26), vimentin, and LN-3. The infiltrating lymphocytes were T cells (CD45RO+, CD43+, CD20-) which variably expressed LN-3. The bile ducts were positive for the keratin cocktail, AE-1, AE-3, and keratin-19, but only occasionally positive for EMA and LN-3. There was no significant difference in the staining patterns of either the bile duct cells or lymphocytes between the three groups. With the antibodies that we used, there does not appear to be a significant difference in the antigenic phenotype of the bile ducts in GVH as compared to normal or reactive livers.
Localized herpetic lymphadenitis is an extremely uncommon complication of herpes simplex virus (HSV) infection. The authors report two cases of localized herpetic lymphadenitis, both showing well-circumscribed areas of necrosis containing cells with diagnostic intranuclear inclusions. Electron microscopic studies in both cases revealed characteristic viral particles, and in situ hybridization studies using a herpes simplex genomic probe demonstrated HSV DNA in both specimens. Immunohistochemical studies demonstrated that the cells containing the inclusions were stromal, not lymphoid, cells. Combining the current two cases with the six well-documented cases previously reported in the literature, seven of the eight cases of HSV lymphadenitis have developed in inguinal lymph nodes, with four occurring in patients with previously or subsequently diagnosed hematopoietic malignancies, including both patients in the current series.
Explore the source record for details and available documents.
We studied two cases of a recently recognized systemic lymphoproliferative disease with morphological features of Castleman's disease: multicentric giant lymph node hyperplasia. Both patients developed Kaposi's sarcoma and had laboratory evidence of immune abnormalities, including reversed T4 to T8 ratios. One patient's disease had a subacute course with fevers of unknown origin, mucocutaneous candidiasis, and progressive thrombocytopenia, while the other patient's disease had a fulminant course with anemia, thrombocytopenia, and splenic lymphoma. Both patients were elderly, and both died of complications of multicentric giant lymph node hyperplasia.