Giant cell arteritis

Giant cell arteritis: Description, Causes and Risk Factors:ICD-10: M31.6.Abbreviation: GCA.Alternative Name: Temporal arteritis, cranial arteritis, extracranial arteritis, granulomatous arteritis, Horton arteritis.Giant cell arteritisGiant cell arteritis is a systemic inflammatory vasculitis that affects medium-sized to large arteries. Arterial wall inflammation leads to luminal occlusion and tissue ischemia, which cause the clinical manifestations of this vasculitis. Susceptible sites include: the vascular bed of the cranial nerves, optic nerve, masseter muscles, and the posterior circulation of the central nervous system. Involvement can extend to the aorta and its primary and secondary branches, including the subclavian and axillary arteries, which leads to upper-extremity ischemia.Giant cell arteritis is more frequent among people of Scandinavian and Northern European descent, irrespective of their place of residence. Women affected at least twice as often as men. Its overall incidence is 15 to 25 per 100000/year in individuals over the age of 50 years.While the exact etiology of GCA is unknown, a variety of infectious agents have been suggested as potential immune triggers for the disease, including herpes virus, parainfluenza virus, cytomegalovirus, parvovirus B19, chlamydia and mycoplasma. There is little doubt that immune-mediated processes factor in the pathogenesis of GCA, and both the adaptive and innate immune systems have been implicated.Current theory regarding the etiology of giant cell arteritis holds that a maladaptive response to endothelial injury leads to an inappropriate activation of cell-mediated immunity via immature antigen-presenting cells. The subsequent release of cytokines within the arterial vessel wall can attract macrophages and multinucleated giant cells, which gives diseased vessels their characteristic histology. This also leads to an oligoclonal expansion of T-cells directed against antigens in or near the elastic lamina. Ultimately, this cascade results in vessel wall damage, intimal hyperplasia, and eventual stenotic occlusion.Some studies have found an association with HLA-DR4 haplotype and 60% of patients express the B1*0401 or B1*0404/8 variant of the HLA-DR4 haplotype. These alleles appear to be a strong risk factor for disease and a marker for steroid resistance in some populations. The intercellular adhesion molecule 1 (ICAM-1) genes may also predispose to GCA. ICAM-1 is strongly expressed in the inflammatory infiltrate of the temporal artery in GCA and G/R 241 polymorphisms in the ICAM-1 gene are associated with GCA susceptibility.Symptoms:Symptoms may include:Excessive sweating.
  • General ill feeling.
  • Fever.
  • Jaw pain, intermittent or when chewing.
  • Loss of appetite.
  • Muscle aches.
  • Throbbing headache on one side of the head or the back of the head.
  • Scalp sensitivity, tenderness when touching the scalp.
  • Blurred, double, and reduced vision.
  • Fatigue.
Additional symptoms may include:Bleeding gums.
  • Face pain.
  • Hearing loss.
  • Joint stiffness.
  • Joint pain.
  • Mouth sores.
Diagnosis:The doctor will examine your head. Touching the head may show that the scalp is sensitive and has a tender, thick artery on one side. The affected artery may have a weak pulse or no pulse.There is no single clinical symptom, sign or laboratory test specificfor GCA.General tests may include:Hemoglobin or hematocrit -- may be normal or low.
  • Liver function tests -- may be abnormal with high levels of alkaline phosphatase.
  • Sedimentation rate and C-reactive protein -- almost always very high.
  • Blood tests cannot specifically diagnose this condition. A biopsy and examination of tissue from the affected artery confirm the diagnosis in most cases.
Several imaging tests may be used in the diagnosis of giant cell arteritis. These include:Ultrasound: Imaging using high-frequency sound waves. This may help to detect swelling of temporal arteritis. Doppler ultrasound may be used to detect narrowing and decreased blood flow of the arteries in the head.
  • Cerebral angiography: A form of minimally invasive x-ray where a flexible tube (catheter) is inserted into an artery and threaded into the cerebral arteries in the brain. A contrast medium is injected and x-rays are taken as the medium fills the arteries. This reveals arterial blood flow and may be used to detect reductions in that flow.
  • CAT scan (computed axial tomography) or MRI (magnetic resonance imaging): This may detect involvement of large arteries. These tests also have the capacity to follow changes in the thickness of arterial walls that cannot otherwise be detected.
Treatment:The goal of treatment is to reduce tissue damage that may occur because of lack of blood flow. Your doctor may prescribe corticosteroids to reduce inflammation. Corticosteroid treatment may be started even before a biopsy confirms the diagnosis. Aspirin may also be recommended. Medications that suppress the immune system are occasionally prescribed.Consultations: 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.A rheumatologist or internist should direct follow-up care for these patients, monitor remissions and recurrence, and manage complications associated with long-term corticosteroid therapy.Exercise plays very important role in treatment of giant cell arteritis. Exercise not only relieves stiffness, pains and fatigue but also improves bone and muscle strength. So everyone should create exercise schedule. It is important for a person with giant cell arteritis to remove stress-inducing events from his life because stress can aggravate arthritis.NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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