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1 Şubat 2017 Çarşamba


Giant cell arteritis (GCA) is the most common systemic vasculitis.
The greatest risk factor for GCA is aging. The disease, which is almost never seen under the age of 50, peaks at ages 70-79.
The disease is a little more common in females. GCA can also be found in patients' families.
Patients with GCA are not associated with increased mortality if there is no significant aortic disease. Approximately 40-60% of GCA patients have polymyalgia rheumatica (PMR), but only 15% of patients with PMR have GCA.
The onset of the disease is mostly subacute, but may also be acute.
Fever is present near the half of the patients and is usually at low levels. However, fever can reach 39° C in 15% of patients, It may also be due to a skipped infection.
Fatigue, weight loss (usually low level) are common.
Headache is present in 2/3 of the patients.
Jaw claudication is an experience where almost half of the patients live. In one analysis, jaw claudication was reported to be the most associated symptom with temporal artery biopsy results.
Amorozis fugax, temporary loss of vision, mostly affecting one eye. It may be an early manifestation. It is valuable in terms of prior notice of permanent blindness.
Persistent vision loss is painless and sudden. It can be partial or complete. It may be unilateral or bilateral. Persistent visual loss in patients with GCA has been reported to be 15-20%, even with appropriate treatment. Once it develops; Rarely returns. Moreover, other eyes of untreated patients may experience visual loss within 1 week (25-50% risk).
If visual loss returns quickly after the appropriate dose of glucocorticoid therapy, the risk of vision loss is virtually eliminated.
If vision loss is already present, this treatment will significantly reduce the risk of further deterioration.
Causes of vision loss;
Arterial ischemic optic neuropathy (AION),
Central or branchial occlusion of the retinal artery (CRAO / BRAO),
Posterior ischemic optic neuropathy (PION,
Cerebral ischemia (rare).

AION accounts for at least 80%. AION typically develops as a consequence of the occlusion of the posterior silier artery, a branch of the ophthalmic artery (the main feeder vessel in the eye) originating from the internal carotid artery .
CRAO is responsible for 10% of permanent blindness due to GCA.
Diplopi % 5
Charles Bonnet Syndrome; Visual hallucinations in the person with vision loss. It may also be associated with glucocorticoid. It's actually a psychiatric syndrome.
Peripheral symmetric synovitis with pit edema occurs in a small proportion of patients.


Aortic aneurysms occur in 10-20% of GCA patients. The thoracic aorta, especially the descending aorta, is frequently involved compared to the abdominal aorta.
A small proportion of patients may have aortic rupture and dissection, with or without aneurysms.
GCA may also affect the subclavian artery from distal to the vertebral artery dissection site, to axillary and proximal brachial arteries.
The upper extremity disease associated with GCA is not symmetrical, but is characteristically bilateral.
Stroke is rare. Ataxia, vertigo, dysarthria, etc. are rare.
Intracranial vessel involvement is very rareApproximately 10% of GCA patients have upper respiratory symptoms. A nonproductive cough is the most common symptom.
Macroglossia, lingual infarct, and scalp necrosis are rarely reported.
Pulses may be felt weakly and may be inconsistent blood pressure arterial measurements.
A murmur of aortic regurgitation should not be skipped because it may be a finding of a descending aortic aneurysm and its associated aortic valve dilatation.

Anemia can sometimes be profound and reactive thrombocytosis may also be present. Leukocytosis tends not to increase even in active disease.
Serum albumin can be slightly lowered and responds quickly to glucocorticoid therapy.
Liver enzymes, especially ALP, have increased slightly in 25-30% of patients. It returns to normal with glucocorticoid therapy.
ESR is typically elevated, and GCA is a disease that can exceed the ESR of 100. The CRP also generally increases proportionally. Neither is specific for GCA.

Increased concentrations of IL-6 appear to be closely related to the clinical activity of GCA. However, the clinical significance is unknown and is not present in routine practice.