title: Predictors for treatment success and expression of glucocorticoid receptor in giant cell arteritis and polymyalgia rheumatica.
abstract: OBJECTIVE
  Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) generally respond well to treatment with glucocorticoids (GC). We sought to determine the value of clinical, histopathologic, immunohistochemical, and genetic findings and the expression of the glucocorticoid receptor (GR) for discriminating between patients who achieve complete remission, or partial remission, or who do not improve with glucocorticoid treatment.
  
  
  METHODS
  We examined biopsies of the temporal artery from 60 patients, of whom 27 had GCA, 13 PMR, and 20 arteriosclerosis.
  
  
  RESULTS
  Of the clinical variables evaluated, jaw claudication was correlated with the histologic classification of the biopsies (p < 0.0001). Erythrocyte sedimentation rate was significantly higher in patients with PMR and GCA than in patients with arteriosclerosis (p < 0.0001). There were significant differences between patients with GCA versus PMR in the numbers of CD3-, CD8-, and CD4-positive T cells, in CD68-positive monocytes (p < 0.0001), and antigen-presenting cells (p < 0.0001). CD138-positive and CD20-positive cells were absent in patients with PMR but present in patients with GCA (p < 0.0001). In GCA and chronic inflammation most monocytes and lymphocytes expressed GR (88.9%). The number of CD68-positive cells and the extent of GR-staining in chronic inflammation reflected the success of treatment in logistic regression analysis (p < 0.05). GR polymorphism showed that more than 90% of patients had the wild-type (homozygote) of the R23K or N363S polymorphism. There was no evidence that this polymorphism influenced response to treatment with GC (Fisher's exact test 1.0).
  
  
  CONCLUSIONS
  Expression of GR and the presence of CD20-, CD3-, CD4-, CD8-, CD68-, CD138-positive cells and antigen-presenting cells differ between GCA and PMR. The presence of CD68-positive cells and the extent of GR-staining in chronic inflammation are suitable to predict complete remission in GCA.
authors.affiliation: Division of General Internal Medicine and Nephrology, Department of Internal Medicine, Robert-Bosch Hospital Stuttgart, 70376 Stuttgart, Germany. Niko.Braun@rbk.de
authors.forename: Niko
authors.initials: N
authors.lastname: Braun
authors.forename: Peter
authors.initials: P
authors.lastname: Fritz
authors.forename: Anja
authors.initials: A
authors.lastname: Rieth
authors.forename: Werner
authors.initials: W
authors.lastname: Schroth
authors.forename: Martin
authors.initials: M
authors.lastname: Kimmel
authors.forename: Dagmar
authors.initials: D
authors.lastname: Biegger
authors.forename: David
authors.initials: D
authors.lastname: Zakim
authors.forename: Mark Dominik
authors.initials: MD
authors.lastname: Alscher
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001706:Biopsy; D016022:Case-Control Studies; D005260:Female; D013700:Giant Cell Arteritis / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology / Q000473:pathology; D011111:Polymyalgia Rheumatica / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D011237:Predictive Value of Tests; D011965:Receptors, Glucocorticoid / Q000378:metabolism*; D012074:Remission Induction; D012189:Retrospective Studies; D013699:Temporal Arteries / Q000378:metabolism / Q000473:pathology; D016896:Treatment Outcome; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; C067980:CD68 antigen, human; D000097382:CD68 Molecule