title: Anti-tumor necrosis factor alpha therapy in fifteen patients with AA amyloidosis secondary to inflammatory arthritides: a followup report of tolerability and efficacy.
abstract: OBJECTIVE
  Because anti-tumor necrosis factor alpha (anti-TNF) has emerged as a highly effective treatment for numerous inflammatory arthritides, which are a common cause of AA amyloidosis, we retrospectively evaluated the safety and efficacy of anti-TNF in a nationwide study.
  
  
  METHODS
  The rheumatology departments of all French teaching hospitals were contacted by mail to obtain the files of patients with histologically proven secondary AA amyloidosis and renal involvement who were treated with anti-TNF. Efficacy was assessed as a sustained decrease in 24-hour proteinuria and a stable/improved glomerular filtration rate (GFR).
  
  
  RESULTS
  Among the 15 patients studied, the 24-hour proteinuria was 4.5 +/- 3.6 gm (mean +/- SD), creatininemia was 178.4 +/- 74.9 micromoles/liter, and GFR was 46 +/- 23 ml/minute before starting anti-TNF. Ten patients received infliximab, 4 received etanercept, and 1 received both types of treatment. The mean followup was 10.4 months. No severe adverse events were recorded; one episode of herpes zoster in the first branch of the trigeminal nerve occurred after one infusion of infliximab. Amyloidosis progressed in 7 patients and was stabilized in 5 patients. Three patients (receiving infliximab alone, infliximab plus methotrexate [MTX], or etanercept plus MTX) experienced rapid, dramatic, and sustained decreases in proteinuria (>or=80%), with the GFR increasing 15-78%.
  
  
  CONCLUSIONS
  Anti-TNF was well-tolerated and safe in the 15 patients with AA amyloidosis and renal involvement. The pathogenic role of TNF in AA amyloidosis, the sustained proteinuria decrease in 3 patients, and the stabilization of renal parameters in 5 other patients make anti-TNF a promising candidate to treat AA amyloidosis secondary to inflammatory arthritides.
authors.affiliation: Hôpital de Bicêtre, Paris, France.
authors.forename: Jacques-Eric
authors.initials: JE
authors.lastname: Gottenberg
authors.forename: Florence
authors.initials: F
authors.lastname: Merle-Vincent
authors.forename: Fabrice
authors.initials: F
authors.lastname: Bentaberry
authors.forename: Yannick
authors.initials: Y
authors.lastname: Allanore
authors.forename: Francis
authors.initials: F
authors.lastname: Berenbaum
authors.forename: Bruno
authors.initials: B
authors.lastname: Fautrel
authors.forename: Bernard
authors.initials: B
authors.lastname: Combe
authors.forename: Antoine
authors.initials: A
authors.lastname: Durbach
authors.forename: Jean
authors.initials: J
authors.lastname: Sibilia
authors.forename: Maxime
authors.initials: M
authors.lastname: Dougados
authors.forename: Xavier
authors.initials: X
authors.lastname: Mariette
mesh_terms: D000328:Adult; D000368:Aged; D000686:Amyloidosis / Q000188:drug therapy* / Q000209:etiology; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000009:adverse effects; D018501:Antirheumatic Agents / Q000008:administration & dosage* / Q000009:adverse effects; D001053:Apolipoproteins / Q000276:immunology; D001168:Arthritis / Q000150:complications / Q000188:drug therapy*; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000009:adverse effects; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000188:drug therapy / Q000209:etiology; D018124:Receptors, Tumor Necrosis Factor / Q000008:administration & dosage; D012189:Retrospective Studies; D000685:Serum Amyloid A Protein / Q000276:immunology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D001053:Apolipoproteins; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept