What is it giant cell arteritis?
Giant cell arteritis is a form of vasculitis most commonly affecting the arteries of the scalp and head; as such it is also known as temporary arteritis [1]. Giant cell arteritis can also cause previous ischemic optical neuropathy, cerebral arteritis and the aortic arc syndrome.
It is characterized by a strong headache, visual symptoms, discomfortand fever [2].
Who gets giant cell arteritis?
the incidence Giant cell arteritis varies from 5.8 to 31.3 per 100,000 of the population, and the predominance it is estimated at 30.4 cases per 100,000 [2].
Giant cell arteritis occurs only in adults over the age of 50 and peaks between the ages of 70 and 80. [one]. It is more frequent in women than in men and affects Caucasians more frequently [1].
In 50% cases, giant cell arteritis is associated with polymyalgia rheumatic (PMR), a rheumatic condition that causes extended pain and stiffness. It is estimated that 5 to 15% of people with PMR can develop giant cell arteritis. [one].
What causes giant cell arteritis?
Giant cell arteritis is a vasculitis of the great vessels of unknown cause. [one]. Giant cell arteritis symptoms are due to occlusion of the affected arteries.
Age, genetics and infection it may be involved in its causality [3]. The human White blood cell antigen (HLA) The DR4 serotype has been correlated with giant cell arteritis and PMR [3].
What are the clinical features of giant cell arteritis?
The clinical features of giant cell arteritis are typically [1]:
- A new persistent headache
- A scalp and tender temples
- Mandible claudication
- Abrupt onset of visual changes, such as blurred vision, double vision, and blindness.
- Flu-like symptoms, such as fatigue, fever, and loss of appetite.
- Decreased or temporarily absent, occipitalor pulses of the facial artery.
the cutaneous manifestations of giant cell arteritis
Cutaneous manifestations of giant cell arteritis are rare and can occur months after the onset of other symptoms; these manifestations include [2,4]:
- Erythema, purple, hardeningand bullas
- Offer nodules, ulcers or necrosis
- Periorbital ecchymosis
- Glossitis
- Facial edema
- Hair lost.
Late skin manifestations include ulceration and necrosis of the frontotemporal scalp and tongue [4].
Giant cell arteritis rarely affects another site, such as the lower limb, but generalized skin lesions are rare. This type of injury are caused by the occlusion of small vessels in the dermis or subcutis [2].
What are the complications of giant cell arteritis?
It is estimated that 13 to 19% of patients with giant cell arteritis experience ischemia of an optic artery, causing sudden partial or complete loss of vision that may be permanent [1,2].
Patients who develop necrosis of the scalp are at increased risk of vision loss and mortality. [two].
Other complications may include gangrene of the tongue or nasal pulp [5].
How is giant cell arteritis diagnosed?
The diagnosis of giant cell arteritis is based on the clinical characteristics and the results of the investigations.
- the inflammatory markers, erythrocytes sedimentation rate (ESR) and C-reactive protein, they are raised.
- Biopsy reveals granulomatous inflammation of great blood vessels - more commonly, the branches of the external carotid and vertebral arteries [2].
- the histology of a skin lesion is not specific and a negative biopsy does not exclude the diagnosis.
- Blood cultures may be necessary to exclude a systemic infection.
- Imaging of the temporal artery and other large blood vessels can be helpful. [6].
The American College of Rheumatology has suggested five criteria for diagnosing giant cell arteritis; these criteria are [5]:
- Age greater than or equal to 50 years.
- New start of a located headache
- Temporal artery tenderness.
- High ESR (> 50 mm / hour)
- Inflammatory infiltrators and multinucleated giant cells in biopsy
The presence of three or more criteria has a sensitivity of 93.5% and a specificity of 91.2% for diagnosis. [5].
Which is the differential diagnosis for giant cell arteritis?
The differential diagnosis for giant cell arteritis may include [3]:
- Other forms of vasculitis with constitutional symptoms and elevated inflammatory markers.
- Takayasu's arteritis, which has indistinguishable histopathological findings but occurs at a younger age, typically before age 40
- Non-arteritic anterior ischemic optic neuropathy, presenting with sudden monocle vision loss but lacks other features of giant cell arteritis.
- Systemic infection, which causes fever, myalgia, arthralgia, headache and elevated inflammatory markers.
What is the treatment for giant cell arteritis?
If there is a strong clinical suspicion of giant cell arteritis, systemic steroid treatment should be started immediately to decrease the risk of vision loss [6].
Typically 40-60 mg of oral prednisone per day is prescribed for a minimum of 4 weeks, which may be preceded by intravenous methylprednisolone sodium succinate if there is visual impairment. The steroid dose gradually decreases over 1 to 2 years. [5]. Bone protection, such as calcium and vitamin D supplements or bisphosphonate medication, may be necessary for some patients due to the side effects of prolonged corticosteroid use. [one].
In some cases, attached immunomodulator Medications such as methotrexate or tocilizumab [6] can be used.
Low-dose aspirin is prescribed simultaneously to prevent ischemic events [6].
Occasionally, a skin graft is required to repair persistent ulceration. [two].
What is the result of giant cell arteritis?
Giant cell arteritis is usually self-limiting and resolves for months or years. [3]. Relapses It can occur as the corticosteroid dose is reduced and requires the dose to be temporarily increased [6].
New-onset visual loss is rare once corticosteroid therapy is started [3].
Giant cell arteritis is associated with a cardiovascular increase morbidity and mortality [2].