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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. OPG levels were measured immediately before and after an infliximab infusion. Correlations of OPG levels with disease activity, clinical characteristics, systemic inflammation, metabolic syndrome features, adipokines and biomarkers of endothelial activation were assessed. Changes in OPG concentration following an infusion of anti-TNF-α monoclonal antibody-infliximab were also analysed., Results: We found a positive correlation between OPG levels and markers of disease activity such as BASDAI and VAS spinal pain (r=0.497, p=0.01; r=0.390; p=0.04, respectively). No differences in OPG levels according to specific clinical features of the disease were seen. An inverse correlation between OPG levels and total cholesterol and LDL-cholesterol was also found (r=-0.451; p=0.02 and r=-0.411; p=0.03, respectively). A correlation between OPG and asymmetric dimethylarginine, a biomarker of endothelial cell activation, was also disclosed (r=0.533; p=0.01). No correlation between OPG level and insulin resistance was observed. An infliximab infusion did not lead to a significant reduction in OPG levels., Conclusions: OPG shows a correlation with markers of disease activity and endothelial activation in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.

Objectives: To determine whether circulating gelsolin (GSN) levels in patients with ankylosing spondylitis (AS) undergoing TNF-α antagonist-infliximab-therapy are altered compared with controls and to establish whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating GSN levels in these patients., Methods: We assessed GSN serum concentrations in a series of 30 non-diabetic AS patients without cardiovascular (CV) disease undergoing TNF-α antagonist-infliximab therapy and 48 matched controls. GSN levels were measured immediately before and after an infliximab infusion. Correlations of GSN serum levels with disease activity, systemic inflammation and metabolic syndrome were assessed. Potential changes in GSN concentration following an infusion of anti-TNF-α monoclonal antibody-infliximab were also analysed., Results: Although at the time of the study AS patients undergoing anti-TNF-α therapy had adequate control of the disease (mean BASDAI 2.94), they showed lower GSN serum levels than healthy controls (mean±SD: 38660.42±23624.6 ng/ml versus 68975.43±31246.79 ng/ml; p<0.0001). When AS patients were stratified according to sex, we observed that GSN levels were significantly lower in men than in women (p=0.032). However, no differences in GSN levels according to the specific clinical features of the disease were seen. No association was found between GSN concentration and adipokines or biomarkers of endothelial cell activation. However, correlation between basal GSN levels and insulin resistance was observed. A single infliximab infusion did not lead to significant changes in GSN levels., Conclusions: GSN concentration is reduced in AS patients undergoing periodical anti-TNF-α therapy and low disease activity. Potential association with some metabolic syndrome features seems to exist.

Objectives: To determine whether circulating osteopontin (OPN) levels in patients with ankylosing spondylitis (AS) undergoing TNF-α antagonist-infliximab-therapy are increased compared with controls and to establish whether disease activity, systemic inflammation, metabolic syndrome, adipokines and biomarkers of atherosclerosis are potential determinants of circulating OPN levels in these patients., Methods: We assessed OPN serum concentrations in a series of 30 non-diabetic AS patients without cardiovascular disease undergoing TNF-α antagonist-infliximab therapy and 48 matched controls. OPN levels were measured immediately before and after an infliximab infusion, at time 0 and at time 120 minutes respectively. Correlations of OPN serum levels with clinical features, disease activity, systemic inflammation, metabolic syndrome and several biomarkers of atherosclerosis were assessed. Potential changes in OPN concentration following an infusion of anti-TNF-α monoclonal antibody-infliximab were also analysed., Results: At the time of the study AS patients undergoing anti-TNF-α therapy had low disease activity (mean BASDAI 2.94) and they showed similar OPN serum levels to healthy controls. No differences in OPN levels according to the specific clinical features of the disease were seen. Also, no correlation between OPN concentration and insulin resistance and adipokines was observed. However, a positive correlation between OPN and angiopoietin-2 (Angpt-2) serum levels was found (r=0.397; p=0.04). In addition, a single infliximab infusion led to a marginal statistically significant reduction in OPN levels (24112.19±14608.73 pg/ml at time 0 versus 21806.62±11390.83 pg/ml at time 120'; p=0.05)., Conclusions: OPN and Angpt-2 serum levels are correlated in non-diabetic AS patients undergoing TNF-α antagonist 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. Serum ghrelin levels were determined immediately prior to and after an infliximab infusion. Correlations of ghrelin serum levels with disease activity, systemic inflammation and metabolic syndrome were assessed. Potential changes in ghrelin concentration following an infusion of infliximab were analysed., Results: We observed a negative correlation between ghrelin concentration and insulin resistance (HOMA-IR immediately before infliximab infusion- at time 0 and at the end of infliximab infusion- at time 120') (r=-0.496; p=0.01 at time 0; r=-0.393; p=0.047 at time 120', respectively). We also found a positive correlation with insulin sensitivity (QUICKI) (r=0.415; p=0.035 at time 0; r=0.465; p=0.017 at time 120'). A correlation was found between ghrelin and resistin prior to infliximab infusion (r=0.429; p=0.046), and a negative correlation between serum ghrelin levels at time 0 and triglycerides (r=-0.416; p=0.035). No differences in ghrelin levels according to specific clinical features of the disease were seen. A single infliximab infusion led to mild but not significant increase in ghrelin serum concentration., Conclusions: In AS patients undergoing periodical treatment with anti-TNF-α monoclonal antibody-infliximab a link between insulin resistance and serum ghrelin concentration was observed.

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. Also, potential changes in ADMA concentration following an infusion of the anti-TNF-α monoclonal antibody-infliximab were analysed., Results: A higher concentrations of ADMA in men (p=0.012) and patients with hypertension was found (p=0.001). There was also a marginally positive correlation of ADMA serum levels with C-reactive protein levels (p=0.08). Moreover, a significant negative correlation between ADMA levels and total cholesterol and LDL-cholesterol was observed (p= 0.05). No differences in ADMA levels according to the specific clinical features of the disease were seen. A single infliximab infusion did not lead to significant changes in ADMA serum levels., Conclusions: In AS patients undergoing periodical treatment with the anti-TNF-α monoclonal antibody-infliximab a link between some features of metabolic syndrome and ADMA concentrations was observed.

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. Also, potential changes in apelin concentration following an infusion of the anti-TNF-α monoclonal antibody-infliximab were analysed., Results: No significant correlation between apelin concentration and demographic features, inflammation, adiposity and metabolic syndrome features was seen. Neither differences were seen in basal apelin in different categorical variables associated to AS. Following infliximab infusion, a reduction of apelin serum levels was observed. In this regard, the median (interquartile range) values of apelin decreased from 0.99 (0.74-1.25) ng/ml immediately prior to infliximab infusion to 0.92 (0.72-1.39) ng/ml at the end of the infusion (time 120 minutes). However, the reduction in apelin serum levels following administration of the drug did not achieve statistical significance., Conclusions: The present study shows that in non-diabetic patients with AS on treatment with infliximab apelin serum levels do not correlate with disease activity or metabolic syndrome. A single infusion of infliximab does not yield a significant change of apelin serum levels in AS patients.

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. Leptin and visfatin levels were also determined immediately after administration of an infliximab dose., Results: Significant differences in leptin concentrations between men (8.85±5.31 ng/ml) and women (18.96±9.72 ng/ml) were observed (p=0.001). A significant correlation between visfatin concentrations and insulin resistance (HOMA at the time of the study) was found (r= 0.493; p=0.009). Circulating leptin and visfatin concentrations did not correlate with disease duration, erythrocyte sedimentation rate, C-reactive protein, BASDAI and VAS at the time of the study and adiponectin and resistin levels prior to infliximab infusion. Likewise, no differences in leptin and visfatin concentrations were observed when patients with a history of anterior uveitis or presence of syndesmophytes were compared with the remaining patients who did not exhibit these features. Leptin and visfatin levels did not change upon infliximab administration., Conclusions: The present study indicates that in non-diabetic patients with AS on treatment with infliximab leptin and visfatin serum levels do not correlate with disease activity or systemic inflammation. Nevertheless, visfatin concentration correlates with insulin resistance.

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., Results: A significant correlation between adiponectin concentrations and insulin sensitivity (QUICKI at the time of the study) was seen (r=0.384; p=0.05). Also, a marginally significant negative correlation between adiponectin serum levels and the body mass index was observed (r=-0.367; p=0.07). Circulating adiponectin and resistin concentrations did not correlate with disease duration, erythrocyte sedimentation rate, C-reactive protein, BASDAI or VAS at the time of the study. However, AS patients with hip involvement or synovitis and/or enthesitis in other peripheral joints had higher adiponectin concentrations than those who did not have these complications (p-value for both comparisons =0.01). Adiponectin and resistin levels did not change upon infliximab administration., Conclusions: The present study shows that in non-diabetic patients with AS on treatment with infliximab adiponectin and resistin serum levels do not correlate with disease activity. Nevertheless, adiponectin concentration correlates with insulin sensitivity. This finding raises the possibility that low circulating adiponectin concentrations may be involved in the pathogenesis of the CV disease in AS.

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. Fasting blood samples were taken for determination of plasma glucose and serum insulin levels immediately before (time 0) and after infliximab infusion (time 120)., Results: At the time of the study only 8 (26.7%) of the 30 patients fulfilled definitions for insulin resistance as HOMA index was in most cases less than 2.29. Nevertheless, a statistically significant reduction in the HOMA values was observed when results found at time 0 (mean±SD: 1.72±1.22) were compared with those observed immediately after infliximab infusion (1.18±0.94) (p<0.001). The reduction in HOMA values was more important in those patients with the higher values of HOMA before infliximab infusion. Also, a significant improvement of insulin sensitivity was observed in most patients when QUICKI values before (0.37±0.04) and after infusion (0.39±0.04) were compared (p=0.004)., Conclusions: The present study shows that non-diabetic patients with AS on treatment with infliximab experience a rapid improvement of insulin sensitivity following administration of this drug.