Genetic markers of treatment response to tumour necrosis factor-α inhibitors in the treatment of psoriasis

2014 ◽  
Vol 39 (4) ◽  
pp. 519-524 ◽  
Author(s):  
C. Ryan ◽  
J. Kelleher ◽  
M. F. Fagan ◽  
S. Rogers ◽  
P. Collins ◽  
...  
Keyword(s):  
Treatment Response ◽  
Tumour Necrosis Factor ◽  
Genetic Markers ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Treatment response, drug survival and safety of anti-tumour necrosis factor α therapy in 193 patients with psoriatic arthritis: A twelve-year “real life” experience

2015 ◽  
Vol 82 (1) ◽  
pp. 31-37 ◽  
Author(s):  
Anne-Sophie Soubrier ◽  
Peggy Bele-Philippe ◽  
Bernard Cortet ◽  
Nassima Ramdane-Sebbane ◽  
Marie-Astrid Bacle-Boutry ◽  
...  
Keyword(s):  
Psoriatic Arthritis ◽  
Treatment Response ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Life Experience ◽  
Real Life ◽  
Tumour Necrosis Factor Α ◽  
Drug Survival ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Predictors of Response to Biologics in Patients with Moderate-to-severe Psoriasis: A Danish Nationwide Cohort Study

2021 ◽  
Author(s):  
Christopher Willy Schwarz ◽  
Nikolai Loft ◽  
Mads Kirchheiner Rasmussen ◽  
Christoffer V. Nissen ◽  
Tomas Norman Dam ◽  
...  
Keyword(s):  
Treatment Response ◽  
Tumour Necrosis Factor ◽  
Odds Ratio ◽  
Tumour Necrosis ◽  
Logistic Models ◽  
Patient Characteristics ◽  
Interleukin 12 ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Identifying patient characteristics associated withachieving treatment response to biologics in patients with psoriasis could prevent expensive switching between biologics. The aim of this study was to identifypatient characteristics that predict the efficacy of treatment for biologics that inhibit tumour necrosis factor-α, interleukin-12/-23, and -17A. The study investigated biologic-naïve patients from the DERMBIO registry treated with adalimumab, etanercept, infliximab, secukinumab, or ustekinumab. Multivariable logistic models were conducted to assess associations between patient characteristics and treatment response. A total of 2,384 patients were included (adalimumab n = 911; etanercept n = 327; infliximab n = 152; secukinumab n = 323; ustekinumab n = 671). Smoking (odds ratio 0.74; 95% confidence interval (CI) 0.56–0.97; p = 0.03) and higher bodyweight (odds ratio 0.989; 95% CI 0.984–0.994; p < 0.001) reduced the odds of achieving response defined as Psoriasis Area and Severity Index ≤2.0 after 6 months of treatment. In conclusion, higher bodyweight and smoking were associated with a reduced probability of treatment response for tumour necrosis factor-α inhibitors, ustekinumab, and secukinumab.

Clinical response, drug survival and predictors thereof in 432 ankylosing spondylitis patients after switching tumour necrosis factor α inhibitor therapy: results from the Danish nationwide DANBIO registry

2012 ◽  
Vol 72 (7) ◽  
pp. 1149-1155 ◽  
Author(s):  
Bente Glintborg ◽  
Mikkel Østergaard ◽  
Niels Steen Krogh ◽  
Ulrik Tarp ◽  
Natalia Manilo ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Disease Activity ◽  
Treatment Response ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Drug Survival ◽  
Treatment Responses ◽  
Factor Α ◽  
Necrosis Factor

ObjectiveTo investigate frequencies and reasons for switching, treatment responses and drug survival in patients with ankylosing spondylitis (AS) switching tumour-necrosis-factor-α inhibitor (TNFi) treatment in routine clinical care.MethodsAS patients were identified in the Danish nationwide DANBIO registry. Disease activity, treatment responses (50% or 20 mm reduction in Bath AS Disease Activity Index (BASDAI)), duration and rates of drug survival and predictors thereof were studied in patients receiving ≥2 different biological drugs.ResultsOf 1436 AS patients starting TNFi treatment, 432 patients (30%) switched to a second and 137 (10%) to a third biological drug. Compared with non-switchers, switchers were more frequently women (33%/22%), had shorter disease duration (3 years/5 years) and higher BASDAI (62(52–76) mm/56(43–69) mm (median(interquartile-range))), Bath AS Functional Index (BASFI) (54(39–71) mm/47(31–65) mm) and visual-analogue-scale (VAS) global, pain and fatigue scores when they started the first TNFi (all p<0.01). Main reason for switching was lack of response (56%). During the first, second and third treatment BAS- and VAS scores had decreased after 6 months' treatment (all p<0.05). Median drug survivals were 3.1, 1.6 and 1.8 years respectively (p<0.001). After 2 years of treatment 52% of switchers and 63% of non-switchers had achieved response (number needed to treat 1.9 and 1.6, respectively, p=0.01). Drug survivals were similar regardless of the reason for switching. Male gender and low BASFI predicted drug survival of the second TNFi.ConclusionsNearly one-third of AS patients in clinical practice switched biological treatment. Response rates and drug survivals were lower among switchers, however, half of switchers achieved treatment response.

Genetic markers of tumour necrosis factor α in aggressive and chronic periodontitis

2008 ◽  
Vol 35 (6) ◽  
pp. 493-500 ◽  
Author(s):  
Susanne Schulz ◽  
Helmut K. G. Machulla ◽  
Wolfgang Altermann ◽  
Jana Klapproth ◽  
Uta Zimmermann ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Genetic Markers ◽  
Chronic Periodontitis ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Substrate specificity and inducibility of TACE (tumour necrosis factor α-converting enzyme) revisited: the Ala-Val preference, and induced intrinsic activity

2003 ◽  
Vol 70 ◽  
pp. 39-52 ◽  
Author(s):  
Roy A. Black ◽  
John R. Doedens ◽  
Rajeev Mahimkar ◽  
Richard Johnson ◽  
Lin Guo ◽  
...  
Keyword(s):  
Substrate Specificity ◽  
Recent Work ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Transforming Growth Factor ◽  
Intrinsic Activity ◽  
Converting Enzyme ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Tumour necrosis factor α (TNFα)-converting enzyme (TACE/ADAM-17, where ADAM stands for a disintegrin and metalloproteinase) releases from the cell surface the extracellular domains of TNF and several other proteins. Previous studies have found that, while purified TACE preferentially cleaves peptides representing the processing sites in TNF and transforming growth factor α, the cellular enzyme nonetheless also sheds proteins with divergent cleavage sites very efficiently. More recent work, identifying the cleavage site in the p75 TNF receptor, quantifying the susceptibility of additional peptides to cleavage by TACE and identifying additional protein substrates, underlines the complexity of TACE-substrate interactions. In addition to substrate specificity, the mechanism underlying the increased rate of shedding caused by agents that activate cells remains poorly understood. Recent work in this area, utilizing a peptide substrate as a probe for cellular TACE activity, indicates that the intrinsic activity of the enzyme is somehow increased.

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