Plasma viscosity in giant cell arteritis as a predictor of disease activity.

Guðmundsson, M. T.; Nordborg, E; Bengtsson, Bengt‐Åke; Bjelle, A

doi:10.1136/ard.52.2.104

Cited by 22 publications

(13 citation statements)

References 26 publications

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“…Rat liver cells in vitro have been shown to respond to DEX by increasing the synthesis of FBG mRNA, whereas no induction of the FBG-polypeptide mRNA was observed in vivo at various times after the injection of different doses of GCs into the livers of rats (79). When GCs are used in the setting of increased inflammatory activity, they significantly decreased FBG (56,71,78,80). This biphasic response is explained by the dose-dependency of GC anti-inflammatory effects on the acute phase response (including FBG) (70) (Fig.…”

Section: Coagulation Cascadementioning

confidence: 99%

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

Isidori

Minnetti

Sbardella

et al. 2015

European Journal of Endocrinology

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: Coagulation Cascadementioning

confidence: 99%

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

Isidori

Minnetti

Sbardella

et al. 2015

European Journal of Endocrinology

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%

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

169

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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“…However, a study by Gudmundsson et al [6] report that 10% of GCA patients present with normal CRP. Furthermore, PV proved best at predicting flare-ups, while CRP did not.…”

Section: Discussionmentioning

confidence: 99%

“…PV is a hemorheological marker associated with the acute phase response that was repeatedly shown to be elevated in GCA patients [5,6,7] and in patients with vascular disease [8,9,10]. Here, PV and inflammatory markers ESR, CRP and fibrinogen were determined in GCA patients and in a sample of patients with various nonrheumatic inflammatory conditions.…”

Section: Introductionmentioning

confidence: 99%

Plasma Viscosity in Giant Cell Arteritis

Finke

Schroeter²,

Kalus³

et al. 2011

Eur Neurol

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Background: Diagnosis of giant cell arteritis (GCA) is based on criteria of the American College of Rheumatology. However, not all GCA patients meet these criteria and treatment may be delayed in individual patients, leading to an increased risk of complications. Methods: In an observational study, we investigated acute phase response markers in GCA and non-GCA patients matched for erythrocyte sedimentation rate and CRP levels. Results: Plasma viscosity (PV) was significantly elevated in all GCA patients, but normal in non-GCA patients. Conclusions: Our data suggest that PV may reflect a more specific component of the acute inflammatory response in patients with GCA. Analysis of PV may significantly contribute to a reliable diagnosis early in the course of the disease, particularly in patients with suspected GCA that do not meet current diagnostic criteria.

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Plasma viscosity in giant cell arteritis as a predictor of disease activity.

Cited by 22 publications

References 26 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

Plasma Viscosity in Giant Cell Arteritis

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