Plasma levels of beta-thromboglobulin and factor viii-related antigen in diabetic children and adults

104

Diabetes mellitus is associated with a variety of vascular complications like diabetic retinopathy, myocardial infarction, stroke and peripheral vessel disease. These complications are of utmost importance because they lead to disability and premature death of the patients. The pathogenesis of these lesions has been thought to depend at least partly on defects in the hemostatic system. Many alterations of the coagulation and the fibrinolytic system as well as of the reaction of platelets have been found in diabetics. In general these tend to suggest a state of slightly activated coagulation, of increased platelet reactivity and of decreased fibrinolysis. However, no conclusive picture of the role of hemostasis in the development of vascular lesions in diabetics has emerged yet, as contradictive results have been found by many investigators. The aim of this review article is to sum up the knowledge that has accumulated in the last years in controlled clinical trials concerning the state of the diabetic hemostatic system.

Section: Platelet Release Reactionmentioning

confidence: 99%

Factors of the Hemostatic System in Diabetic Patients

Ostermann¹,

Loo²

1986

104

“…Endothelial cells synthesize several glyco proteins which play a major role in haemosta sis: von Willebrand factor (vWF) [1], tissuetype plasminogen activator (t-PA) [2], plas minogen activator inhibitor-1 [3] and throm bomodulin [4], There are a number of clinical conditions such as liver cirrhosis [5], athero sclerosis [6], malignancies [7] in which sus-tained elevation of vWF has been reported. The mechanism of the increase in plasma vWF level in these diseases is not necessarily the same.…”

Section: Introductionmentioning

confidence: 99%

Endothelium Releases More von Willebrand Factor and Tissue-Type Plasminogen Activator upon Venous Occlusion in Patients with Liver Cirrhosis than in Normals

Tornai

Hársfalvi

Boda

et al. 1993

Self Cite

Venous occlusion was used in 8 patients with liver cirrhosis and in 10 normals to investigate the pathomechanism of long-term elevation of plasma von Willebrand factor antigen (vWFAg) in liver cirrhosis. The following parameters were determined at baseline, and immediately, 60 min and 24 h after 10 min venous occlusion: vWFAg, ristocetin cofactor (RiCoF), in vitro platelet retention (Adeplat T), and tissue-type plasminogen activator (t-PA). Every baseline value in the liver cirrhosis group was significantly higher than in the controls. In both groups the 10-min values were significantly higher than their corresponding baseline results. Hence, comparing the two groups, in liver cirrhosis a significantly higher release of vWFAg and t-PA could be observed. These findings suggest on the one hand that the increased release contributes substantially to the sustained elevation of plasma vWF level in liver cirrhosis. On the other hand, the results indicate that not only the vascular surface of the diseased liver but most probably the total endothelium plays an important role in this phenomenon.

“…This glyco protein has a unique structure, consisting of a series of different molecular weight multimers of a 270-kD monomer [1], von Wille brand's disease (vWD) is a bleeding disor der, which is characterized by quantitative or qualitative defects of the vWF molecule [2], Although vWD is mainly inherited, ac quired forms have also been described [3]. In addition, a number of other clinical condi tions, such as diabetes mellitus [4], athero sclerosis [5], liver cirrhosis [6], solid tumors [7], uremia [8], pregnancy-induced hyperten sion (P1H) [9] and thrombotic thrombocyto penic purpura [10] with sustained elevated plasma vWF antigen (vWFAg) levels have been described, often associated with either a lack [8] or an excess [10] of the highest multimers.…”

Section: Introductionmentioning

confidence: 99%

Measurement of von Willebrand Factor Antigen in Plasma and Platelets with an Enzyme-Linked Immunosorbent Assay Based on Two Murine Monoclonal Antibodies

Tornai¹,

Declerck²,

Smets³

et al. 1991

Two murine monoclonal antibodies, raised against von Willebrand factor (vWF), were used to construct an enzyme-linked immunosorbent assay (ELISA), for quantitation of vWF antigen (vWFAg) in human plasma and platelets. This assay had a lower limit of sensitivity of 0.0001 IU/ml in buffer, and thus is one to two orders of magnitude more sensitive than other ELISA assays which have been reported. The intraassay, interassay and interdilution coefficients of variation were 4.1, 10.4 and 9.9%, respectively. In normal plasma (n = 20), the vWFAg level was 0.83 (range: 0.42–1.25) IU/ml. In normal washed platelets (n = 10), 0.35 (0.25–0.49) IU/10⁹ platelets was found. In plasma obtained from various patient groups the following vWFAg levels (geometric mean and range) were observed: von Willebrand’s disease (n = 19): 0.18 (0.02–0.77) IU/ml; patients with liver cirrhosis (n = 20): 3.73 (1.68–9.20) IU/ml; patients with pregnancy-induced hypertension (n= 20): 4.14 (2.28–7.44) IU/ml and patients with malignant disease (n = 10), 2.54 (1.51–5.60) IU/ml. A linear correlation was found between vWFAg levels measured with a polyclonal antibody based Laurell electroimmunoassay (r = 0.92, n = 58) or with a polyclonal antibody based ELISA (r = 0.94, n = 64). The present assay is based on stable and reproducible reagents and allows the specific measurement of vWFAg in plasma and in platelets. This assay may constitute a useful tool for the further investigation of clinical conditions associated with changes in vWFAg levels. In addition, its high sensitivity may facilitate a more detailed study of platelet vWFAg in normal and in pathological conditions.