Correlation of interleukin-6 production and disease activity in polymyalgia rheumatica and giant cell arteritis

Arthritis Rheum. 1993 Sep;36(9):1286-94. doi: 10.1002/art.1780360913.


Objective: To explore the role of proinflammatory cytokines in giant cell arteritis (GCA) and polymyalgia rheumatica (PMR), two clinically related syndromes characterized by an intense acute-phase reaction. In particular, to determine plasma concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF alpha) and to correlate changes in plasma IL-6 levels with clinical symptoms during corticosteroid therapy.

Methods: IL-6 and TNF alpha concentrations were determined in plasma samples from patients with untreated PMR or GCA, and plasma IL-6 levels were monitored in patients receiving long-term therapy (14 months) with corticosteroids. To identify IL-6-producing cells, the polymerase chain reaction was used to detect IL-6 messenger RNA. In vitro production of IL-6 and IL-2 by peripheral blood mononuclear cells (PBMC) from treated and untreated patients was quantified using IL-6- and IL-2-specific bioassay systems.

Results: IL-6 concentrations were increased in PMR and GCA patients, whereas TNF alpha concentrations were similar to those in normal donors. Administration of corticosteroids rapidly reduced the levels of circulating IL-6 but did not correct the underlying mechanism inducing the increased IL-6 production. In individual patients, changes in plasma IL-6 levels and clinical manifestations during prolonged therapy were closely correlated. Short-term withdrawal of corticosteroids, even after several months of treatment, was followed by an immediate increase in plasma IL-6 concentrations. To identify the cellular source of plasma IL-6, PBMC from treated and untreated patients with PMR or GCA were analyzed for their ability to secrete IL-6 and the T cell-specific cytokine IL-2. Polyclonal T cell stimulation caused a rapid release of IL-6, which was shown to be derived exclusively from CD14+ cells.

Conclusion: Increased production of IL-6, but not TNF alpha, is a characteristic finding in patients with PMR or GCA. Corticosteroids rapidly suppress IL-6 production but do not correct the underlying mechanism inducing the increased IL-6 production. The close correlation of plasma IL-6 concentrations with clinical symptoms suggests a direct contribution of this cytokine to the disease manifestations and presents the possibility that monitoring IL-6 levels would be useful in making decisions on adjustment of corticosteroid dosage in individual patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Base Sequence
  • Giant Cell Arteritis / metabolism*
  • Giant Cell Arteritis / pathology
  • Giant Cell Arteritis / physiopathology
  • Humans
  • Interleukin-6 / biosynthesis*
  • Interleukin-6 / blood
  • Longitudinal Studies
  • Middle Aged
  • Molecular Sequence Data
  • Monocytes / metabolism*
  • Osmolar Concentration
  • Polymyalgia Rheumatica / metabolism*
  • Polymyalgia Rheumatica / pathology
  • Polymyalgia Rheumatica / physiopathology
  • Prednisone / therapeutic use
  • Reference Values
  • T-Lymphocytes / physiology
  • Tumor Necrosis Factor-alpha / biosynthesis*


  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Prednisone