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Background Mondor's disease (MD) is considered an inflammatory condition of superficial vasculitis that develops mainly in the anterolateral thoracoabdominal wall. The pathogenesis of the disease has been controversial, however, because of the lack of histopathologic methods for differentiating between the small vein and the lymphatic vessel. Aim To objectively examine the origin of vascular lesions in MD, we investigated the endothelial cells of their blood and lymphatic vessels. Methods Immunohistochemical examinations were carried out on specimens involving vascular lesions from 16 patients with MD, using antibodies against von Willebrand factor and human lymphatic vessel endothelial hyaluronan receptor-1, which specifically discriminate between lymphatic and blood vessels. Results The histopathologic findings clearly showed thrombophlebitis in 14 patients, a lesion originating in the lymphatic vessel in one patient, and sclerosis that consisted of the artery together with veins in another. Conclusion This study suggests that almost all cases of MD are due to thrombophlebitis, with a small minority due to lymphangitis or other conditions. We believe this study will contribute to the better recognition of the factual changes in the condition designated MD. [ABSTRACT FROM AUTHOR]

Aims: The renal lymphatics have not been fully documented in humans. The aim of this study was to clarify the morphology of the human renal lymphatic system under normal and pathological conditions by immunohistochemistry using anti-D2-40 antibody. Methods and results: Normal and pathological renal tissues obtained at autopsy as well as nephrectomy specimens with renal cell carcinoma (RCC) were used. Thin sections were immunostained with antibodies against D2-40 and CD31. In normal kidney, D2-40+ lymphatics were abundant in the interstitium around the interlobar and arcuate arteries/veins but sporadic in those around the glomeruli or between the tubules in the cortex. A few lymphatics contained erythrocytes in their lumina. Lymphatics were seldom present in the medulla. In RCC cases, lymphatics were evident at the tumour margin, whereas CD31+ capillaries were abundant throughout the tumour and lymphatics were increased in the fibrous interstitium around the tumour. Lymphatic invasion by RCC cells was also detectable. D2-40+ lymphatics were evident in other pathological conditions and end-stage kidney had a denser lymphatic distribution than normal kidney. Conclusions: Lymphatics are abundant around the arteries/veins and are also present in the renal cortex and medulla. D2-40 immunostaining is helpful for investigating the pathophysiological role of renal lymphatics. [ABSTRACT FROM AUTHOR]

Aims: Secretory phospholipase A2 is associated with ischaemic injury in the human heart, but the distribution of type V secretory phospholipase A2 (sPLA2-V) remains unknown. The significance of sPLA2-V in myocardial infarction was investigated histopathologically. Methods: Sequential changes in the localization of sPLA2-V and its mRNA in myocardial tissues obtained from 30 autopsied hearts were examined by immunohistochemistry and in situ hybridization and compared with those of fibronectin, vascular endothelial growth factor (VEGF), interleukin (IL)-1 β, tumour necrosis factor (TNF)-α, and cyclooxygenase-2 (COX-2). Results: No expression of sPLA2-V was observed in normal heart, but it was promptly expressed in wavy myofibres positive for fibronectin just after the onset of infarction. sPLA2-V was subsequently expressed in ischaemic cardiomyocytes around the lesion. The expression decreased at the granulation tissue and disappeared at the chronic stage with scar formation. The distribution of the signal for sPLA2-V mRNA paralleled that of the protein. Ischaemic myocytes around the lesion expressed VEGP, IL-1 β, TNF-α and COX-2 at all stages. Conclusions: sPLA2-V production in myocardium is limited to the acute phase of infarction. sPLA2-V may play a dual role, acting both to remove degraded cell-membrane through cooperative activity with COX-2 in necrotic areas and to attack ischaemic myocytes around the lesion via degradation of membrane phospholipids. [ABSTRACT FROM AUTHOR]