| ObjectiveAnkylosing spondylitis (AS) is a chronic progressive inflammatorydisease, with major violation of the human central axis joint system andperipheral large joints, the cause of AS is not yet very clear, the clinicalfeatures are low back pain and the gradual emergence of sacroiliitis, as well asthe spinal of the lesions partly or completely which induced by the chronicinflammatory. If clinical diagnosis in late-stage has missed the best treatmentopportunity, it could bring serious damage to the patient’s physical and mentalhealth. Axial spondyloarthritis (aSpA) as an early manifestation of AS, typicalradiological bone destruction will appear in the majority of patients after2to5years. If we seize this chance, early diagnosis and effective treatment areexpected to change the condition and improve patients, prognosis.After10to20years continuously explore, numerous cytokine familymembers have become increasingly prominent in the medical treatment inSpA. It has been confirmed that multiple cytokines involved in the erosionprocess of SpA bones. TNF-α is the most important inflammatory cytokines inthe pathogenesis of AS, the application of TNF-α antagonists can significantlyimprove the clinical symptoms, ease AS conditions, also underlined theimportance of TNF-α in the pathogenesis of AS. The conventional wisdom isthat AS patients have high levels of TNF-α expression, rather than elevatedexpression of IL-1in the junction area of bone and cartilage. Therefore, somescholars believe that IL-1is not a major pathogenic factor in AS, but the latestresearch shows that, due to the gene polymorphism of IL-1, the role in thepathogenesis of AS is also different.Interleukin33(IL-33) is a recently discovered member in the family ofIL-1cytokines, it plays an important role in a variety of autoimmune diseases, allergic diseases and other inflammatory immune process. Studies have shownthat IL-33is highly expressed in the serum of AS, it has the ability to promotethe peripheral blood mononuclear cells to release TNF-α and IL-6, therefore,as an early inflammatory mediators, whether it highly expresses in the serumof AS patients with early performance-aSpA? No research coveraged at homeor abroad.From the rheumatoid arthritis (Rheumatoid arthritis, RA) research,TNF-α antagonists may inhibit the expression of IL-33and its receptor (ST2),Whether the the same effect will appears in the AS? It is also not yetreported. In this study we observed the expression levels of IL-33in the serumof patients with aSpA, investigate the relationship between IL-33and diseaseactivity, as well as the changes before and after treatment with etanercept. Thepurpose is to explore the pathogenic role of IL-33in the aSpA, as well as thetherapeutic effect of etanercept. Provide a theoretical basis to take effectivetreatment measures to control the disease progression.Methods80aSPA patients were included, who were collected from the out-patientand in-patient in the Second Hospital of Hebei Medical rheumatism fromJanuary to December in2012.They are all in line with the classification standards released by ASAS in2009. Aged from16to35.Including23cases before treatment,24patientsreceived traditional drug treatment (Including:14cases of patients treatmentedfor1month,10cases of patients treatmented for3months) as DMARDstreatment group,24patients received Etanercept treatment (including:15cases of patients treatmented for1month,18cases of patients treatmented for3months) as a biological treatment group. Screening the other20cases whatthe gender,age-matched healthy volunteers as normal control group, no seriousbacterial and viral infections for two weeks before their treatment, no historyof immunization for4weeks,no history of rheumatism both in themselves andtheir family.Exclude:(1) clinical and imaging tips spine has entasia (2) in acute or chronic infection period including tuberculosis, hepatitis B, hepatitis C orAIDS patients,(3) patients with malignant tumors, or have a family history (4)women were not in the period of pregnancy or lactation.Traditional treatment group received a sufficient amount of non-steroidalanti-inflammatory drug sulfasalazine plus1.0g each time, twice a day orally.Biological treatment group received etanercept50mg.w-1, subcutaneousinjection. Record ESR, CRP, PLT and the BASDAI ratings in each group ofpatients, IL-33concentration in the serum detected by ELISA. Statisticalanalyses were performed by SPSS19.0（SPSS Company, Chicago，Illinois，USA）Results1Compare the clinical datasAmong the normal control group, the treatment before group, DMARDstreatment group and the etanercept treatment group, their gender, age, couse ofdisease were not statistically different.2The change of clinical activity indicators and IL-33levels in patientstreated with DMARDs drugs.Compared with the normal control group, IL-33level was significantlyelevated, compared with patients before treatment, their ESR, CRP, BASDAIand IL-33levels were significantly decreased after1month,s treatment,compared with patients treated for1month, the ESR, CRP, BASDAI, IL-33level also reduced significantly after3months,treatment.3The change of clinical activity indicators and IL-33levels in patientstreated with Etanercept.Compared with the level before treatment, the ESR, CRP, BASDAI,IL-33level were decreased significantly after treated for1month, as the timeof treatment gone, ESR, the reduce of CRP, PLT, BASDAI level wastime-dependent.4Chang of IL-33level in DMARDs treatment group and the etanerceptgroup The IL-33level had no statistical significance between the DMARDstreatment group and the etanercept group.after1month treatment. But there is statistical significance between the DMARDs treatment group and theetanercept group.after3month treatment. The etanercept group is lower5Chang of ESR in DMARDs treatment group and the etanercept groupThe average level of ESR is lower than DMARDs treatment group, afteretanercept treatment both in one month and three months. Statisticalprocessed that there was statistical difference between the two groups afterthree months,treatment.6Chang of CRP in DMARDs treatment group and the etanercept groupThe average level of ESR is lower than DMARDs treatment group, afteretanercept treatment both in one month and three months.7Chang of PLT in DMARDs treatment group and the etanercept groupThere was no statistical significance between the DMARDs treatmentgroup and the etanercept group both in1month and3months.8Analysis the correlation between the IL-33level and clinical activityindexSpearman correlation analysis showed: both in the DMARDs treatmentgroup and the etanercept group, IL-33expression levels was positivelycorrelatedwith BASDAI score,(r=0.361，P=0.033) and (r=0.324，P=0.012), therewas no correlation with ESR, CRP, PLT.Conclusions1High levels of IL-33expressde in serum of aSpA in activity period,suggesting that IL-33is an important virulence factor for aSpA patients.2There was positively correlation between IL-33and BASDAI score.suggesting that IL-33may reflect disease activity of ankylosing spondylitis tosome extent.3The combination of Sufficient amount of non-steroidal anti-inflammatory drugs and salicylazosulfapyridine(SASP) or etanerceptmonotherapy can reduce the expression of IL-33, ease patient’s conditionpartly, eta nercept is superior to traditional oral medication in reducinginflammatory markers. This experiment is proceeding from the clinical observation, research theexpression of IL-33and its relationship with disease activity in the early stageof AS-aSpA, observed the intervention effects of traditional drugs andetanercept at the same time., preliminarily confirmed that IL-33was involvedin the pathogenesis and disease activity in the early stage of AS, earlyintervention for IL-33, could alleviate the condition as soon aspossible,improve the quality of patients,life. Continue to investigate theimmunological function of IL-33in the peripheral blood of aSpA patients, notonly helps to improve the pathogenesis of AS,but also provide a basis forexploring new disease-specific intervention target and new ways of lookingfor specific biological targeted therapies. |
