Cytokines in Polymyalgia and Giant Cell Arteritis

Although it has been postulated that giant cell arteritis and polymyalgia rheumatica are a continuum of the same HLA-DR-associated disease process, the exact relation between the two conditions is still unknown. Giant cell arteritis is a well-characterized clinical entity. Histopathologic studies show a granulomatous, inflammatory reaction with a dense mononuclear leukocytic infiltration in the intima and media of large- and medium-sized arteries, along with giant cell infiltration of the internal elastic lamina [1]. Polymyalgia rheumatica is diagnosed primarily by clinical presentation of characteristic muscle pain and stiffness in the proximal portions of the extremities and torso, by increased erythrocyte sedimentation rate, and by response to glucocorticoids [2], but it has no pathognomonic histopathologic characteristics.

In this issue, Weyand and colleagues [3] report a study designed to determine whether specific cytokine patterns distinguish giant cell arteritis from polymyalgia rheumatica. That the research team found evidence of macrophage and T-cell activation in giant cell arteritis is neither new nor unexpected. However, the investigators were able to distinguish between temporal artery biopsy specimens from patients with polymyalgia rheumatica and those from patients with giant cell arteritis based on their lymphokine profiles. This is an important new observation. Further, based on the patterns of T-cell derived cytokines, the authors postulated that TH1 cells are critically involved in the granulomatous infiltrate of giant cell arteritis. This conclusion is based on the finding that interferon-γ is present only in patients with giant cell arteritis (albeit in only 67% of the samples). Pathologic studies also found that the macrophage component of the inflammatory response is shared between polymyalgia rheumatica and giant cell …