Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

This paper contains a review of the signs and symptoms of giant cell arteritis, especially speech and respiratory manifestations of the disease, which are demonstrated by a new case history. An elderly woman presented with speech that was falsetto, breathy, and marked by downward pitch breaks and phonation breaks. In addition, she had visual loss, headache, edema along the scalp and pharyngeal arteries, polymyalgia rheumatica, elevation of Westergren erythrocyte sedimentation rates, and positive arterial biopsy results. Her speech disorder recurred during an exacerbation. A vascular mechanism is proposed to explain her unusual speech, acute recurrence, and rapid recovery. This explanation (reversible ischemia of the laryngeal musculature) has been proposed by other authors in previous studies.
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PMID:Speech pathology in giant cell arteritis. Review and case report. 281 76

On 91 patients with temporal arteritis (TA) and/or polymyalgia rheumatica (PMR), we observed 7 females aged 62 to 73 years with upper extremities ischemia. Arm claudication and/or Raynaud's phenomenon were the initial manifestations of the disease in 2 cases, or appeared simultaneously with other symptoms in 2 cases, or complicated decreasing corticosteroid therapy in 3 cases. A temporal artery biopsy was performed on 6 patients with, in all of them, typical giant cell granulomatous arteritis pathology findings. Angiograms showed, in all cases, multiple bilateral smooth stenosis and/or obliterations of post vertebral subclavian arteries and/or axillary arteries. Symptoms always improved on corticosteroid treatment and no patient needed reconstructive surgery. In conclusion, large arteries involvement, which can occur in TA and/or PMR, affect in our experience most commonly the subclavian and axillary arteries, with female predominance as found in Takayasu's arteries. These disorders should be considered in cases of occlusive disease of the arms in elderly women and the response to steroids is usually adequate to eliminate the need for early surgical intervention. Early recognition of asymptomatic large artery involvement by Doppler evaluation, in all TA and/or PMR patients, and transient anticoagulant therapy might prevent vessels occlusions.
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PMID:[Involvement of arterial trunks of the upper limbs in giant cell arteritis. Apropos of 7 cases]. 361 48

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common diseases in the elderly. The arteritis usually affects medium sized vessels, but large vessel involvement can also occur leading to arm claudication, bruits, loss of pulses and pallor of the upper extremities. The differential diagnosis of large vessel arteritis includes atherosclerosis and Takayasu's disease. Atherosclerosis, which affects patients of similar age to GCA is usually confined to the lower limbs and can be differentiated on the basis of the clinical setting and investigations such as the ESR, arteriography and temporal artery biopsy. Takayasu's arteritis' although histologically and arteriographically indistinguishable from GCA, is predominantly a disease of young women. A patient is described who presented with upper limb ischemia. A clinical examination revealed absence of right radial pulses and presence of murmurs at level of the carotids. The blood pressure was unrecordable in the upper right limb. The ESR was 102 mm/hr and the C-reactive protein was 11.66 mg/dl. A selective arteriography of the aortic arch and its branches revealed a right subclavian artery obstruction with good collateral circulation and a left subclavian artery stenosis. The biopsy of left temporal artery showed a typical GCA in acute stage. Treatment with prednisolone 30 mg/day was started and four weeks later, the ESR had fallen to normal. In addition this case confirms that PMR implies a systemic arteritis.
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PMID:[Giant cell arteritis and polymyalgia rheumatica presenting as subclavian artery obstruction]. 823 15

Three patients with visual loss and normal fundi were discovered to have choroidal ischemia on fluorescein angiography. Each patient had a markedly increased Westergren erythrocyte sedimentation rate, but only one described symptoms of polymyalgia rheumatica, neck pain, and jaw claudication. Biopsy of the temporal artery confirmed giant cell arteritis in the two patients without constitutional symptoms. In one patient, typical anterior ischemic optic neuropathy developed the following day, whereas in the other two, anterior ischemic optic neuropathy later occurred despite the prompt administration of intravenous high-dose corticosteroids. Choroidal ischemia may be the first sign of giant cell arteritis in elderly patients with visual loss. Early diagnosis and treatment are mandatory in an attempt to forestall the development of anterior or posterior ischemic optic neuropathy, or central retinal artery occlusion in the affected or fellow eye.
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PMID:Visual loss caused by choroidal ischemia preceding anterior ischemic optic neuropathy in giant cell arteritis. 829 97

The authors report the case of a woman aged 67 years who presented an acute ischemia of the lower limbs. A surgical exploration showed no atherosclerosis or thrombus. A biopsy of the femoral artery found an extensive mononuclear cell infiltration of the media and a fragmentation of internal elastic lamina. The diagnosis of Horton disease was considered and confirmed by the presence of clinical signs of polymyalgia rheumatica and inflammatory syndrome (erythrocyte sedimentation rate: 75 mm). Corticosteroid therapy was started with success. A year after discharge there was no recurrence of ischemic manifestations and the erythrocyte sedimentation rate was normal. Involvement of lower limbs in Horton disease is rare and exceptionally proven. But postmortem studies indicate that it is more frequent than previously reported. The diagnosis should be considered in the differential diagnosis of any unexplained case of peripheral vascular disease occurring in the middle-aged or elderly.
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PMID:[Horton disease disclosed by a specific inflammatory arteriopathy of the lower limbs]. 936 38

Molecular studies of giant cell arteritis indicate that T cells are recruited to the wall of medium-sized and large arteries, are activated locally, produce IL-2 and IFN-gamma, and regulate the activity of tissue-infiltrating macrophages. Downstream effects of T cell activation include the production of proinflammatory cytokines, metalloproteinases, and growth factors. Growth factors are instrumental in the process of intimal hyperplasia, leading to luminal occlusion and tissue ischemia. The amounts of IL-2, IFN-gamma, and the growth factor PDGF in the vascular lesions varies among patients and are correlated with differences in patterns of clinical manifestations. Giant cell arteritis complicated by cranial ischemia, such as anterior optic neuropathy or stroke, is characterized by high levels of IFN-gamma and PDGF. If the IFN-gamma-PDGF loop is less developed, fever and wasting can dominate the disease. Dominant production of IL-2 is associated with polymyalgia rheumatica. The finding of different inflammatory pathways translating into different clinical phenotypes may reflect differences in the contribution of the arterial wall. Alternative hypotheses include a role of multiple disease-inducing antigens with different tissue distributions or tropisms.
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PMID:Giant cell arteritis--a molecular approach to the multiple facets of the syndrome. 992 95

Systemic vasculitis occurs in a heterogeneous group of primary disorders or can be a manifestation of infection, an adverse drug reaction, malignancy or a connective tissue disease. A vasculitic process should be suspected in patients with unexplained ischemia or multiple organ involvement, especially when such features as polymyalgia rheumatica, inflammatory arthritis, palpable purpura, glomerulonephritis or multiple mononeuropathy are also present. The clinical features of systemic vasculitis depend on the organs involved and, in turn, organ involvement is largely influenced by the size of the affected blood vessels. The diagnostic work-up should be tailored to the clinical situation and geared toward a tissue or angiographic diagnosis, bearing in mind that the findings from these studies are not always pathognomonic. Emphasis should also be placed on exclusion of a secondary process. The diagnosis of the specific type of vasculitis may be made on the basis of the clinical features and the histopathologic or angiographic findings. Initial therapy for most types of systemic vasculitis consists of high-dose corticosteroids, with the addition of immunosuppressive therapy in certain patients.
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PMID:An approach to diagnosis and initial management of systemic vasculitis. 1052 86

Diagnosis and management of giant cell (temporal) arteritis (GCA) should be performed by physicians who can accurately monitor the ophthalmologic, neurologic, and systemic sequelae of the disease as well as the numerous side effects of systemic corticosteroids, which are typically necessary for treatment. When the diagnosis of giant cell arteritis is seriously entertained, early treatment with adequate doses of oral or intravenous corticosteroids should not be delayed until laboratory confirmation has been obtained. Unilateral or bilateral temporal artery biopsy should be performed on all patients with suspected GCA. A positive biopsy result mandates that higher doses of corticosteroids be used during the first 2 months, which comprise the critical period for risk of new ocular ischemia. A definitive, biopsy-proven diagnosis requires at least 6 months, and typically 12 months, of corticosteroid therapy. Common pitfalls include increasing the dose and prolonging the use of corticosteroids in response to increases in the erythrocyte sedimentation rate (ESR) unrelated to GCA or visual blurring that may be related to benign tear film abnormalities, corticosteroid-induced lens changes, and other ophthalmic conditions. The muscle stiffness of polymyalgia rheumatica (PMR) must be distinguished from the osteoarthritis and other painful conditions common in the elderly. After corticosteroid therapy has begun, continuing ophthalmologic evaluation is necessary to evaluate the effectiveness of treatment and whether ocular complications, such as glaucoma or cataract, develop. Careful attention must be given to early detection and prevention of systemic side effects of corticosteroid treatment. Patients may be given gastrointestinal protective agents, such as histamine (H(2))-blocking agents; vitamin D and calcium; oral hypoglycemic agents; and, if necessary, insulin and antihypertensive drugs. If bone density measurements warrant, hormones/supplementation to prevent or reverse osteoporosis may be prescribed. After the initial diagnosis and first 4 weeks of treatment, elevation of the ESR or C-reactive protein alone should generally not be used as signs of disease activity nor as a reason to increase the daily dose of steroids. If symptoms or signs of disease activity occur, the dose should be raised regardless of test results. Even with vigorous physician-patient education, however, a patient is occasionally unable to provide adequate historical information about response to therapy, and the physician is forced to rely on laboratory values as a measure of disease activity. After initial high-dose corticosteroid therapy, patients without a classic history and with negative biopsy results will generally receive a rapid taper to low doses of corticosteroids. The role of repeated temporal artery biopsy in the clinical management of GCA is unclear. Despite persistence of PMR and, in some cases, histologic evidence of inflammation in temporal arteries, patients do not frequently have recurrence of symptomatic GCA after 6 months or more of corticosteroid therapy. Under these circumstances, late vision loss is rare.
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PMID:Giant Cell Arteritis. 1109 95

Giant cell arteritis is a vasculitis of large and medium size arteries, especially those of the aortic arch with an extracranial distribution, but also the aorta and some of its larger branches. It is characterised by the presence of mononuclear inflammatory infiltrates close to the internal elastic lamina formed by lymphocytes and macrophages, which in slightly more than 50% of the cases contain multinucleate giant cells. The morbidity associated with this disease is related to phenomena of distal ischemia to the luminal stenosis of the inflamed arteries, and to a lesser extent to the formation of aneurisms due to the weakening of the arterial wall. With an unknown aetiology, its pathogenesis is immune through the migration and location of gamma-INF -producing T cells in the adventitia of the inflamed arteries, it being assumed that this is the place of immune stimulation by a still unidentified antigen. The recruitment and activation of macrophages by this cytokine is one of the most important points of its pathogenesis. The destruction by these of the arterial elastic tissue is a relevant phenomenon, as is the production of other factors promoting neoangiogenesis and a proliferation of neointime, responsible through obliterating light for the ischemic manifestations of the disease. The process is accompanied by an important systemic repercussion characterised by a strong reaction of acute phase and general but barely specific symptoms of disease. On the other hand, an important percentage of patients show a clinical picture of polymyalgia rheumatica, an entity that has a historical and controversial relationship to this arteritis. In recent years important contributions have been made to the understanding of the immune mechanisms involved in its pathogenesis.
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PMID:[Etiopathogenesis of giant cell arteritis]. 1275 11


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