A rare case of cardiac sarcoidosis in a patient with progressive systemic sclerosis, Sjogren's syndrome, and polymyositis.

A 56-year-old woman with overlap syndrome of progressive systemic sclerosis (PSS), Sjogren's syndrome, and polymyositis is reported. She developed complete atrioventricular (AV) block and progressive bilateral hilar adenopathy, and was diagnosed as having sarcoidosis by histological examination of the hilar lymph nodes biopsied thoracoscopically. Although coexistence of one or two autoimmune diseases with sarcoidosis is not uncommon, coexistence of three or more autoimmune diseases with sarcoidosis is rare. To our knowledge, the described case is the first case in which the three above-mentioned autoimmune diseases were accompanied by myocardial sarcoidosis.

Reduction of rat myocardial ischaemia/reperfusion injury by a synthetic selectin oligopeptide.

Neutrophils infiltrate into myocardial tissue subjected to ischaemia followed by reperfusion and play a major role in myocardial reperfusion injury. The infiltration of neutrophils begins within 2 h after reperfusion, indicating the engagement of rapidly inducible adhesion molecules, such as P-selectin, on vascular endothelial cells of myocardial tissue. To investigate the essential role of P-selectin in myocardial reperfusion injury, this study examined the expression of P-selectin in rat hearts subjected to 30 min of ischaemia followed by reperfusion. The induction of P-selectin was also evaluated on the surface of cultured rat vascular endothelial cells subjected to 60 min of hypoxia, followed by reoxygenation in vitro. Finally, the effects of in vivo administration of a synthetic selectin oligopeptide on myocardial necrosis were analysed. Reperfusion of ischaemic myocardial tissue resulted in enhanced expression of P-selectin on the luminal surface of vascular endothelium and surface expression of P-selectin was induced on cultured vascular endothelial cells by hypoxia/reoxygenation in vitro. The in vivo administration of a synthetic selectin oligopeptide significantly reduced the area of myocardial infarction produced by 30 min of ischaemia, followed by 48 h of reperfusion. These data offer therapeutic possibilities for acute myocardial infarction.

Induction of sialyl Lewis(X) on the surface of cultured rat vascular endothelial cells and cardiac myocytes by hypoxia/reoxygenation in vitro.

Neutrophils adhere to and roll on vascular endothelial cells (VECs) through interaction of selections and their carbohydrate ligands in the early stages of inflammation; this adhesion is then later strengthened through interaction of integrins on neutrophils with intercellular adhesion molecule-1 (ICAM-1) on endothelial cells. Recent, as yet unpublished studies showed that myocardial ischaemia/reperfusion caused rapid expression of sialyl Lewis(X) (SLe(X)), one of the carbohydrate ligands of selections, on VECs and cardiac myocytes and that an anti-SLe(X) monoclonal antibody (MAb) significantly reduced myocardial reperfusion injury in vivo, In the present study, to investigate whether or not ischaemia/reperfusion itself can induce the expression of SLe(X) on VECs and cardiac myocytes, the expression of SLe(X) on cultured rat VECs and cardiac myocytes was examined by treatment with hypoxia/reoxygenation in vitro, because ischaemia/ reperfusion stimuli may partly be due to hypoxia/reoxygenation. The expression of SLe(X) was induced rapidly and temporarily on the surface of cultured rat cardiac myocytes and VECs by hypoxia/reoxygenation in vitro. This strongly suggests that the expression of SLeX on the surface of myocardial cells is induced initially and directly by ischaemia/reperfusion, which results in the rolling attachment of neutrophils in the early stages of myocardial reperfusion injury.

Expression of sialyl Lewis(X) in rat heart with ischaemia/reperfusion and reduction of myocardial reperfusion injury by a monoclonal antibody against sialyl Lewis(X)

Neutrophils which infiltrate into the myocardial tissue subjected to ischaemia, followed by reperfusion, play a major role in myocardial reperfusion injury. It is known that early rolling attachment of neutrophils is mainly mediated by the selection family of cell-adhesion molecules and that this adhesion is then strengthened through the interaction of integrins and intercellular adhesion molecule-1. To investigate the role of sialyl Lewis(X) (SLe(X)), which is a ligand of all three members of the selections, in myocardial reperfusion injury, the expression of SLe(X) was examined in rat hearts subjected to 30 min of ischaemia followed by reperfusion. The effects were also analysed of in vivo administration of an anti-SLe(X) monoclonal antibody (MAb) on myocardial necrosis in a rat model of myocardial reperfusion injury. Reperfusion of ischaemic myocardial tissue resulted in enhanced expression of SLe(X) on the luminal surface of vascular endothelial cells (VECs), as well as cardiac myocytes. Furthermore, the in vivo administration of an anti-SLe(X) MAb significantly reduced the extent of the myocardial infarction developed after 30 min of ischaemia followed by 48 h of reperfusion. These findings indicate that SLe(X) plays a critical role in the development of myocardial reperfusion injury and offer a potentially useful immune therapy to protect against this injury.