Unlike PMR treatment, GCA therapy begins with higher doses of prednisone or its equivalents. The main principle is to commence the glucocorticoid treatment in patients with suspected GCA as soon as possible, upon meeting of three or more ACR criteria or in case of GCA history with exacerbation of neuro-ophthalmologic complications, including jaw claudication, amaurosis fugax and other visual disturbances. The initial dose of prednisone ranges around 40–60 mg daily. In case of a risk of severe ischaemic complications (amaurosis fugax, monocular vision loss, initial manifestations of visual disturbances in the other eye), the patient receives intravenous pulse methylprednisolone therapy at the dose of 500–1000 mg daily for three days, which then continues in the form of oral treatment. Alleviation of subjective complaints is reported by patients within 48–72 h of commencement of treatment. During 2–4 weeks, inflammatory parameters (ESR, CRP) decrease or return to normal. The initial dose is administered usually for 4 weeks, and then it is gradually reduced, maximally by 10 % of the total daily dosage at 1- or 2-week intervals [7, 78, 79].

Patients are monitored during the treatment due to a risk of both disease relapse and of adverse effects of the therapy. At the beginning of the disease, checks must be more frequent, with the recommended intervals at week 0, 1, 4, 8 and 12 and afterwards at month 3, 6, 9 and 12 during the 1st year [67]. Disease relapse should be considered with ESR > 40mmHg and the presence of at least one GCA clinical manifestations: fever (≥38 °C), PMR, headache or scalp tenderness, loss of vision, pain in the tongue/jaw or jaw claudication, claudication pain in extremities, thickening, palpation tenderness or swelling of the temporal or occipital arteries, angiographic changes indicating vasculitis of the aorta or its branches, TIA or stroke [67, 80].

The risk of ischaemic complications in patients with GCA is reduced by antiplatelet or anticoagulation therapy [81].

In order to reduce the cumulative dose of prednisone, also other DMARDs are added to glucocorticoid treatment, particularly methotrexate, however with a varying effect on reduction of the monitored parameters reported in individual studies [80, 82]. Several recent studies have presented promising results of anti-cytokine therapy (primarily infliximab and etanercept) used in patients with PMR and GCA, although the cohorts of patients were small [83, 84].

The drug of choice for treatment of both PMR and GCA still remain glucocorticoids. In order to reduce the risk of adverse effects, the patients receive simultaneously H₂ receptor blockers or proton pump inhibitors, calcium and vitamin D supplementation and where appropriate bisphosphonates, depending on the bone density values.

The British Society for Rheumatology published the following guidelines for GCA treatment [67]:

Treatment of PMR and primarily GCA must be multidisciplinary due to their systemic nature. Early diagnosis, a timely and appropriate treatment and lifelong follow-up of patients in view of the risk of ischaemic complications may prevent both development of severe complications of the disease and adverse effects of the treatment (Figs. 8.1, 8.2, 8.3, 8.4, 8.5, 8.6, and 8.7).