Giant cell arthritis

Giant cell arthritis

This entity was first described by Hutchinson in 1890. Horton was in 1930 when histology revealed granulomatous arthritis of temporal vessels. And 20 years later postulated the relationship between temporal arthritis and polymyalgia rheumatica (in fact many authors consider to be two different phases of the same disease)

We define temporal arthritis, also called giant cell arthritis(GCA) or Horton as a chronic systemic vasculitis of large vessels and medium caliber. That is, is characterized by chronic inflammation of large blood vessels. Although potentially can affect all vessels, usually affecting cranial branches of arteries originating from the aortic arch.

It usually affects older than 50 years (with a peak age between 70 and 80 years) and predominantly in women. Mortality is similar to that of the general population of the same sex and age.

Giant cell arthritis
Horton disease
Granulomatous Arthritis
Cranial Arthritis
Temporal arthritis

There are diagnostic criteria formulated by the American College of Rheumatology in 1990. By these criteria, is diagnosed when a patient presents at least 3 of the 5 criteria set. These criteria are:

1) development of symptoms after 50 years.
2) Debut or appearance of a new type of headache location.
3) Changes in the temporal artery such as a decrease in pulse palpation of the artery (due to arteriosclerosis of cervical arteries.
4) glomerular sedimentation rate and # 8805, 50 per hour, and
5) Changes in temporal artery biopsy.

We recommend biopsy of the temporal artery in all patients with suspected GCA. Inflammation of the arteries is usually discontinuous at a biopsy is needed about 3-5 cm, and if this is normal should consider performing a contralateral biopsy. When possible, it should be biopsied before starting treatment.

Causes

Probably the GCA is a polygenic disease in which involve multiple genetic and environmental factors. Several of these factors discussed but not confirmed are: high latitudes, viral causes such as parainfluenza type 1 virus, Mycoplasma pneumoniae, Chlamydia pneumoniae, parvovirus B19, associations with HLA complement genes, and so on.

Clinical Manifestations

The onset of this disease is usually gradual, but can be abrupt. The most common symptom (in 2 / 3) is a frontotemporal headache (although it can affect the occipital area) intense, non-pulsatile, irradiated jaw and may be associated with scalp tenderness, fever, constitutional syndrome (asthenia, anorexia and weight loss), jaw claudication (40%), polymyalgia rheumatica (50%) and optic neuritis (which can cause blindness).

Jaw claudication occurs in about half of patients with GCA. Occasionally, they may have claudication of the muscles of the tongue and those involved in swallowing.

One of the major symptoms is the partial or complete loss of vision. Occurs in 20% of patients and is often an early manifestation of the disease. Patients typically describe it as “a shadow that covers one eye,” which progresses to total blindness. If untreated, the other eye is affected in one or two weeks. Once established, the visual deficit is usually permanent. Amaurosis fugax (transient loss of vision) is an important visual symptom that precedes visual loss by 44%. Double vision and visual hallucinations are less frequent. The loss of vision due to optic nerve ischemia as a result of arthritis and ophthalmic branch arteries and less commonly filiares later by occlusion of the arterioles.

Other symptoms include neurological manifestations (30%) and less frequently neuropathies and transient ischemic attacks or stroke in the territory of the carotid or vertebrobasilar, alterations in the respiratory tract manifestations in the musculoskeletal system, there may be surrender of arms involvement of the aortic arch branches.

Special mention thoracic aortic aneurysms. This is a late complication, usually several years after diagnosis. The aneurysm may rupture causing death. An annual radiographic screening is suitable for screening of thoracic aortic aneurysm.

Treatment

Corticosteroids are the treatment of choice for ACG. In patients with recent vision loss can be treated with an intravenous bolus of methylprednisolone. Corticosteroids may prevent but usually do not reverse vision loss.

The response to corticosteroids is rapid, with resolution of symptoms within a few days of treatment. If not, we must question the diagnosis. Also, about 30-50% of patients suffer exacerbations of the disease, especially during the first 2 years, regardless of steroid regime.

The evolution of symptoms, ESR or CRP are usually the parameters used for monitoring patients

Corticosteroid treatment is not without adverse effects. Thus, the observed increase in diabetes and osteoporotic fractures (so you should take calcium and vitamin D). Some studies have postulated the use of methotrexate to reduce the dose of corticosteroids in patients requiring high doses to control the activity of the disease and suffer serious adverse effects.

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