Complications
Clinically significant stenoses of branches of the aortic arch, especially the subclavian and axillary arteries, occur in about 10% to 15% of patients.[7]
GCA patients are 17 times more likely to develop thoracic aortic aneurysms and 2.4 times more likely to develop isolated abdominal aortic aneurysms, compared with unaffected people of the same age and sex.[102] Management of aneurysms depends on size. Smaller aneurysms can be managed medically with tight blood pressure control, whereas larger ones require surgical intervention. The incidence of aortic aneurysm after diagnosis of GCA may be as high as 30%.[7]
The treatment of GCA is associated with significant toxicity; therefore, measures to prevent or treat glucocorticoid-related adverse effects are very important. These may include managing glucocorticoid-induced diabetes, monitoring for and treating elevated blood pressure. Strategies to prevent glucocorticoid-induced bone loss include optimized intake of dietary and supplemental calcium and vitamin D based on age-appropriate national recommended daily allowances.[68] Patients ages ≥40 years receiving long-term glucocorticoids and deemed to be at high risk of fracture should receive oral bisphosphonates. Other agents including intravenous bisphosphonates, parathyroid hormone/parathyroid hormone related protein agonists (e.g., teriparatide, abaloparatide) or denosumab are also options. Selection of an agent should be based on patient and physician preferences.[68] If available, bone mineral density testing is recommended within 6 months of starting glucocorticoid therapy for adults and every 1-2 years thereafter while continuing glucocorticoid therapy.[68]
Appropriate immunizations, including influenza and pneumococcal vaccines, should be administered. While patients are receiving >20 mg of prednisone daily, they should be given prophylaxis for Pneumocystis jirovecii pneumonia (PJP).[108] Although PJP is rare in patients with GCA, it is associated with significant morbidity and is potentially life-threatening.[109]
Once blindness has occurred, it is usually irreversible. Hence, treatment with glucocorticoids should be started immediately in patients with visual symptoms or a high clinical suspicion of GCA (while awaiting confirmation of diagnosis, including results of temporal artery biopsy and acute-phase reactants).[64]
The risk of vision loss after starting glucocorticoid therapy is about 1% for patients with no preceding loss of vision. In patients with impaired vision before treatment, the risk of progressive vision loss is about 13%. Data are based on a 5-year period of follow-up.[106]
The presence of constitutional symptoms or polymyalgia rheumatica may be associated with a reduced risk of blindness.[107]
Treatment is intravenous methylprednisolone 1 g bolus daily for 3 days, followed by standard oral prednisone regimen.[66]
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