title: Detection of antibodies to anti-TNF agents in psoriatic patients: a preliminary study.
abstract: OBJECTIVE
  The efficacy of anti-TNFα agents in psoriasis (Pso) has been established in different clinical trials and in every day practice. However, a portion of patients (non-responder patients) persists with active disease or relapses even during current biological therapy. In addition to this, the use of biologic agents can give adverse drug reactions. All these factors may be due to the immunogenicity of these new biological drugs. All the biological proteins, including fully human proteins, have the potential to induce immunogenicity which leads to the development of specific antidrug antibodies (ADAs).
  
  
  METHODS
  In a retrospective way, we studied ADAs, using ELISA test, in a group of 51 patients with moderate to severe Pso treated with anti TNF α drugs: 18 Etanercept (ETN), 15 infliximab (IFX) and 18 adalimumab (AdA).
  
  
  RESULTS
  Anti-IFX antibodies were positive in 13.3%, anti AdA in 16.6% while all the patients treated with ETN did not present ADAs. Our opinion is that it is important to verify non-responder patients due to neutralizing ADAs so that we can change the drug before patients get worse. Moreover, it is important to detect ADAs since positive patients are more likely to develop acute hypersensitivity reactions. The development of antimonoclonal specific IgGs may also lead to an effector mechanism involving complement activation and production of anaphylotoxins which determine side effects that can be, in some cases, very severe. ADAs can be responsible of the poor response to the drugs and can impact the safety profile of the drugs.
  
  
  CONCLUSIONS
  We think that the detection of ADAs will be useful for the management of the drugs and the disease in all patients with psoriasis in treatment with anti biological drugs as a routine clinical practice.
authors.affiliation: IRCCS Azienda Ospedaliera Universitaria, San Martino - IST, Genoa, Italy. emanuele.cozzani@unige.it
authors.forename: E
authors.initials: E
authors.lastname: Cozzani
authors.forename: M
authors.initials: M
authors.lastname: Burlando
authors.forename: A
authors.initials: A
authors.lastname: Parodi
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000906:Antibodies / Q000097:blood / Q000276:immunology*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D003879:Dermatologic Agents / Q000627:therapeutic use*; D004351:Drug Resistance / Q000276:immunology; D000068800:Etanercept; D019317:Evidence-Based Medicine; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use*; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000188:drug therapy* / Q000276:immunology*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000906:Antibodies; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D003879:Dermatologic Agents; D007074:Immunoglobulin G; D007155:Immunologic Factors; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept