Temporal arteritis medical therapy
|
Temporal Arteritis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Temporal arteritis medical therapy On the Web |
|
American Roentgen Ray Society Images of Temporal arteritis medical therapy |
|
Risk calculators and risk factors for Temporal arteritis medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2]
Overview
The mainstay of treatment for temporal arteritis is corticosteroids. Damage may be irreversible if treatment is delayed beyond 48 hours. Oral prednisone 40-60 mg/day should be started, with a temporal artery biopsy performed within 1 week. Prednisone doses of 80-100 mg/day have been suggested for patients with visual or neurologic symptoms of temporal arteritis and follow-up care within 72 hours after starting therapy should be arranged. Patients with acute visual changes from temporal arteritis can be started on intravenous (IV) methylprednisolone at a dose of 1,000 mg daily for 3 days. Initial high-dose IV corticosteroid, methylprednisolone, treatment 15 mg/kg of ideal body weight/day may reduce remission rates. Use of low-dose aspirin (81 mg) for prevention of visual loss and stroke is recommended in temporal arteritis. Improvement of systemic symptoms occurs within 72 hours after initiation of therapy. The elevation in erythrocyte sedimentation rate and ischemic symptoms such as headache and jaw claudication improve over several days. High-dose steroid therapy should be maintained long enough for symptoms to resolve and then be tapered slowly to the lowest dose required to suppress symptoms. Long-term corticosteroid therapy complications include diabetes mellitus, vertebral compression fractures, steroid myopathy, steroid psychosis, and immunosuppression related infections. Tocilizumab has been approved for use in rheumatoid arthritis and is now approved for use in temporal arteritis.
Medical Therapy
The medical therapy for temporal arteritis is as follows:[1][2][3][4][5]
- Pharmacologic medical therapies for temporal arteritis is high-dose corticosteroid therapy.
- Damage may be irreversible if treatment is delayed beyond 48 hours.
- Oral prednisone 40-60 mg/day should be started, with a temporal artery biopsy performed within 1 week.[6]
- Prednisone doses of 80-100 mg/day have been suggested for patients with visual or neurologic symptoms of temporal arteritis and follow-up care within 72 hours after starting therapy should be arranged.[3]
- Patients with acute visual changes from temporal arteritis can be started on intravenous (IV) methylprednisolone at a dose of 1,000 mg daily for 3 days.
- Initial high-dose IV corticosteroid, methylprednisolone, treatment 15 mg/kg of ideal body weight/day may reduce remission rates.[7][8]
- Use of low-dose aspirin (81 mg) for prevention of visual loss and stroke is recommended in temporal arteritis.[9]
British guidelines recommend the following schedule for tapering of standard-regimen corticosteroids:[1]
- Continue prednisolone, 40-60 mg (not <0.75 mg/kg) for 4 weeks (or until symptoms and laboratory abnormalities resolve), then
- Reduce dose by 10 mg every 2 weeks to 20 mg, then
- Reduce dose by 2.5 mg every 2-4 weeks to 10 mg, then
- Reduce dose by 1 mg every 1-2 months, provided no relapse occurs
The guidelines recommend that patients on steroid therapy receive prophylactic treatment with the following medications:[1]
- Low-dose aspirin, 81 mg per day – to decrease cranial ischemic complications
- Proton pump inhibitor – for gastrointestinal protection
- Bisphosphonate, calcium, and vitamin D – for bone protection
- Treatment maintenance is recommended for 2 years to lessen the chances for relapses.[10]
- Long-term corticosteroid therapy complications include diabetes mellitus, vertebral compression fractures, steroid myopathy, steroid psychosis, and immunosuppression related infections.[11]
- Tocilizumab has been approved for use in rheumatoid arthritis and is now approved for use in temporal arteritis.[12]
- Improvement of systemic symptoms occurs within 72 hours after initiation of therapy. The elevation in erythrocyte sedimentation rate and ischemic symptoms such as headache and jaw claudication improve over several days.
- High-dose steroid therapy should be maintained long enough for symptoms to resolve and then be tapered slowly to the lowest dose required to suppress symptoms.
References
- ↑ 1.0 1.1 1.2 Dasgupta B, Borg FA, Hassan N, Alexander L, Barraclough K, Bourke B; et al. (2010). "BSR and BHPR guidelines for the management of giant cell arteritis". Rheumatology (Oxford). 49 (8): 1594–7. doi:10.1093/rheumatology/keq039a. PMID 20371504.
- ↑ Caylor TL, Perkins A (2013). "Recognition and management of polymyalgia rheumatica and giant cell arteritis". Am Fam Physician. 88 (10): 676–84. PMID 24364483.
- ↑ 3.0 3.1 Fraser JA, Weyand CM, Newman NJ, Biousse V (2008). "The treatment of giant cell arteritis". Rev Neurol Dis. 5 (3): 140–52. PMC 3014829. PMID 18838954.
- ↑ Buttgereit, Frank; Dejaco, Christian; Matteson, Eric L.; Dasgupta, Bhaskar (2016). "Polymyalgia Rheumatica and Giant Cell Arteritis". JAMA. 315 (22): 2442. doi:10.1001/jama.2016.5444. ISSN 0098-7484.
- ↑ Matteson, Eric L.; Buttgereit, Frank; Dejaco, Christian; Dasgupta, Bhaskar (2016). "Glucocorticoids for Management of Polymyalgia Rheumatica and Giant Cell Arteritis". Rheumatic Disease Clinics of North America. 42 (1): 75–90. doi:10.1016/j.rdc.2015.08.009. ISSN 0889-857X.
- ↑ Charlton R (2012). "Optimal management of giant cell arteritis and polymyalgia rheumatica". Ther Clin Risk Manag. 8: 173–9. doi:10.2147/TCRM.S13088. PMC 3333461. PMID 22547936.
- ↑ Mazlumzadeh M, Hunder GG, Easley KA, Calamia KT, Matteson EL, Griffing WL; et al. (2006). "Treatment of giant cell arteritis using induction therapy with high-dose glucocorticoids: a double-blind, placebo-controlled, randomized prospective clinical trial". Arthritis Rheum. 54 (10): 3310–8. doi:10.1002/art.22163. PMID 17009270.
- ↑ Prieto-González S, García-Martínez A, Arguis P, Cid MC (2013). "Early improvement of radiological signs of large-vessel inflammation in giant cell arteritis upon glucocorticoid treatment". Rheumatology (Oxford). 52 (7): 1335–6. doi:10.1093/rheumatology/ket161. PMID 23620559.
- ↑ Nesher G, Berkun Y, Mates M, Baras M, Rubinow A, Sonnenblick M (2004). "Low-dose aspirin and prevention of cranial ischemic complications in giant cell arteritis". Arthritis Rheum. 50 (4): 1332–7. doi:10.1002/art.20171. PMID 15077317.
- ↑ Chan CC, Paine M, O'day J (2005). "Predictors of recurrent ischemic optic neuropathy in giant cell arteritis". J Neuroophthalmol. 25 (1): 14–7. PMID 15756126.
- ↑ Durand M, Thomas SL (2012). "Incidence of infections in patients with giant cell arteritis: a cohort study". Arthritis Care Res (Hoboken). 64 (4): 581–8. doi:10.1002/acr.21569. PMID 22184094.
- ↑ Loricera J, Blanco R, Hernández JL, Castañeda S, Mera A, Pérez-Pampín E; et al. (2015). "Tocilizumab in giant cell arteritis: Multicenter open-label study of 22 patients". Semin Arthritis Rheum. 44 (6): 717–23. doi:10.1016/j.semarthrit.2014.12.005. PMID 25697557.