Marginalzonenlymphome: extranodale vom MALT-Typ, nodale und splenische

Marginal zone B-cell lymphomas (MCL) of extranodal, nodal and splenic origin appear to be different lymphoma entities with a similar growth pattern in the marginal zone of the B-follicles. Decisive for the detection of MCL as a distinct lymphoma entity was the "MALT concept" for lymphoid infiltrates in the gastric and intestinal mucosa as described by Isaacson et al. in the 1980's. Immunohistological stainings for the immunoglobulin light and heavy chains and molecular pathological studies of the immunoglobulin heavy chain gene configuration have subsequently confirmed the neoplastic nature of the extranodal infiltrates and differentiated marginal zone cells from mantle zone cells. In 1994, the MCL of MALT type as well as of nodal and splenic origin were included in the REAL classification and in 1998 in the new WHO classification for lymphomas. Meanwhile extranodal MCL of MALT-type have been observed in almost every organ and site of the body, by far most frequently in the gastric mucosa. Beside the typical growth pattern, lymphoepithelial lesions are a distinct diagnostic feature of extranodal MCL. Clinically, the small cell extranodal MCL show a very good prognosis with regression after treatment. As for nodal and splenic MCL, we need further studies to evaluate the prognostic aspects and to compare them with other B-cell lymphomas. The same is true for primary extranodal large B-cell lymphomas or blastic transformation to a large cell lymphoma; in these tumors the diagnosis of a MALT type lymphoma should only be made if a small cell component with MALT-specific criteria can be proved.     

Diffuse lymphocyte-predominant Hodgkin''s disease (diffuse paragranuloma). A variant of the B-cell-derived nodular type.

Lymph node sections from 10 cases of mixed nodular/diffuse and 10 cases of completely diffuse lymphocyte-predominant Hodgkin's disease (LPHD) were immunophenotyped. The results obtained were compared with those of nodular LPHD (nodular paragranuloma). In conventional stains, nodular/diffuse LPHD differed from diffuse LPHD in the presence of nodularity, which can be best demonstrated with silver impregnation. Immunohistologic analysis showed a correlation of the difference in nodularity with the presence or absence and pattern of follicular dendritic cell (FDC) meshwork, ie, a relatively sharply defined and large spherical meshwork was present in nodular areas of nodular/diffuse LPHD, whereas FDCs were either absent or present in a diffuse, ill-defined meshwork, usually of small size, in the diffuse zones of nodular/diffuse LPHD and in diffuse LPHD. The amount of FDC meshwork corresponded roughly to the number of reactive B cells and T cells, meaning that in diffuse areas significantly fewer B cells and more T cells were observed than in nodular areas. The immunohistologic analysis also showed that the antigen profile (positivity with the monoclonal B-cell marker L26 in the majority [14/20] of cases and negativity for CD15 in all but one of 20 cases) of the tumor cells in both nodular/diffuse LPHD and diffuse LPHD were comparable while it was different from the antigen profile (L26- and CD15+) in most cases of nodular sclerosis and mixed cellularity types of HD. This suggests that the considered subtypes of LPHD differ mainly in FDC pattern, but not in origin and nature of the tumor cells. This further justifies assignment of the above-mentioned LPHD subtypes to the category paragranuloma (LPHD).     

Irreversible shock of rats after acute renal vein thrombosis

Summary After occlusion of the renal veins rats die quickly in progressive shock (within 4.5 h), but after ligating the renal hilum of both Kidneys they survive 27 h. To learn why renal vein occlusion is so rapidly lethal, and what substances are given off and by what method from the hemorrhagically infarcted kidneys, we studied eight groups of rats, each containing at least seven animals. The groups differed in the combination of hilar structures (renal veins, ureters, lymphatics) ligated. We compared: survival times, changes in blood pressure, blood volume, levels of plasma kinins, adenosine, and lactate, changes of blood pH, responses to Indomethacin, Trasylol^®, and plasma expanders, tubular and capillary flow rates, histopathological changes in organs and cerebral blood flow and changes in the blood coagulation system. Our results suggest that the venous stasis, anoxia, and hemorrhagic necrosis caused by bilateral venous occlusion release into renal lymphatics toxic substances which reach the systemic circulation and induce irreversible shock. We have excluded prostaglandins and adenosine as the toxic substances inducing shock but could not rule out an action of the kallikrein-kinin-system. We postulate that the striking degenerative changes occurring in the arterioles of the brain after bilateral venous occlusion may mean these vessels are especially susceptible to high levels of lactic acid and that this may explain why these animals die so quickly. Our conclusions should help not only in understanding why high levels of lactate in shock portend a poor prognosis but also help in formulating appropriate therapy for circulatory failure of renal origin and for protracted hypotension after extensive tissue injury.The studies were supported by the German Research Foundation within the SFB 90 Cardiovasculäres SystemPresented in part: Jäckh and Steinhausen, 1976; Dallenbach et al., 1978; Zimmerhackl et al., 1979We dedicate this paper to Wilhelm Doerr, Dr. med., Professor of Pathology, University of Heidelberg on the occasion of his 65th birthday (August 25th, 1979)     

Predictive utility of autistic traits in youth with ADHD: a controlled 10-year longitudinal follow-up study

European Child & Adolescent Psychiatry - The objective of this study was to investigate the stability and predictive utility of autistic traits (ATs) in youth with...     

Paraffin section markers for Reed-Sternberg cells. A comparative study of peanut agglutinin, Leu-M1, LN-2, and Ber-H2

Hodgkin's disease (HD) is sometimes difficult to distinguish from non-Hodgkin's lymphomas, and a reliable marker for Reed-Sternberg and related (R-S) cells in paraffin sections would be useful. Ninety-one cases of HD with PNA, anti-Leu M1, and LN-2, and 90 cases with Ber-H2 were studied. The staining results were evaluated independently. R-S cells stained positively with one or more of the reagents in all cases. PNA staining was positive in 78 cases (85.7%); Leu M1, 63 (69.2%); LN-2, 71 (78.0%); and Ber-H2, 80 cases (88.9%). Positively stained cells were readily recognized in 71 cases (91.0%) of PNA+, 51 (80.9%) of Leu M1+, and 51 (71.8%) of LN-2+ and 71 (88.7%) of Ber-H2+ cases; the cells were found only after careful search in the remaining cases. Sixteen cases of peripheral T-cell lymphoma (large cell type, ten; mixed, five; unclassifiable, one) were also stained. Tumor cells did not stain with PNA or anti-Leu M1 in any of the 16 cases but did stain positively with LN-2 in four and with Ber-H2 in five. Thus, the detection rate of R-S cells was the highest with Ber-H2, closely followed by PNA. PNA, however, stained the largest number of R-S cells per case, and the results were least affected by the type of fixative employed. Staining of peripheral T-cell lymphoma appeared to be nil or extremely rare with PNA and Leu M1, whereas it was not uncommon with Ber-H2 and LN-2. In conclusion, to facilitate the detection of R-S cells in paraffin sections, the application of a panel of three markers, PNA, Leu M1, and Ber-H2, appears to be necessary at this point in time.     

Considerations on the development of experimental lead encephalopathy

Summary Experimental lead encephalopathy was produced in developing rats. The cerebellar changes that developed were studied by light and electron microscopy. Although edema was observed in all phases of the encephalopathy, changes in the blood vessels, formation of platelet thrombi, and alterations of the Purkinje cells and their dendrites warranted special attention. The lead and calcium content of the brain and of the blood in the lead poisoned and control groups were determined chemically. The results are discussed from a morphological point of view and a hypothesis of their pathogenesis is presented.

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Zusammenfassung Wir haben bei neugeborenen Ratten eine experimentelle Blei-Encephalopathie hervorgerufen und die cerebellaren Veränderungen licht- und elektronenmikroskopisch untersucht. In allen Stadien der Encephalopathie war ein Ödem vorhanden, darüber hinaus fanden sich Anzeichen für Capillarschäden, Bildung von Plättchenthromben und Veränderungen der Purkinje-Zellen mit ihren Dendriten. Blei- und Calciumgehalt des Gehirnes wie des Blutes von bleivergifteten Ratten und von Kontrolltieren wurden chemisch untersucht. Die Ergebnisse werden aus der Sicht des Morphologen besprochen, die Pathogenese der Veränderungen diskutiert.

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This work was supported by the Deutsche Forschungsgemeinschaft.

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, St. John's Medical College, Bangalore 34, India.     

Low incidence of mbr bcl-2/JH fusion genes in Hodgkin's disease

Lymph node biopsies from 140 cases of Hodgkin's disease (HD) and from 30 non-malignant lesions were screened for the presence of t(14;18) translocations involving the major breakpoint region (mbr) of the bcl-2 gene and the joining region (J)_H of the immunoglobulin heavy chain gene, using a polymerase chain reaction (PCR) assay with subsequent nucleotide sequencing of amplified bcl-2/J_H junctional regions. Expression of the bcl-2 protein within the Hodgkin and Reed-Sternberg (HRS) cells was investigated in 86 cases of HD by immunohistochemistry on cryostat or paraffin sections. Although bcl-2 expression could be found in a proportion of neoplastic cells in up to one-third of HD cases, the frequency of t(14;18) gene fusions detected by PCR was low. We identified such gene fusions in only 3 out of 140 (2 per cent) HD cases, one biopsy of which presented with four clonally distinct bcl-2/J_H sequences. No t(14;18) was found in any of 30 reactive lymph node lesions. All fusion gene sequences were unique regarding the localization of the chromosome 14 and 18 breakpoints and the extranucleotide N-insertions. None of these gene fusions conformed to t(14;18) breakpoint sequences previously characterized in our laboratories. Our findings point to a mere coincidence in some cases of HD lesions and cells carrying a t(14;18) in the same biopsy and argue against a significant role of bcl-2 in the pathogenesis of HD.