Behaviour of Von Willebrand Factor Antigen in Follow-up of Polymyalgia Rheumatica/Giant Cell Arteritis

Ciompi, Maria Laura; Marotta, Giorgio; Puccetti, Lorenzo; Remorini, E.; Petrini, G.; Zuccotti, Mauro; Vispi, M; Baicchi, U; Iacconi, Pietro

doi:10.3109/03009748809098813

Cited by 17 publications

(12 citation statements)

References 13 publications

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“…In contrast, a recent systematic review found that in patients with inflammatory disease (e.g. giant cell arteritis), GCs lowered vWF levels (70, 71,72,73). An acute high-dose of GC has been associated with a rapid activation of endothelial nitric oxide (NO) synthase via a direct non-genomic effect, which in turn enhances NO release (74).…”

Section: Platelet Activationmentioning

confidence: 91%

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

Isidori

Minnetti

Sbardella

et al. 2015

European Journal of Endocrinology

101

107

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Glucocorticoids (GCs) target several components of the integrated system that preserves vascular integrity and free blood flow. Cohort studies on Cushing's syndrome (CS) have revealed increased thromboembolism, but the pathogenesis remains unclear. Lessons from epidemiological data and post-treatment normalisation time suggest a bimodal action with a rapid and reversible effect on coagulation factors and an indirect sustained effect on the vessel wall. The redundancy of the steps that are potentially involved requires a systematic comparison of data from patients with endogenous or exogenous hypercortisolism in the context of either inflammatory or non-inflammatory disorders. A predominant alteration in the intrinsic pathway that includes a remarkable rise in factor VIII and von Willebrand factor (vWF) levels and a reduction in activated partial thromboplastin time appears in the majority of studies on endogenous CS. There may also be a rise in platelets, thromboxane B2, thrombin-antithrombin complexes and fibrinogen (FBG) levels and, above all, impaired fibrinolytic capacity. The increased activation of coagulation inhibitors seems to be compensatory in order to counteract disseminated coagulation, but there remains a net change towards an increased risk of venous thromboembolism (VTE). Conversely, GC administered in the presence of inflammation lowers vWF and FBG, but fibrinolytic activity is also reduced. As a result, the overall risk of VTE is increased in long-term users. Finally, no studies have assessed haemostatic abnormalities in patients with Addison's disease, although these may present as a consequence of bilateral adrenal haemorrhage, especially in the presence of antiphospholipid antibodies or anticoagulant treatments. The present review aimed to provide a comprehensive overview of the complex alterations produced by GCs in order to develop better screening and prevention strategies against bleeding and thrombosis.

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Section: Platelet Activationmentioning

confidence: 91%

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

Isidori

Minnetti

Sbardella

et al. 2015

European Journal of Endocrinology

101

107

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“…Design In total, 17 controlled clinical trials [23,26–41], seven cross‐sectional studies [25,42–47] and 13 drug‐intervention studies were included [44,48–59]. One paper incorporated both a cross‐sectional and a drug‐interventional design [44].…”

mentioning

confidence: 99%

“…Participants Twelve trials investigated healthy subjects [26–31,33,34,36,38–40] and four trials included patients undergoing surgery [23,32,35,37]. Seven papers studied patients with giant cell arteritis or polymyalgia rheumatica [44,48,50,51,54,58,59], three papers included patients with systemic lupus erythematosus [42,43,52], three investigated heart or renal transplant recipients [25,41,57] and another three studied patients with collagen disease [45,46,56]. The four remaining studies included patients with sepsis syndrome [47], Crohn’s disease [53], Henoch Schönlein [55] or other chronic inflammatory diseases [49].…”

mentioning

confidence: 99%

Systematic review on the effect of glucocorticoid use on procoagulant, anti‐coagulant and fibrinolytic factors

Zaane

Nur

Squizzato

et al. 2010

Journal of Thrombosis and Haemostasis

171

131

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To cite this article: van Zaane B, Nur E, Squizzato A, Gerdes VEA, Bü ller HR, Dekkers OM, Brandjes DPM. Systematic review on the effect of glucocorticoid use on procoagulant, anti-coagulant and fibrinolytic factors. J Thromb Haemost 2010; 8: 2483-93.Summary. Background: Whether glucocorticoid use contributes to a hypercoagulable state, and thereby enhances the thrombotic risk, is controversial. Objective: We aimed to examine the effects of glucocorticoid use on coagulation and fibrinolysis. Methods: MEDLINE and EMBASE databases were searched to identify published studies comparing glucocorticoid treatment with a glucocorticoid-free control situation. Subjects could be either patients or healthy volunteers. Two investigators independently performed study selection and data extraction. Results were expressed as standardized mean difference, if possible; data were pooled with a random-effects model. Results: Of the 1967 identified publications, 36 papers were included. In healthy volunteers, a clear rise in factor (F)VII, VIII and XI activity was observed after glucocorticoid treatment, but these data alone provided insufficient evidence to support hypercoagulability. However, during active inflammation, glucocorticoids significantly increased levels of plasminogen activator inhibitor-1 (PAI-1), whereas levels of von Willebrand factor (VWF) and fibrinogen decreased. Perioperative use of glucocorticoids inhibited the increase in tissue-type plasminogen activator induced by surgery. Conclusions: The present study showed differential effects of glucocorticoids depending on the clinical situation in which it is given, most likely as a result of their disease modifying properties. Clinical outcome studies are needed to adequately assess the risk-benefit of glucocorticoid use per population when thrombotic complication is the focus.

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“…Other workers, such as Ciompi et al, have expressed an opposite view, stating that vessel injury is a common feature of scleroderma, glomerulonephritis, diabetes mellitus, Behqet's syndrome, systemic lupus erythematosus, rheumatoid arthritis, and vasculitis in general. 5 There seems to be little disagreement about the presence of raised vWFAg in a large number of conditions, some of which may be characterised by histological evidence of injury to the vasculature. However, the exact mechanism, in many cases, is unclear.…”

Section: Jiri T Beranek Division Of Cardiologymentioning

confidence: 99%

Endothelium damage and von Willebrand factor antigen.

P¹,

Olsson²,

Elling³

1993

Annals of the Rheumatic Diseases

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was noted with low doses of prednisone, however, in contrast with the dramatic improvement obtained in the original papers.5 6 On the other hand, synovial biopsy in our case did not show malignant infiltration. Thus it is reasonable to suggest that the rheumatic manifestations belong to a paraneoplastic syndrome, as has been previously reported with other neoplasms.7To our knowledge this is the first description of peripheral synovitis and pitting oedema as an initial manifestation of non-Hodgkin's lymphoma. We would like to

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Behaviour of Von Willebrand Factor Antigen in Follow-up of Polymyalgia Rheumatica/Giant Cell Arteritis

Cited by 17 publications

References 13 publications

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

Systematic review on the effect of glucocorticoid use on procoagulant, anti‐coagulant and fibrinolytic factors

Endothelium damage and von Willebrand factor antigen.

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