Anti-TNF-α therapy reduces endothelial cell activation in non-diabetic ankylosing spondylitis patients.

Endothelial dysfunction can be detected by the presence of elevated levels of biomarkers of endothelial cell activation. In this study, we aimed to establish whether correlations of these biomarkers with characteristics of patients with ankylosing spondylitis (AS) exist. We also studied the effect of anti-TNF-α therapy on these biomarkers.

IGF-1 and ADMA levels are inversely correlated in nondiabetic ankylosing spondylitis patients undergoing anti-TNF-alpha therapy.

Like rheumatoid arthritis, ankylosing spondylitis (AS) is also an inflammatory disease associated with accelerated atherosclerosis and the presence of metabolic syndrome (MeS) features. AS patients often display osteoporosis as well as new bone formation. Insulin-like growth factor 1 (IGF-1) is a protein involved in both inflammation and bone metabolism.

Osteoprotegerin correlates with disease activity and endothelial activation in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.

Objectives: Osteoprotegerin (OPG) has been associated with increased risk and severity of atherosclerotic disease in the general population. Since ankylosing spondylitis (AS) is a chronic inflammatory disease associated with accelerated atherosclerosis, we aimed to assess whether OPG levels correlate with disease activity, systemic inflammation, metabolic syndrome, adipokines and biomarkers of endothelial cell activation in patients with AS undergoing TNF-α antagonist therapy.

Methods: We assessed OPG plasma concentration in 30 non-diabetic AS patients without cardiovascular disease undergoing TNF-α antagonist-infliximab therapy.

Patients with ankylosing spondylitis and low disease activity because of anti-TNF-alpha therapy have higher TRAIL levels than controls: a potential compensatory effect.

Objective: TRAIL is a potential biomarker of cardiovascular (CV) disease. Ankylosing spondylitis (AS) is a chronic inflammatory disease associated with metabolic syndrome (MeS) and accelerated atherosclerosis. We assessed whether disease activity, systemic inflammation, and MeS features were associated with circulating TRAIL levels in AS patients undergoing TNF-α antagonist infliximab therapy and if infliximab infusion modified TRAIL levels.

Adipokines, biomarkers of endothelial activation, and metabolic syndrome in patients with ankylosing spondylitis.

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease associated with accelerated atherosclerosis and increased risk of cardiovascular (CV) disease. AS patients also display a high prevalence of features clustered under the name of metabolic syndrome (MeS). Anti-TNF- α therapy was found to be effective to treat AS patients by suppressing inflammation and also improving endothelial function.

Correlation between insulin resistance and serum ghrelin in non-diabetic ankylosing spondylitis patients undergoing anti-TNF-α therapy.

Objectives: To evaluate whether anti-TNF-α therapy (infliximab) administration alters circulating levels of ghrelin, an anti-inflammatory gastric peptide. We also assessed possible associations of circulating ghrelin concentrations with CRP and ESR levels, metabolic syndrome, demographic characteristics and other adipokines in ankylosing spondylitis (AS) patients.

Methods: We studied 30 consecutive non-diabetic AS patients, without history of cardiovascular (CV) events, on periodical treatment with infliximab.

Asymmetric dimethylarginine serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.

Objectives: This paper aims to determine whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating asymmetric dimethylarginine (ADMA) in ankylosing spondylitis (AS) patients undergoing TNF-α antagonist-infliximab-therapy.

Methods: We investigated ADMA serum concentrations in a series of 30 non-diabetic AS patients without history of cardiovascular (CV) events that were treated with the TNF-α antagonist infliximab, immediately prior to an infliximab infusion. Correlations of ADMA serum levels with disease activity, systemic inflammation and metabolic syndrome were assessed.

Leptin and visfatin serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.

Objectives: This paper aims to determine whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating leptin and visfatin levels in ankylosing spondylitis (AS) patients undergoing TNF-α antagonist therapy. We also assessed whether the infusion of infliximab may alter circulating leptin and visfatin concentrations in these patients.

Methods: We investigated leptin and visfatin serum concentrations in a series of 30 non-diabetic AS patients without history of cardiovascular (CV) events that were treated with the TNF-α antagonist infliximab, immediately prior to an infliximab infusion.

Apelin serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.

Objectives: To determine whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating apelin in ankylosing spondylitis (AS) patients undergoing TNF-α antagonist-infliximab therapy.

Methods: We investigated apelin serum concentrations in a series of 30 non-diabetic AS patients without history of cardiovascular (CV) events that were treated with the TNF-α antagonist infliximab, immediately prior to an infliximab infusion. Correlations of apelin serum levels with disease activity, systemic inflammation and metabolic syndrome were assessed.

Adiponectin and resistin serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.

Objectives: The objective of this paper is to assess if disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating adiponectin and resistin levels in ankylosing spondylitis (AS) patients undergoing TNF-α antagonist therapy.

Methods: We investigated adiponectin and resistin serum concentrations in a series of 29 non-diabetic AS patients without history of cardiovascular (CV) events that were treated with the TNF-α antagonist infliximab, immediately prior to an infliximab infusion. Adipokine levels were also determined immediately after administration of an infliximab dose.

TNF-alpha antagonist therapy improves insulin sensitivity in non-diabetic ankylosing spondylitis patients.

Objectives: Since insulin resistance can promote endothelial dysfunction, and anti-TNF-α treatment improves endothelial function in ankylosing spondylitis (AS) patients, in the present study we sought to assess whether an infusion of the anti-TNF-α monoclonal antibody-infliximab may improve insulin sensitivity in non-diabetic AS patients.

Methods: We assessed a series of 30 non-diabetic patients with AS attending hospital outpatient clinics who fulfilled the modified New York diagnostic criteria for AS. In all cases, the drug was given as an intravenous infusion in a saline solution over 120 minutes.

Megestrol acetate-induced adrenal insufficiency.

Megestrol acetate is a synthetic progestin that has been used since the 1970s for the treatment of advanced cancer and subsequently to treat anorexia, cachexia and weight loss in AIDS patients. It has been shown that high doses or prolonged treatment with this drug may cause Cushing's syndrome, new-onset diabetes and suppression of plasma ACTH and cortisol levels. Megestrol acetate may cause suppression of the pituitary-adrenal axis due to the affinity of this compound for the glucocorticoid receptor.