at low doses of prednisone (<20 mg/day), during the first year of treatment, and the most common signs of relapse are headache and polymyalgia rheumatica. Associated conditions The varicella-zoster virus (VZV) antigen was found in 74% of temporal artery biopsies that were GCA-positive, suggesting that the VZV infection may trigger the inflammatory cascade. The disorder may co-exist (in about half of cases) with polymyalgia rheumatica (PMR), which is characterized by sudden onset of pain and stiffness in muscles (pelvis, shoulder) of the body and is seen in the elderly. GCA and PMR are so closely linked that they are often considered to be different manifestations of the same disease process. PMR usually lacks the cranial symptoms, including headache, pain in the jaw while chewing, and vision symptoms, that are present in GCA. Giant cell arteritis can affect the aorta and lead to aortic aneurysm and aortic dissection. Up to 67% of people with GCA having evidence of an inflamed aorta, which can increase the risk of aortic aneurysm and dissection. There are arguments for the routine screening of each person with GCA for this possible life-threatening complication by imaging the aorta. Screening should be done on a case-by-case basis based on the signs and symptoms of people with GCA. Mechanism The pathological mechanism is the result of an inflammatory cascade that is triggered by an as of yet undetermined cause resulting in dendritic cells in the vessel wall recruiting T cells and macrophages to form granulomatous infiltrates. These infiltrates erode the middle and inner layers of the arterial tunica media leading to conditions such as aneurysm and dissection. Activation of T helper 17 (Th17) cells involved with interleukin (IL) 6, IL-17, IL-21 and IL-23 play a critical part; specifically, Th17 activation leads to further activation of Th17 through IL-6 in a continuous, cyclic fashion. This pathway is suppressed with glucocorticoids, and more recently it has been found that IL-6 inhibitors also play a suppressive role. Diagnosis Physical exam Palpation of the head reveals prominent temporal arteries with or without pulsation. The temporal area may be tender. Decreased pulses may be found throughout the body Evidence of ischemia may be noted on fundal exam. Bruits may be heard over the subclavian and axillary arteries Laboratory tests Erythrocyte sedimentation rate, an inflammatory marker, >60 mm/hour (normal 1–40 mm/hour). C-reactive protein, another inflammatory marker, may be elevated. LFTs, liver function tests, are abnormal