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Giant Cell Arteritis (Temporal Arteritis) Treatment & Management

  • Author: Mythili Seetharaman, MD; Chief Editor: Herbert S Diamond, MD  more...
 
Updated: Nov 04, 2015
 

Approach Considerations

The universally accepted treatment of giant cell arteritis (GCA) is high-dose corticosteroid therapy.[49, 19, 6, 131, 132, 133] The major justification for the use of corticosteroids is the impending danger of blindness in untreated patients. Patients who present with visual symptoms have a 22-fold increased chance of visual improvement if therapy is started within the first day. Damage may be irreversible if treatment is delayed beyond 48 hours.

Few studies exist regarding dosing protocols for corticosteroids in GCA. It is generally agreed that most patients with suspected GCA should be started on oral prednisone 40-60 mg/day, with a temporal artery biopsy performed within 1 week.[100] Prednisone doses of 80-100 mg/day have been suggested for patients with visual or neurologic symptoms of GCA.[134] Follow-up care within 72 hours after starting therapy should be arranged.

Alternatively, patients with acute visual changes from GCA can be started on intravenous (IV) methylprednisolone at doses of 250-1,000 mg daily for 3 days. In addition, limited data suggest that initial high-dose IV corticosteroid treatment (eg, methylprednisolone, 15 mg/kg of ideal body weight/day) may reduce remission rates.[135, 136] However, further study is warranted before this is routinely practiced.

Improvement of systemic symptoms (eg, headache, lethargy) typically occurs within 72 hours of initiation of therapy. The elevation in erythrocyte sedimentation rate (ESR) and ischemic manifestations (eg, temporal headache, jaw claudication) diminish in several days. The ESR often drops even in patients with a normal baseline reading.

Patients with multi-infarct dementia from GCA should not expect immediate cognitive recovery; however, longitudinal follow-up should show no further deterioration and may show modest improvement. Even with prompt treatment, visual loss may be permanent.

High-dose steroid therapy should be maintained only long enough for symptoms to resolve. Steroids should then be tapered slowly to the lowest dose required to suppress symptoms. Both clinical signs and sequential measurements of the ESR (or C-reactive protein level) assist in monitoring the patient's response. Patients with visual involvement usually require slower tapering of corticosteroids.

British guidelines recommend the following schedule for tapering of standard-regimen corticosteroids[49] :

  • 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[49] :

  • 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

Sequential ESR determination may assist in determining the success of corticosteroid therapy. Once the signs of clinical inflammation are suppressed and the ESR is maintained at a low level, corticosteroids may be tapered In almost all patients, the steroid dosage can be significantly decreased; however, the inflammatory process may ebb and flow, and temporary dose increases may be needed to control disease flares. Relapse occurs in 25-60% of cases.

The dose of prednisone should be increased only if clinical manifestations recur, and not simply on the basis of an elevation of the ESR. An elevated ESR without accompanying symptoms or signs of GCA could be related to an infection.

No absolute guidelines exist as to the length of treatment with corticosteroids for GCA.[100] It may be reasonable to maintain the patient on treatment for 2 years to lessen the chances for relapses. Even then, relapses have been reported.[137] Some patients may need treatment for as long as 5 years. Because the incidence of new visual damage appears to decrease with disease duration, consider a repeat temporal artery biopsy before restarting corticosteroids in patients who relapse after 18-24 months.

Long-term corticosteroid therapy has frequent and potentially serious consequences, including diabetes mellitus, vertebral compression fractures, steroid myopathy, steroid psychosis, and immunosuppression-related infections.[138] Indeed, the cumulative morbidity associated with long-term therapy often exceeds that of the underlying disease.

Alternative immunosuppressant agents (eg, cyclosporin, azathioprine, methotrexate) may be started later in the course of treatment. They can be useful as steroid-sparing agents in patients who require prolonged treatment with high doses of steroids (more than 5-10 mg/d) and those who experience significant steroid-related complications.

Most patients with GCA can be treated on an outpatient basis. Hospital admission may be indicated for patients with particularly severe symptoms or those unable to provide self-care at home. After resolution of acute GCA, patients require regular followup to monitor for disease recurrence, steroid complications during steroid therapy, and long-term complications such as aortic aneurysm.

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Alternatives to Corticosteroids

Trials of other immunosuppressant agents, including cyclophosphamide, azathioprine, methotrexate, and dapsone, have been attempted for their steroid-sparing effects. Steroid dosages have been lowered successfully but inconsistently in some patients on each of these drugs. Toxicity can be a significant problem, particularly with dapsone and cyclophosphamide.

Limited experience suggests that cyclophosphamide may be the most consistently effective immunosuppressant. It may permit more rapid steroid tapering when instituted after a relapse. Cyclophosphamide may be administered in monthly pulses.[122]

Azathioprine, in an average dosage of 1.5-2.7 mg/kg/day, reduced steroid requirements in a double-blind, placebo-controlled study that included 31 patients with GCA, polymyalgia rheumatic, or both. However, the advantage of azathioprine over placebo did not reach statistical significance until 1 year.[139]

Methotrexate has been used as a steroid-sparing agent, in doses of 15-25 mg/wk. However, evidence regarding its efficacy remains inconclusive.[140, 141, 142, 143]

In a formal meta-analysis, adjunctive methotrexate, 7.5-15 mg/wk, reduced the risk of a first relapse by 35% and of a second relapse by 51%. In addition, methotrexate reduced the cumulative exposure to steroids. However, the superiority of the treatment effect of methotrexate over placebo fully appeared only after a latency period of 24-36 weeks, and no between-group difference was noted in the occurrence of adverse events.[141]

Tumor necrosis factor (TNF) inhibitors (eg, infliximab, etanercept) are being evaluated in clinical trials for the treatment of GCA. A randomized controlled trial showed that adding infliximab to steroids provided no measurable benefit in the management of newly diagnosed GCA.[144]

A double-blind, placebo-controlled trial of etanercept in steroid-refractory GCA yielded mixed results. The study included 17 patients who required a stable dose of prednisone of 10 mg/d to maintain clinical remission and had at least one steroid-related adverse effect. After 12 months, more of the patients in the etanercept group had successfully discontinued prednisone (50% versus 22.2% of placebo patients), but the difference was not significant. No difference was noted in the number and type of adverse events.[145]

However, patients in the etanercept group did have a significantly lower cumulative dose of accumulated prednisone during the first year of treatment (p = 0.03). The researchers noted that a larger trial with longer follow-up is needed to determine the role of etanercept in GCA therapy.[145]

In an open-label study, treatment with the interleukin-6 receptor antagonist tocilizumab led to rapid and maintained improvement in 19 of 22 patients whose GCA was refractory to corticosteroid treatment, or who had experienced unacceptable corticosteroid side effects. However, serious infection-related complications--including a fatal stroke associated with infective endocarditis--occurred in three patients.[146]

A number of clinical trials of GCA are either actively recruiting or are active but not yet recruiting. For a complete list, see these List Results from ClinicalTrials.gov.

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Diet and Activity

Patients with GCA who are on steroid therapy should be monitored carefully for the steroid-related complications of diabetes mellitus, hypertension, peripheral edema, and weight gain. Management of dietary sugar, salt, and caloric intake may help to prevent such complications.

No activity restrictions are necessary in a patient with GCA who is asymptomatic on adequate therapy. If a patient has ischemic eye or brain symptoms, then bedrest in a supine position may be desirable before or when first beginning steroid therapy. Some patients may have orthostatically sensitive amaurosis fugax, but this is rare.

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Consultations

Immediate consultation with a rheumatologist is suggested when initiating high-dose steroid therapy for presumed GCA prior to performance of a temporal artery biopsy (TAB). Therapy should not be delayed if consultation is not available immediately, however.

Rheumatologic consultation also is indicated to consider the need for steroid therapy when biopsy results are negative, but the clinical presentation strongly suggests GCA. The occasional patient with GCA who does not respond adequately to steroid therapy requires a referral for reconsideration of the diagnosis and for other forms of immunosuppressive therapy.

Surgical consultation is necessary for TAB. Depending on the institution, this procedure can be performed by a neurosurgeon, plastic surgeon, ophthalmologist, or general surgeon.

It is imperative that the treating physician be familiar and confident with the laboratory that is evaluating the TAB specimen, since this is the criterion standard for GCA diagnosis. A myriad of laboratory errors (eg, specimen handling, fixation, sectioning) can, if they occur, result in a misdiagnosis (most often a false-negative result).

An ophthalmologist should be consulted for a complete, dilated ocular examination to rule out other causes of vision loss, particularly when the diagnosis is uncertain. Consultation with neurologist is helpful for excluding other causes of headache.

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Long-Term Monitoring

Because giant cell arteritis (GCA) is a potentially blinding and lethal disease, regular follow-up care after a successful initial management of the acute process is considered a standard of care. Routine follow-up should include asking about symptoms of upper extremity claudication or ischemia, listening for bruits, and taking blood pressure in both arms. Ongoing monitoring of symptoms and the erythrocyte sedimentation rate (ESR) is mandatory.

The ESR often normalizes within days of instituting steroid therapy. With tapering of steroid doses, ischemic complications may occur at any time but tend to occur a median of 1 month after beginning therapy.

British guidelines recommend that patients with GCA have follow-up visits at weeks 1, 3, and 6 and then months 3, 6, 9, and 12 in the first year after diagnosis, with extra unscheduled visits as necessary if relapse or adverse events occur.[49] The typical patient with GCA remains on steroid therapy for roughly 2 years. Followup is recommended until 1 year after discontinuation of therapy.

During corticosteroid therapy, monitoring for complications of long-term use of these drugs is indicated. Patients should be screened for diabetes, hypertension, and cataracts.

Given the high risk of corticosteroid-induced osteoporosis, patients should have baseline bone densitometry at the start of therapy. All patients on corticosteroids need adequate calcium and vitamin D for protection against osteoporosis (1500 mg of calcium and 800 IU of vitamin D3 daily).

American College of Rheumatology guidelines provide an algorithm for determining whether a patient receiving corticosteroids is at low, medium, or high risk for osteoporosis. The guidelines also offer recommendations for treatment—including, where appropriate, pharmacologic treatment with alendronate, risedronate, zoledronic acid, or teriparatide, with the choice of agent determined partly by risk level.[147]

Vaccination against influenza and pneumococcal disease is of heightened importance, because of relative immunosuppression from steroids. Long-term high-dose steroid therapy increases risk for peptic ulcer disease, particularly in patients older than 65 years, so prophylaxis with histamine-2 blockers, proton pump inhibitors, or antacids is justified, especially in patients who are also taking nonsteroidal anti-inflammatory drugs.[148]

Retrospective but impressive data from Nesher and colleagues support the use of low-dose aspirin (81 mg) in patients with GCA for prevention of visual loss and stroke.[149] This therapy should be initiated in every patient diagnosed with GCA who does not have contraindications to its use.

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Contributor Information and Disclosures
Author

Mythili Seetharaman, MD Consultant Rheumatologist, OAA; Clinical Assistant Professor, Thomas Jefferson University Hospital, St Christopher's Hospital for Children

Mythili Seetharaman, MD is a member of the following medical societies: American College of Rheumatology, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

C Stephen Foster, MD, FACS, FACR, FAAO, FARVO Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution

C Stephen Foster, MD, FACS, FACR, FAAO, FARVO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, Sigma Xi

Disclosure: Nothing to disclose.

John G Albertini, MD Private Practice, The Skin Surgery Center; Clinical Associate Professor (Volunteer), Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine; President-Elect, American College of Mohs Surgery

John G Albertini, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery

Disclosure: Received grant/research funds from Genentech for investigator.

Stephen A Paget, MD Physician-in-Chief Emeritus, Joseph P Routh Professor of Medicine, New York Hospital, Weill Cornell Medical College; Program Director, Cornell Arthritis and Multipurpose Arthritis and Musculoskeletal Diseases Center (MAMDC), Hospital for Special Surgery

Stephen A Paget, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, New York Academy of Sciences

Disclosure: Nothing to disclose.

Manolette R Roque, MD, MBA, FPAO Section Chief, Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Section Chief, Ocular Immunology and Uveitis, International Eye Institute, St Luke's Medical Center Global City; Senior Eye Surgeon, The LASIK Surgery Clinic; Director, AMC Eye Center, Alabang Medical Center

Manolette R Roque, MD, MBA, FPAO is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Philippine Medical Association, American Uveitis Society, International Ocular Inflammation Society, Philippine Ocular Inflammation Society, American Society of Ophthalmic Administrators, American Academy of Ophthalmic Executives, Philippine Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Lawrence H Brent, MD Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

Richard J Caselli, MD Professor, Department of Neurology, Mayo Medical School; Chair, Department of Neurology, Mayo Clinic of Scottsdale

Disclosure: Nothing to disclose.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting

Hyland Cronin, MD Resident Physician, Dermatology Department, Geisinger Health System

Disclosure: Nothing to disclose.

Ann G Egland, MD Consulting Staff, Department of Operational and Emergency Medicine, Walter Reed Army Medical Center

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Gino A Farina, MD, FACEP, FAAEM Associate Professor of Emergency Medicine, Hofstra North Shore LIJ School of Medicine and Albert Einstein College of Medicine; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Kilbourn Gordon III, MD, FACEP Urgent Care Physician

Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society

Disclosure: Nothing to disclose.

Russell Hall, MD J Lamar Callaway Professor And Chair, Department of Dermatology, Duke University Medical Center, Duke University School of Medicine

Russell Hall, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Federation for Medical Research, American Society for Clinical Investigation, and Society for Investigative Dermatology

Disclosure: Novan Consulting fee Consulting; Stieffel, a GSK company Consulting fee Consulting; Society for Investigative Dermatology Salary Board membership

Jean Marie Hammel, MD Assistant Professor, Associate Residency Director of Emergency Medicine Residency Program, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine

Jean Marie Hammel, MD is a member of the following medical societies: Alpha Omega Alpha and Phi Beta Kappa

Disclosure: Nothing to disclose.

Leslie W Jackson, MD, LTC, MC Assistant Professor, Department of Medicine, Uniformed Services University of the Health Sciences; Assistant Chief, Rheumatology Service, Department of Medicine, Walter Reed Army Medical Center

Disclosure: Nothing to disclose.

B Mark Keegan, MD, FRCPC Associate Professor of Neurology, College of Medicine, Mayo Clinic; Master's Faculty, Mayo Graduate School; Consultant, Department of Neurology, Mayo Clinic, Rochester

B Mark Keegan, MD, FRCPC is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Minnesota Medical Association

Disclosure: Novartis Consulting fee Consulting; Bionest Consulting fee Consulting; Bristol Meyers Squibb Consulting fee Consulting; Caridian BCT Grant/research funds Other

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Christopher H Lee, MD Clinical Instructor, Section of EMS, Department of Emergency Medicine, Yale University School of Medicine

Christopher H Lee, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Evan Leibowitz, MD Fellow, Department of Internal Medicine, Division of Rheumatology, Valley Hospital

Evan Leibowitz, MD is a member of the following medical societies: Alpha Omega Alpha and American Medical Association

Disclosure: Nothing to disclose.

Victor J Marks, MD Associate, Department of Dermatology, Section Chief, Dermatologic Surgery, Geisinger Health System

Victor J Marks, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American College of Physicians, American Medical Association, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Jorge E Mendizabal, MD Consulting Staff, Corpus Christi Neurology

Jorge E Mendizabal, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, National Stroke Association, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Elisabetta Miserocchi, MD Fellow in Immunology and Uveitis Service, Department of Ophthalmology, Harvard Medical School

Disclosure: Nothing to disclose.

Julia R Nunley, MD Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center

Julia R Nunley, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Nephrology, International Society of Nephrology, Medical Dermatology Society, Medical Society of Virginia, National Kidney Foundation, Phi Beta Kappa, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Arun Ramachandran State University of New York Upstate Medical University

Arun Ramachandran is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Tarakad S Ramachandran, MBBS, FRCP(C), FACP, FRCP Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, FRCP(C), FACP, FRCP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, RoyalCollegeofPhysicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine

Disclosure: Boeringer-Ingelheim Honoraria Speaking and teaching

Barbara L Roque, MD Full Partner, Ophthalmic Consultants Philippines Co; Service Chief, Pediatric Ophthalmology and Strabismus, Department of Ophthalmology, Asian Hospital and Medical Center; Active Staff, International Eye Institute, St Luke's Medical Center Global City; Visiting Ophthalmologist, AMC Eye Center, Alabang Medical Center

Barbara L Roque, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Cataract and Refractive Surgery, Philippine Academy of Ophthalmology, Philippine Society of Cataract and Refractive Surgery, and Philippine Society of Pediatric Ophthalmolo

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska

Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Florian P Thomas, MD, MA, PhD, Drmed Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine

Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Paraplegia Society, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, and Sigma Xi

Disclosure: Nothing to disclose.

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of Medscape Reference gratefully acknowledge the assistance of Ryan I Huffman, MD, with the literature review and referencing for this article.

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Hematoxylin- and eosin-stained superficial temporal artery biopsy specimen, cross section. The hallmark histologic features of GCA shown here include intimal thickening with luminal stenosis, mononuclear inflammatory cell infiltrate with media invasion and necrosis, and giant cell formation in the media.
Lumbar angiogram showing stenosis and occlusion of femoral artery branches due to vasculitis.
Hematoxylin- and eosin-stained femoral artery branch, cross section, taken from a lower limb amputation specimen. Mononuclear cell invasion and necrosis in the media of this large artery can be observed. Extensive lower limb vasculitis from GCA resulted in ischemic necrosis of the lower limb, necessitating amputation.
Hematoxylin and eosin stain, low power. Temporal artery. Note the thrombosis in the lumen, intimal hyperplasia, and infiltration of the arterial wall muscular layers with inflammatory cells. A multinucleated giant cell is seen internal to the muscularis at the area of the internal elastic lamina (upper right).
Anterior ischemic optic neuropathy. Image courtesy of Richard Kho, MD, Q.C. Eye Center, Quezon City, Philippines.
Branch retinal vein occlusion in a patient with giant cell arteritis. Image courtesy of Manolette Roque, MD, Roque Eye Clinic, Manila, Philippines.
 
 
 
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