Elsevier

Joint Bone Spine

Volume 77, Issue 1, January 2010, Pages 50-52
Joint Bone Spine

Original article
Effects of 14 weeks of TNF alpha blockade treatment on lipid profile in ankylosing spondylitis

https://doi.org/10.1016/j.jbspin.2009.05.012Get rights and content

Abstract

Objective

Cardiovascular morbidity and mortality seem to be increased in ankylosing spondylitis, perhaps as the result of biological inflammation and consecutive dyslipidemia. This study aims to investigate the impact of TNF alpha-inhibitors, an effective treatment, on lipid profile.

Methods

Thirty-four ankylosing spondylitis (AS) patients with active disease undergoing anti-TNF alpha therapy (n = 20, infliximab; n = 7, etanercept; n = 7, adalimumab) were recruited. Disease activity parameters, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were assessed at baseline and after 14 weeks of treatment.

Results

After 14 weeks of TNF alpha blockade treatment, there was a significant increase in levels of total cholesterol (5.08 ± 1.20 vs. 4.73 ± 1.12 mmol/l; p = 0.01) and HDL-cholesterol (1.61 ± 0.47 vs. 1.47 ± 0.35 mmol/l; p = 0.008), but no resulting change in the atherogenic index (3.43 ± 1.13 vs. 3.35 ± 0.93; p = 0.87). There was also no change in concentrations of triglycerides (1.33 ± 1.22 vs. 1.27 ± 0.98 mmol/l; p = 0.794) and LDL-cholesterol (3.15 ± 0.99 vs. 2.91 ± 0.93 mmol/l; p = 0.24). TNF alpha inhibitor treatment was followed by a significant improvement in all disease activity parameters: VAS pain or VAS disease activity, BASDAI or BASFI and systemic inflammation. Sub-group analysis showed that monoclonal antibodies increased total and LDL-cholesterol levels but did not change the atherogenic index. Conversely, 14 weeks of etanercept treatment was followed by no change in lipid profile.

Conclusion

TNF alpha inhibitors may be successful in reducing cardiovascular risk in AS, as in RA, but not by affecting lipid profile. However, there is insufficient documented evidence, and long-term investigations are needed to define the possible protective mechanisms of TNFalpha inhibitor treatment in spondylarthropathies.

Introduction

Increased cardiovascular morbidity and mortality have been observed in several inflammatory rheumatic diseases, including rheumatoid arthritis (RA) and spondylarthropathies [1], [2], [3], [4], [5], [6]. Patients with ankylosing spondylitis (AS) have an overall mortality of about 1.6–1.9 times that of the general population, and excess mortality from circulatory or cardiovascular disease (CVD) has been estimated at 20–40% [6]. The causes underlying this increased incidence of CVD are not entirely understood. AS patients have dyslipidemia with decreased HDL-cholesterol and increased atherogenic index [7]. In a recent survey of men with AS, there was an increased percentage of smokers and a higher rate of body mass index compared with age-matched healthy controls [8]. In RA, traditional coronary risk factors such as hyperlipidemia, smoking, hypertension and diabetes have been implicated in but do not account for the increased risk of CVD [9]. Conversely, disease severity has consistently been associated with an increased risk of CVD, indicating that systemic inflammation is a major determinant of vascular comorbidity [10]. In AS, C-reactive protein (CRP), interleukin-6 and fibrinogen were significantly elevated, which suggests that systemic inflammation may predispose to CVD, but conclusive evidence is lacking [8]. Inflammatory biomarkers are good predictors for cardiovascular events in both the general population and inflammatory polyarthritis patients [11], [12].

TNF alpha inhibitor treatments have properties that might decrease cardiovascular risk in RA [13], but only in patients who respond to anti-TNF therapy [14]. This decrease may be due to a decrease in biological inflammation or to improvement of the pro-atherogenic lipid profile, which has already been observed after TNF alpha blockade treatment in RA [15]. However, reports on the effects of anti-TNF alpha therapy on lipid profile in RA are conflicting, and in AS, there is a lack of documented evidence.

In the present study, we assessed the effect of 14 weeks’ treatment of TNF alpha blockade on lipid profile in patients with AS.

Section snippets

Methods

We studied 34 patients with AS who all met the New York diagnostic criteria [16]. Clinical assessment and laboratory examinations were recorded at baseline and after 14 weeks of TNF alpha blockade.

Results

Ten female and 24 male (70.59%) patients with a mean age of 43 ± 12 years were enrolled. At baseline, 13 patients were on NSAID (38.24%), seven on methotrexate (20.59%) with a median dose of 7.5 mg/week, one on other DMARDs [sulfasalazine (n = 1)] and one was receiving prednisone. Dose of DMARDs, steroids and NSAIDs were stable during the study. Twenty patients were started on infliximab (58.82%), seven on etanercept (20.59%) and seven on adalimumab (20.59%) for an active disease (Table 1).

Fourteen

Discussion

We found that 14 weeks of TNFalpha inhibitor treatment and especially monoclonal antibodies induced a significant increase in both total cholesterol and HDL-cholesterol levels. However, these changes did not modify the atherogenic index, an important risk factor for future cardiovascular events that should be taken into account in treatment of dyslipidemia in RA [19]. At the same time, there was a significant decrease in clinical disease activity and in biological inflammation.

It is now well

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