Efficacy of golimumab in the treatment of ankylosing spondylitis and rheumatoid arthritis (own experience)

2020 ◽  
Vol 5-6 (215-216) ◽  
pp. 24-31
Author(s):  
Madina Murzabayeva ◽  

Genetic engineering drugs are used to treat rheumatic diseases. Based on the results of multicenter studies, the effectiveness and safety of golimumab, a representative of the group of tumor necrosis factor inhibitors in various categories of patients, was proved.. Purpose of research.To evaluate the effectiveness of golimumab in the treatment of ankylosing spondylitis and rheumatoid arthritis. Material and methods. The efficacy of golimumab was analyzed based on clinical and laboratory data in 7 patients with ankylosing spondylitis and 6 patients with rheumatoid arthritis. These studies are described against the background of a one-year follow-up of patients. Results and discussion. The observation group consisted of 7 patients with ankylosing spondylarthritis (as) and 6 patients with a diagnosis of rheumatoid arthritis. In all patients with (as) at the beginning of the study, the BASDAI index >6 points, and in 5 patients, the ASDASRB index was 3.5±0.45. In 4 patients with the diagnosis (as), the BASFI index was 7±0.67, and in three patients-5±0.3. the BASMI Index in all studied patients revealed pronounced disorders and was 7.5±0.85. Positive dynamics was observed during golimumab therapy. A patient with a high degree of BASDAI activity >6 showed improvement on the 4th injection of golimumab, the Average score of BASDAI and BASFI indices on golimumab was lower by the 20th week, compared with the start of therapy. By the 24th week of therapy, the BASDAI index was down 31%. The follow-up group with the diagnosis of rheumatoid arthritis consisted of 6 patients, including 1 male and 5 female, with an average age of 38±0.5 years. In a male patient, the DAS-28 index was 5.2±0.06, the SDAI index was 27±0.05, and the CDAI index was 23±0.03. In women, the DAS-28 index was 3.8±0.03, and the SDAI index was 19±0.3 in 5 patients, and the CDAI index was 20±0.3. after adding golimumab, the General condition of all patients improved clinically after the second injection, and all indicators of inflammatory activity decreased. Golimumab is a human monoclonal antibody to tumor necrosis factor (TNF)α. The effect of golimumab is due to the binding and neutralization of soluble and membrane-bound forms of TNF)α. TNF)α. it is a cytokine detected in patients with rheumatoid arthritis, ankylosing spondylarthritis. Conclusion. Against the background of the use of golimumab, the clinical effect was noted in the form of complete relief of joint pain and positive dynamics according to the studied laboratory parameters. Keywords: rheumatoid arthritis, ankylosing spondylitis, golimumab, efficacy.

2014 ◽  
Vol 41 (8) ◽  
pp. 1675-1682 ◽  
Author(s):  
Johannes C. Nossent ◽  
Sylvia Sagen-Johnsen ◽  
Gunnstein Bakland

Objective.Despite the clinical efficacy of tumor necrosis factor inhibitors (TNFi), the manner in which TNF-α contributes to disease in patients with ankylosing spondylitis (AS) remains unresolved. We investigated the relationship between TNF-α gene promoter region polymorphism, serum TNF-α levels, and clinical phenotype.Methods.We did a cross-sectional and longitudinal cohort study in TNFi-naive patients with AS (n = 335). Clinical data and biological samples were collected during a research visit with genotyping for TNF-α −238 A/G and −308 A/G performed by Taqman RT-PCR and TNF levels determined by sandwich ELISA. Longitudinal TNF levels were monitored in unselected patients (n = 61).Results.TNF-α −308 GA/AA genotype was present in 14% and TNF-α −238 GA/AA genotype in 1% of patients. TNF-α −308 GA/AA genotype was associated with a reduced risk of uveitis and better spinal function, while TNF-α −238 GA/AA genotype was associated with later age of onset and lower erythrocyte sedimentation rate (ESR). Serum TNF-α level was lower in patients with AS (151 pg/ml) than in controls (263 pg/ml), because more patients with AS had undetectable serum TNF-α (66 vs 25%, p < 0.001). TNFi treatment did not influence serum TNF-α. There was no effect of TNF-α −308/−238 or HLA-B27 genotype on serum TNF-α or subsequent initiation of TNFi.Conclusion.TNF-α −238 or −308 GA/AA genotypes in patients with AS are associated with signs of less severe disease. Serum TNF-α is, however, undetectable in two-thirds of patients with AS and is not influenced by TNF-α promoter genotype or TNFi therapy. These data suggest a more significant role for TNF-α at local sites of inflammation in AS than through systemic effects.


2011 ◽  
Vol 38 (12) ◽  
pp. 2548-2556 ◽  
Author(s):  
BOULOS HARAOUI ◽  
MARIA BOKAREWA ◽  
IAN KALLMEYER ◽  
VIVIAN P. BYKERK

Objective.To evaluate the safety and effectiveness of rituximab (RTX) in combination with methotrexate in patients with active rheumatoid arthritis (RA) after failure of a single tumor necrosis factor-α (TNF-α) inhibitor. Changes in patient-reported outcomes after primary treatment or retreatment with RTX and factors determining retreatment in clinical practice were also evaluated.Methods.In this phase 3b open-label, multicenter trial, patients received 2 slow infusions of RTX 1000 mg 14 days apart after premedication (primary treatment). Patients with a clinically relevant response could receive retreatment between 24 and 48 weeks. The primary endpoint was evaluation of safety. Secondary outcomes were safety of retreatment, effectiveness of primary treatment and retreatment, and changes in patient-reported outcomes after primary treatment or retreatment.Results.Of 120 patients enrolled at 36 centers and receiving primary RTX treatment, 77 received retreatment, 112 completed the 24-week primary treatment period, and 25 completed the 48-week primary treatment and retreatment period following a single course of RTX. The most common adverse events were mild to moderate nausea, vomiting, nasopharyngitis, and headache. No infections or infusion reactions were considered life-threatening. At 24 weeks, 58%, 27%, and 7% of patients achieved American College of Rheumatology 20, 50, and 70 improvements, respectively, and similar improvements were seen after retreatment.Conclusion.RTX was well tolerated, with a low incidence of infusion reactions and infections. Efficacy results, including enhanced response in rheumatoid factor-positive patients, were comparable to those reported in the literature. Based on its efficacy and safety profile and retreatment schedule, RTX is an attractive treatment option for patients that have not responded to a single TNF-α inhibitor.


2012 ◽  
Vol 15 (3) ◽  
pp. 330-335 ◽  
Author(s):  
Ahmed M. Dewedar ◽  
Medhat A. Shalaby ◽  
Sulaiman Al-Homaid ◽  
Ahmed M. Mahfouz ◽  
Osama A. Shams ◽  
...  

2012 ◽  
Vol 39 (5) ◽  
pp. 946-948 ◽  
Author(s):  
ANDRONIKI BILI ◽  
STEPHANIE J. MORRIS ◽  
JENNIFER A. SARTORIUS ◽  
H. LES KIRCHNER ◽  
JANA L. ANTOHE ◽  
...  

Objective.To determine the association of use of tumor necrosis factor-α (TNF-α) inhibitors with differences in lipid levels in patients with rheumatoid arthritis (RA).Methods.We studied 807 patients with incident RA to compare differences in lipid levels in TNF-α inhibitor users versus nonusers, with adjustment for relevant covariables.Results.TNF-α inhibitor use was not associated with differences in levels of low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), triglycerides, LDL:HDL, or TC:HDL compared to nonusers.Conclusion.Use of TNF-α inhibitor was not associated with differences in lipid levels in patients with RA.


2012 ◽  
Vol 39 (7) ◽  
pp. 1418-1423 ◽  
Author(s):  
JULIEN PACCOU ◽  
MARIE-ASTRID BACLÉ-BOUTRY ◽  
ELISABETH SOLAU-GERVAIS ◽  
PEGGY BELE-PHILIPPE ◽  
RENÉ-MARC FLIPO

Objective.While remission is possible in patients with ankylosing spondylitis (AS), it is often unclear what attitude should be adopted once remission has occurred. We investigated whether dosage adjustment is an effective means of maintaining remission.Methods.This was a retrospective study drawn from clinical situations. Remission was defined using clinical measures [Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) ≤ 20/100 and no peripheral joint disease] and biological measures [C-reactive protein (CRP) levels ≤ normal value]. The tumor necrosis factor-α (TNF-α) inhibitors used were infliximab, adalimumab, and etanercept. Response predictors of remission were evaluated by logistic regression (age, CRP, HLA-B27 positivity, sex, duration of disease, and anti-TNF-α naivety). CRP and BASDAI were evaluated before and after dosage adjustment at about 6, 12, 24, and 36 months.Results.One hundred eighty-nine patients with AS were included in the study, with a mean followup of 43.5 (± 17.9) months after the introduction of the first anti-TNF-α inhibitor. Mean age was 45.6 (± 12.5) years. Remission had occurred in 65 patients (35%). Significant response predictors of remission were male sex (p = 0.003) and anti-TNF-α naivety (p < 0.001). Dosage adjustment was observed 49 times, and progressively reducing treatment frequency was effective to maintain remission in a large number of patients for 36 months. The cumulative probability of continuing anti-TNF-α after dosage adjustment was 79.0% at 12 months, 70.5% at 24 months, and 58.8% at 36 months.Conclusion.Remission had occurred in 35% of the patients with AS under anti-TNF-α inhibitor therapy. Dosage adjustment and progressively reducing treatment frequency was effective in maintaining remission.


2002 ◽  
Vol 06 (02) ◽  
pp. 63-71 ◽  
Author(s):  
Koichiro Takahi ◽  
Tetsuya Tomita ◽  
Takanobu Nakase ◽  
Motoharu Kaneko ◽  
Hiroshi Takano ◽  
...  

The purpose of this study is to investigate the expression of tumor necrosis factor-α converting enzyme (TACE) in the synovium and subchondral bone region of patients with rheumatoid arthritis (RA) and to determine the contribution of the enzyme to the pathogenesis of RA. Joint tissues were obtained during total knee arthroplasty from patients with RA and osteoarthritis (OA). The expression of TACE and TNF-α mRNA was detected by in situ hybridization. Characterization of TACE expressing cells was performed by immunohistochemistry using serial sections. We found that TACE mRNA was expressed in both synovium and subchondral bone region and co-localized with TNF-α mRNA in RA. On the other hand, TACE mRNA expression was scarcely detectable in OA samples. TACE was expressed in mononuclear cells, such as CD3 and CD14 positive cells in RA samples. In conclusion, the expression of TACE is up-regulated in the rheumatoid synovium and subchondral bone region, and the results in this study demonstrate that TACE may be involved and play a role in the pathogenesis of RA.


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