Postoperative development of sarcopenia is a strong predictor of a poor prognosis in patients with adenocarcinoma of the esophagogastric junction and upper gastric cancer

Background

There were few studies assessed the postoperative sarcopenia in patients with cancers. The objective of present study was to assess whether postoperative development of sarcopenia could predict a poor prognosis in patients with adenocarcinoma of esophagogastric junction, (AEG) and upper gastric cancer (UGC).

Five percent, 7.5% or 10% hypertonic saline prevents delayed neuronal death in gerbils

PURPOSE: To clarify the appropriate concentration and dose of hypertonic saline solution (HSS) for preventing delayed neuronal death in the hippocampal CA1 subfield after transient forebrain ischemia in gerbils. METHODS: Thirty gerbils were randomly assigned to five groups: physiological saline solution (PSS) group, ischemia/reperfusion treated with PSS 2 mL x kg(-1); 5% HSS group, treated with 5% HSS 2 mL x kg(-1); 7.5% HSS group, treated with 7.5% HSS 2 mL x kg(-1); 10% HSS group, treated with 10% HSS 2 mL x kg(-1); 20% HSS group, treated with 20% HSS 2 mL x kg(-1). Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes. Five days later, histopathological changes in the hippocampal area were examined, and the degenerative ratio of the pyramidal cells were measured according to the following formula: (number of degenerative pyramidal cells/total number of pyramidal cells per 1 mm of hippocampal CA1 subfield) x 100. RESULTS: In PSS and 20% groups, neuronal cell damage was observed five days after ischemia. In the other three groups, these changes were not observed. The degenerative ratios of pyramidal cells were as follows; PSS group: 91.6 +/- 5.6%, 5% HSS group: 7.2 +/- 1.6%, 7.5% group: 8.3 +/- 1.4%, 10% HSS group: 6.2 +/- 1.1%, 20% HSS group: 85.8 +/- 8.7% (P < 0.05; PSS and 20% HSS vs three other groups). CONCLUSION: This study demonstrates that 5, 7.5 or 10% HSS 2 mL x kg(-1) may prevent delayed neuronal death in the hippocampal CA1 subfield after cerebral ischemia/reperfusion in gerbils.     

Granulocytic sarcoma presenting with lymph node infarction at disease onset

A completely infarcted lymph node is an unusual event. However, lymph node infarction should alert the pathologist to the considerable likelihood of malignant lymphoma. We report two unusual cases of acute myeloid leukemia presenting with granulocytic sarcoma at disease onset with a lymph node lesion exhibiting extensive lymph node infarction. The infarcted tissue contained numerous eosinophilic cell ghosts. There were some islands of degenerated, pyknotic medium-sized nuclei resembling lymphoblasts present in the necrotic area. By immunohistochemistry, these medium sized cells were CD3-, CD20-, CD34+, CD43+, CD45RO-, CD68-, CD79a- and myeloperoxidase+ in both cases. Differentiation of granulocytic sarcoma from malignant lymphomas is important for adequate therapy. The present cases indicate that granulocytic sarcoma should be added to the list of differential diagnoses for lymph node infarction.     

Primary pulmonary low-grade marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue type with prominent hyalinosis. A case report

We report a case of primary pulmonary low-grade marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue (MALT)-type with prominent sclerosis, which morphologically resembled pulmonary hyalinizing granuloma (PHG) or inflammatory pseudotumor (IPT) of the lung. The patient, a 66-year-old Japanese female with a history of Sj?gren's syndrome and primary biliary cirrhosis, presented with a lower left lobe mass 6.8 cm in diameter. Histologically, the lesion is characterized by dense bundles of collagen with scattered plasma cells, mature small lymphocytes, and histiocytes among the collagen bundles. Only the peripheral area of the nodule contained dense lymphoplasmacytoid and histiocytoid infiltrates. A few centrocyte-like cells were obscured by the numerous plasma cells and plasmacytoid cells. In addition, lymphoepithelial lesions and colonalized lymphoid follicles were identified by immunohistochemistry alone. Although PHG and IPT are unlikely to be confused with pulmonary MALT-type lymphomas, the present case suggests that MALT-type lymphoma should be added to the list of differential diagnoses for PHG and IPT.     

Follicular hyperplasia presenting with a marginal zone pattern in a reactive lymph node lesion

Histologically, the marginal zone pattern of the lymph node is characterized by lymphoid follicles with three distinct layers. The inner layer is composed of follicular center zones, the middle layer of darkly stained mantle zones, and the outer layer of marginal zones. However, the marginal zone pattern is rarely seen in reactive lymph nodes except for mesenteric lymph nodes. We describe the clinicopathologic, immunohistochemical and genotypic findings of six cases of reactive follicular hyperplasia exhibiting the marginal zone pattern. The patients comprised three males and three females (age range 24 to 63 years; medium 56 years). Follow-up data were obtained from five patients. None of them developed malignant lymphomas during the follow-up period of from 5 to 204 months (median 68 months). Histologically, the lesion was characterized by numerous lymphoid follicles and partial distortion of lymph node structure. Varying degrees of progressive transformation of the germinal center (PTGC) were noted in the four cases. The marginal zone pattern was observed in some or most of the lymphoid follicles including PTGC. The marginal zone B cells were small to medium-sized lymphocytes with round or slightly indented nuclei and a broad rim of pale cytoplasm. Some of them had a monocytoid appearance. They were CD20+, CD79a+, sIgM+/-, sIgD-, CD5-, CD10-, CD21-, CD23-, CD43-, CD45RO-, Bcl-6-, cyclin D1-, EMA- and p53-. A portion of them were Bcl-2 positive. Occasional large lymphoid cells with round or indented nuclei and moderate amounts of cytoplasm were observed in the marginal zone in four cases. These large lymphoid cells were usually CD20 positive, but Bcl-6 negative. A small number of them contained polytypic intracytoplasmic immunoglobulins. The polytypic nature of B lymphocytes was demonstrated by immunohistochemistry and polymerase chain reaction. Recognition of unusual marginal zone hyperplasia in reactive lymph node lesions is important to avoid confusion with nodal involvement in various low-grade B cell lymphomas presenting a marginal zone distribution pattern.     

Inflammatory pseudotumor of lymph nodes: clinicopathologic and immunohistological study of 11 Japanese cases

We report 11 Japanese cases of inflammatory pseudotumor (IPT) of the lymph node. There were 7 males and 4 females with ages ranging from 5 to 68 years (median; 48). Only 2 patients had systemic lymphadenopathy, and all others had involvement of only 1 lymph node group. Constitutional symptoms such as fever were present in 8 patients and laboratory abnormalities were detected in 5. All patients recovered and were alive and well after 2 to 180 months (median; 32 months). Histologically, the process mainly involved the connective tissue framework of the lymph node, secondarily spreading into the lymph node parenchyma and the perinodal tissue. It was characterized by a storiform growth pattern of myofibroblasts, marked vascularity with associated vascular lesions, and a polymorphous reactive cellular infiltrate in a collagen-rich stroma. An immunohistochemical study revealed numerous myofibroblasts, histiocytes, and vascular endothelial cells expressing vascular endothelial growth factor (VEGF) in 6 cases. It was suggested that VEGF may be involved, in part, in the induction of the angiogenesis of IPT. Moreover, the present study indicates that follicular dendritic cell sarcoma, nasal T/natural killer cell lymphoma, and anaplastic large cell lymphoma should be added to the differential diagnosis from IPT of the lymph node. Int J Surg Pathol 9(3):207-214, 2001     

Different roles of arteriosclerosis in the rupture of intracranial dissecting aneurysms

AIMS: Although intracranial dissecting aneurysm (IDA) is a newly described variant of the brain aneurysms that affects mainly the vertebrobasilar arterial system, its pathogenesis remains obscure. We aimed to clarify the role of arteriosclerosis in the pathogenesis of IDA based on histopathological findings in seven autopsy cases of IDA. METHODS AND RESULTS: All cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited subarachnoid haemorrhage. Two types of dissection were recognized in the vertebral artery. Six of seven IDA cases showed a widespread disruption of the entire thickness of the arterial wall with the formation of a dilated pseudoaneurysm, which consisted of thin adventitia (arterial wall disruption type). Medial disruption of the arterial wall and subadventitial dissecting haemorrhage were also found, resulting in the formation of a false lumen and stenosis of the 'true' lumen of the artery. However, these lesions were connected to the site of rupture of the entire arterial wall. Within 1 day after onset of IDA, the autopsy cases showed formation of fibrin thrombus, marked leucocyte infiltration and necrosis of the arterial wall at the site of the lesion. Cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration in the lesions. These cases showed no atherosclerotic plaque, but non-atherosclerotic fibrocellular intima. The thickness of intima and media was significantly less in the vertebral artery of IDA patients than that of non-IDA patients with systemic hypertension. On the other hand, the remaining case showed severe atherosclerosis with haemorrhage into the lipid core without connection to the arterial lumen (intra-atheromatous plaque haemorrhage type). However, unusual arterioles and neovascularization of the intra-and peri-arterial walls were observed. CONCLUSIONS: Our results suggest that disruption of the entire arterial wall may be a critical event in the development of IDA and result in the medial disruption and subadventitial haemorrhage. Non-atheromatous intima might function as a protective factor in arterial wall disruption. On the other hand, atherosclerosis may predispose to intra-atheromatous plaque haemorrhage type of IDA through intramural haemorrhage originating from the newly formed vessels.     

Lymph node necrosis in systemic lupus erythematosus. A histopathological and immunohistochemical study of four cases

The lymph node lesions of lupus lymphadenitis are characterized by necrosis sometimes accompanied by hematoxylin bodies, but only a few immunohistological analyses of this unique lesion have been reported. In this study we investigated the immunopathogenesis of these lesions. Lymph node specimens from four patients were analyzed immunohistochemically by applying recently developed monoclonal antibodies to immunocompetent cells. Necrosis occupied almost the entire lymph node in two cases (extensive type), whereas small foci of necrosis were found in the paracortex in the remaining two (localized type). No hematoxylin body formation was detected in any of the samples. Necrosis of the small muscular arteries, arterioles and venules was seen in the necrotic areas in all four cases. In one case of the localized type, necrotizing angitis was seen in a few arterioles and venules in the non-necrotic area. By immunohistology, amorphous depositions of immunoglobulins and C3 were demonstrated in the walls of the arterioles and venules in two cases. Our findings indicate that vasculitis due to local deposition of immune complexes in the blood vessels may play an important role in the pathogenesis of necrosis in lupus lymphadenitis.     

Analysis of intestinal HLA-DR bound peptides and dysregulated immune responses to enteric flora in the pathogenesis of inflammatory bowel disease

Isolation of antigenic peptides from the MHC-groove has contributed to the understanding of T cell responses. However, these MHC-associated peptides have been isolated from various murine and human cell lines. The specific antigen responsible for the pathogenesis of inflammatory bowel disease is unknown. We examined antigenic peptides bound to the class II major histocompatibility complex (MHC) groove in human intestine by ion-trap tandem mass spectrometry equipped with online reverse-phase high performance liquid chromatography. We detected 55 parent proteins from 4 controls, 9 patients with ulcerative colitis, and 9 patients with Crohn's disease. The calculated molecular masses (m/z) of these peptides ranged from 874.4 to 2727.4, representing 10-26 amino acid residues. Fifty-one of these 55 parent proteins were exogenous proteins. Escherichia coli-, Saccharomyces cerevisiae-, and Caenorhabditis elegans-derived peptides were found frequently in patients with inflammatory bowel disease. The present results suggest that in vivo antigen processing by antigen-presenting cells and T lymphocytes in human intestine participate with exogenous antigen presentation. Increased immune responses against E. coli, S. cerevisiae and C. elegans found in patients with inflammatory bowel may participate as dysregulated immune responses to enteric flora in the pathogenesis of inflammatory bowel disease.     

Follicular lymphoma of the salivary gland: a clinicopathological and molecular study of six cases

To clarify the clinicopathologic, immunohistologic, and genotypic features of follicular lymphoma arising from the salivary glands, we examined 20 cases of operatively resected primary salivary gland lymphoma and identified 6 such cases. There were 4 women and 2 men with ages ranging from 38 to 64 years (median 50 years). The tumor arose from the parotid gland in 4 cases and the submandibular gland in the remaining 2. Four patients were stage IE and 2 were stage IIE-1. The median follow-up period was 49 months and all patients were alive and well at the time of going to press. Histologically, 5 patients were follicular lymphoma grade 2, and 1 was grade 3. In all specimens in noninfiltrating salivary gland tissue, there was periductal lymphocytic infiltration near the lymphoma. Moreover, myoepithelial sialoadenitis was noted in 2 lesions. An immunohistochemical study revealed all 6 cases were CD10+, CD79a+, bcl-6+, CD3-, CD5-, CD21-, CD23-, and CyclinD1-. The tumor cells expressed bcl-2 in 3 cases and p53 oncoprotein in 4 cases. Two cases revealed clonal bands with polymerase chain reaction (PCR) assay for the immunoglobulin heavy (IgH) gene. The bcl-2/IgH translocation at the major breakpoint region was detected in 1 case (16%). We found a relatively high incidence of follicular lymphomas (30%) in salivary gland lymphomas. Among the mucosa-associated lymphoid tissue (MALT) system, follicular lymphomas appeared to occur frequently in the salivary glands as well as the duodenum and skin. Moreover, follicular lymphoma arising from the salivary glands appeared to have some of the characteristics of MALT-type lymphoma including indolent prognosis, presence of myoepithelial sialoadenitis, and rarity of the BCL-2 gene rearrangement.