title: Effect of the TNF-α inhibitor adalimumab in patients with recalcitrant sarcoidosis: a prospective observational study using FDG-PET.
abstract: BACKGROUND
  Tumour necrosis factor-alpha (TNF-α) plays a crucial role in sarcoidosis. In severe disease, treatment with TNF-α inhibitors may be effective.
  
  
  OBJECTIVE
  Changes in sarcoid disease activity were assessed by fluorine-18-fluorodeoxyglucose positron emission tomography (FDG-PET) in patients with recalcitrant sarcoidosis treated with adalimumab.
  
  
  METHODS
  Prospective 24-week observational study. Patients continued medication with steroids and antimetabolites and received adalimumab 40 mg subcutaneously every other week. Ten patients with biopsy-proven sarcoidosis (two men) were included with a median age of 47 years (range 35-73). An FDG-PET showing uptake indicating sarcoid activity was required at inclusion and repeated at the end of the study. FDG-PET uptake was assessed by calculated standardised uptake value (SUV). Blood samples and lung function tests were performed regularly. Quality of life was assessed by the short-form health survey (SF-36) questionnaire.
  
  
  RESULTS
  Following treatment with adalimumab, FDG-PET uptake decreased in nine patients (P = 0.011) and increased in one patient. Maximum SUV fell from median 14.1 to 7.0 (P < 0.03), and mean SUV fell from median 6.5 to 2.9 (P < 0.02). Six patients had uptake in the lungs, which decreased after treatment (P = 0.035). Six patients had uptake in the lymph nodes, which decreased after treatment in five patients (P = 0.035). Four patients had non-lymphatic extrathoracic uptake, which decreased after treatment (P = 0.05). There was no effect of adalimumab on pulmonary function tests, serum angiotensin I converting enzyme and blood lymphocyte (CD3+, CD4+, CD8+) concentrations. Physical component summary score (SF-36) increased during treatment, mental component summary score was unchanged.
  
  
  CONCLUSIONS
  In sarcoidosis, treatment with adalimumab can reduce disease activity, as assessed by FDG-PET.
authors: Department of Rheumatology and Institute for Inflammatory Research, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. nils.mil@dadlnet.dk
authors: Nils
authors: N
authors: Milman
authors: Niels
authors: N
authors: Graudal
authors: Annika
authors: A
authors: Loft
authors: Jann
authors: J
authors: Mortensen
authors: Janni
authors: J
authors: Larsen
authors: Bo
authors: B
authors: Baslund
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D001707:Biopsy, Needle; D015331:Cohort Studies; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D005260:Female; D019788:Fluorodeoxyglucose F18; D005500:Follow-Up Studies; D006801:Humans; D007150:Immunohistochemistry; D007279:Injections, Subcutaneous; D008171:Lung Diseases / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods*; D011239:Prednisolone / Q000627:therapeutic use; D011446:Prospective Studies; D012129:Respiratory Function Tests; D012507:Sarcoidosis / Q000000981:diagnostic imaging* / Q000188:drug therapy* / Q000473:pathology; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000627:therapeutic use
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D014409:Tumor Necrosis Factor-alpha; D019788:Fluorodeoxyglucose F18; D011239:Prednisolone; D000068879:Adalimumab