摘要:

A 49-year-old man with multiple myeloma (IgG-Λ, Bence-Jones protein positive) presented a bleeding tendency: characterized intramuscular hemorrhage. Coagulation studies showed a von Willebrand factor (vWF) defect (Duke bleeding time > 20 min; ristocetin cofactor activity [vWF:RC] < 6%; significant reduction of large multimers of vWF. Mixing study suggested the presence of inhibitor directed against vWF:RC activity and collagen binding activity of vWF. The inhibitor was identified as an antibody of the IgG class. The inhibitor blocked the interaction of vWF with glycoprotein Ib in the presence of ristocetin, as did the pepsin-digested fragment of the inhibitor [F(ab)2], but neither blocked botrocetin-mediated interaction of vWF with glycoprotein Ib. They also inhibited the binding of vWF to immobilized collagen type I. The inhibitor and the F(ab)2 reacted strongly with native vWF and fragment I (amino acids 911–1365) and with the 39/34 kDa fragment (amino acids 480/481–718), but not with fragment II (amino acids 1366–2050) and fragment III-T2 (heavy chains, amino acids 273–511; light chains, amino acids 674–728). We conclude that the IgG antibody inhibits both vWF:RC activity and the binding of vWF to collagen by reacting with the epitopes present on the Al loop and A3 domains of vWF. Blood Coag Fibrinol 9:91–97 × 1998 Rapid Science Ltd.

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Cell surface adhesion molecule expression is likely to be important in inflammation, atherosclerosis and cancer, and soluble forms of many of these molecules are present in plasma. We measured levels of the soluble form of platelet endothelial cell adhesion molecule-1 (sPECAM) by ELISA in the serum of 77 patients with frank atherosclerosis, 69 patients with inflammatory connective tissue disease, and 39 patients with cancer. Each group of patients was controlled by an equal number of age- and sex-matched healthy subjects. There was no difference between sPECAM in patients with atherosclerosis and their matched controls or between patients with connective tissue disease and their controls. However, sPECAM levels were lower (16.6 × 5.0 ng/ml, mean × SD) in patients with cancer than in their controls (21.1 × 4.4 ng/ml, P < 0.001). No differences were found in sPECAM levels between the major subgroups of each type of disease, or as a result of factors such as age, sex or smoking in the controls. In contrast to levels of many other soluble adhesion molecules, levels of sPECAM are not altered in inflammatory or atherosclerotic vascular disease and therefore appear to have little relevance in these conditions. However, there may be significant differences in sPECAM levels in patients with low levels in cancer. Additional investigations are therefore justified. Blood Coag Fibrinol 9:99–103 × 1998 Rapid Science Ltd.

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID