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.
INVOLVEMENT OF GREAT BLOOD
VESSELS İN GCA
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.
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