依那西普血清水平與強直性脊柱炎患者療效無相關性

依那西普血清水平與強直性脊柱炎患者療效無相關性

De Vries MK, Wolbink GJ, et al. EULAR 2007. Present ID: FRI0382.

                                      

背景：咱們最近的一研究顯示AS的Infliximab無效者與Infliximab外周血水平低以及和出現Infliximab抗體有關。

目的：評價AS的Etanercept療效是否也與Etanercept水平以及出現Etanercept抗體有關。

方法： 用Etanercept 25mg x2/周治療AS患者。基線時、治療第3和6月時，隨機挑選患者採集血清。 ASAS療效的定義：BASDAI分數出現50%相對變化或絕對改變超過2 cm。用ELISA測定Etanercept血清水平。用經典的抗原結合試驗檢測Etanercept抗體。將臨牀疾病活動度數據與血清 Etanercept水平進行相關分析。

結果：共歸入72例患者。治療後有50例(69.4%)出現ASAS應答。第三、6 月時，Etanercept中位數水平爲2.4 mg/l (範圍：0～7.5, N=63)、2.9 mg/l (範圍：0.8～5.4, N=57)。應對組與非應答組Etanercept水平無顯著差別。BMI、ESR、CRP水平與Etanercept水平之間無相關性。未發現 Etanercept抗體。

結論：Etanercept治療3月後，69% AS患者被判爲治療有效。應答組與非應答組之間的Etanercept血清水平類似。並且與以前研究發現Infliximab抗體明顯不一樣的是，本研究未發現Etanercept抗體。

---

  原文連接或參見如下信息。

[FRI0382] NO DIFFERENCE IN ETANERCEPT LEVELS BETWEEN RESPONDERS AND NON-RESPONDERS IN PATIENTS WITH ANKYLOSING SPONDYLITIS TREATED WITH 25 MG ETANERCEPT TWICE A WEEK

M.K. de Vries ¹, G.J. Wolbink ², M.T. Nurmohamed ³, L.A. Aarden ⁴, S.O. Stapel ⁴, M.J.L. Peters ³, J.C. van Denderen ³, B.A.C. Dijkmans ¹, I.E. van der Horst-Bruinsma ¹. ¹Rheumatology, VU University Medical Center, ²Rheumatology, Sanquin Research, ³Rheumatology, Jan van Breemen Institute, ⁴Immunopathology, Sanquin Research, Amsterdam, Netherlands

Background: Recently we showed in patients with Ankylosing Spondylitis (AS), who were treated with infliximab, that non-response was correlated with undetectable infliximab levels and presence of antibodies to infliximab.
Objectives: To evaluate whether clinical response of AS to etanercept also correlates with etanercept levels, and the presence of antibodies to etanercept.
Methods: AS patients were treated with etanercept 25 mg twice weekly. Sera were collected randomly at baseline, after 3 and 6 months of treatment.
ASAS response was defined as 50% relative change of the BASDAI score or absolute change of 2cm.
Etanercept levels were measured by a newly developed ELISA, measuring binding of etanercept to TNFalpha. Antibodies to etanercept were measured with an antigen binding test and a classical two side assay. Clinical data were used to correlate disease activity with serum etanercept levels.
Results: 72 patients were included. After 3 months of treatment 50 patients (69.4%) were ASAS responders. Median etanercept levels were 2.4 mg/l (range 0-7.5, N=63) and 2.9 mg/l (range 0.8-5.4, N=57), after 3 and 6 months resp. No significant differences were found between the etanercept levels of responders and non-responders. No correlation was found between BMI, ESR, CRP levels and etanercept levels. No antibodies to etanercept were detected with any of the assays used.

Fig. 1. Mean etanercept levels (mg/l) and SD for ASA non-responders and responders after 3 months of treatment of AS with etanercept.

Conclusion: 69% of the patients was classified as responder after 3 months of treatment. Serum etanercept levels of responders and non-responders were similar. Moreover, no antibody formation against etanercept was detected in these patients which is in contrast with our prior study of infliximab in AS.

              

Citation: Ann Rheum Dis 2007;66(Suppl II):395
Session: Spondylarthropathies