An increased factor VIII antigen as an indicator of endothelial damage in measles

Corda, R.; Alberti, Marta; Caocci, L; Putzolu, G.; Pm, Mannucci

doi:10.1016/0049-3848(79)90136-1

Cited by 20 publications

(2 citation statements)

References 12 publications

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“…=high density lipoprotein cholesterol, TG=triglycerides, FFA=free fatty acids, process and the putative associated release of VIIIR :Ag may be slower and lesser in amount than those seen in diffuse acute vasculitis accompanied by elevated plasma levels of VIIIR:Ag. 21 3) The release of VIIIR :Ag may be an intermittent or cyclic phenomenon with elevated plasma VIIIFVAg levels being detectable only at certain times. The two peaks of VIIIR:Ag (Figure 3) at weeks 4 and 22 might be consistent with this possibility, although conceivably the earlier peak might have reflected some residual effect of the mechanical endothelial injury sustained at the time of the sham or coarctation reversal surgery at the 1-week point.…”

Section: Viiir:ag Changesmentioning

confidence: 99%

Changes in plasma factor VIII complex and serum lipid profile during atherogenesis in cynomolgus monkeys.

et al. 1990

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If endotheiial injury plays a prominent role in early atherogenesis, the plasma levels of von Willebrand factor (VWF), which is made within and normally released from endotheiial cells, might be expected to rise as a marker of the cellular damage. To evaluate this hypothesis, we measured plasma VWF (as VIIIR Ag), factor VIII C, and serum lipids serially up to 37 weeks in 29 adult male cynomolgus monkeys on an atherogenic diet. Factor VIII C peaked at 113% above baseline by week 10 (p<0.0001), then fell and remained 53% below baseline (p<0.04) during weeks 20 to 37. However, the overall rise in VWF was not significant. In contrast, serum cholesterol continued to rise after week 21. Serum phospholipids (PL), triglycerides (TG), and free fatty acids (FFA) showed a temporal pattern similar to VIII C. Significant positive correlations with VIII C were noted for PL (r=0.59, p=0.0001) and TG (r=0.36, p=0.0096). At autopsy, small to moderately advanced atherosclerotic lesions were distributed throughout the aortas of the majority of the animals. We conclude that changes in plasma VIIIR Ag do not correlate with atherogenesis in this model. However, the similar course of VIII C, TG, and PL suggests that these substances may be involved and perhaps interrelated early in atherogenesis.

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Section: Viiir:ag Changesmentioning

confidence: 99%

Changes in plasma factor VIII complex and serum lipid profile during atherogenesis in cynomolgus monkeys.

et al. 1990

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“…It serves as a connecting bridge between platelets and injury-exposed vascular subendothelium (10)(11)(12). In laboratory diagnostics the von Willebrand factor serves as a marker of endothelial damage (13,14). The cellular von Willebrand factor is either secreted directly from the cytosol or after stimulation, when von Willebrand factor is released by von Weibel-Palade bodies.…”

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confidence: 99%

Effect of Cyclosporine A on the Release of Tissue Factor Pathway Inhibitor from Endothelial Cells in Heart Transplant Patients and Cell Culture

Tiemann

Prohaska²,

Körfer³

et al. 1997

Clinical Chemistry and Laboratory Medicine

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Summary: We investigated the influence of cyclosporine A on the concentration of tissue factor pathway inhibitor and von Willebrand factor antigen in plasma of heart transplant outpatients.Tissue factor pathway inhibitor was quantified in plasma of blood donors (n = 50) and heart transplant outpatients (n = 50) by a chromogenic substrate assay with a mean of 32.4 μg/l and 98.2 μ^, respectively. Von Willebrand factor antigen was determined with an enzyme-linked immunoassay with a mean of 90.9% for blood donors and 184.5% in plasma of heart transplant recipients.In addition, we investigated the effect of cyclosporine A on endothelial cell cultures over an incubation period of four days. A dose-dependent effect of cyclosporine A on the release of endothelial tissue factor pathway inhibitor and von Willebrand factor antigen was determined in a concentration range from 100 to 200 μg/l cyclosporine A. The tissue factor pathway inhibitor and von Willebrand factor antigen concentrations in the cell culture supernatant increased during the incubation time according to the cyclosporine A concentration 2-3 fold and 2 fold, respectively.For a further elucidation of the cyclosporine A effect we investigated the influence of cremophor EL, the vehicle of cyclosporine A. Cremophor EL alone did not increase the tissue factor pathway inhibitor release. However, the release was enhanced 2-4 fold after co-stimulation with the calcium ionophore A 23187 (10~4mol/l) in a concentration-dependent mode.We conclude that a generalized endothelial damage or activation is most probably caused by cyclosporine A and its vehicle cremophor EL. This process probably depends upon the increase of cytosolic free calcium, as described for the liberation of von Willebrand factor by endothelial cells.

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Increased von willebrand factor antigen in the plasma of patients with vasculitis

Nusinow

Federici

Zimmerman

et al. 1984

Arthritis & Rheumatism

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The plasma concentrations of von Willebrand factor antigen (vWF:Ag) were determined in 101 patients who had the following diagnoses: vasculitis 8 patients, systemic lupus erythematosus (SLE) 51, rheumatoid arthritis (RA) 28, asthma 7, hereditary angioedema 7. The greatest mean concentration of vWF:Ag, 469% (normal 100% k 50), was observed in patients with vasculitis, often without elevation of the erythrocyte sedimentation rate. The mean concentration of vWF:Ag was also increased in both SLE (277%) and RA (194%). Twenty-four patients (15 with SLE, 6 with vasculitis, 3 with RA) had vWF:Ag concentrations >300%. Four of these patients died within 1 year of the date of the study. Of the 15 SLE patients, 9 had vasculitis and 2 had active glomerulonephritis. The 3 RA patients had severe disease associated with extraarticular manifestations. Elevated vWF:Ag may reflect vascular damage, while markedly elevated levels of vWF:Ag appear to indicate a poor prognosis.Vasculitis is a clinicopathologic process associated with the inflammation and/or necrosis of blood Publication number 3283BCR from the

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An increased factor VIII antigen as an indicator of endothelial damage in measles

Cited by 20 publications

References 12 publications

Changes in plasma factor VIII complex and serum lipid profile during atherogenesis in cynomolgus monkeys.

Changes in plasma factor VIII complex and serum lipid profile during atherogenesis in cynomolgus monkeys.

Effect of Cyclosporine A on the Release of Tissue Factor Pathway Inhibitor from Endothelial Cells in Heart Transplant Patients and Cell Culture

Increased von willebrand factor antigen in the plasma of patients with vasculitis

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