Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe an 18-year-old white male who developed lower extremity ischemia requiring amputation. He presented at 14 with pulmonary infiltrates, hepatosplenomegaly, fever, rash, adenopathy, uveitis, and arthralgias; clinical and laboratory findings were consistent with Mycoplasma pneumoniae infection. Despite adequate treatment with antibiotics, he developed chronic arthralgias and fevers, with rash and pericardial effusion. Criteria for the diagnosis of systemic lupus erythematosus were not met; juvenile rheumatoid arthritis was diagnosed presumptively. Over the subsequent 4 years he developed lymphadenopathy with biopsy-proven nonnecrotizing granulomas, chronic leg ulceration with granulomatous histology, and acute-onset impending gangrene of the left foot. A biopsy of the posterior tibial artery demonstrated giant cell arteritis. Although the histologic features were consistent with Takayasu's arteritis, complete aortic arteriography was normal. Examination of the amputated leg showed multifocal segmental giant cell arteritis. Clinicopathologic features suggested, but were not fully consistent with, juvenile systemic granulomatosis. His disease may represent a separate sarcoid-like entity in the broad spectrum of vasculitis.
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PMID:Giant cell vasculitis with extravascular granulomas in an adolescent. 205 10

Stiffness of the jaw was noted in the first descriptions of temporal arteritis. It was only in 1944 that Horton used the term intermittent claudication and related this sign to effort ischemia due to thrombosis of facial arteries. The introduction of ultrasound techniques has enabled the permeability of facial arteries to be confirmed in spite of induration and absence of pulsatility clinically. Anatomical studies have defined the preponderant role of the internal maxillary artery in the vascular supply of the masseter muscles and have enabled the localization of an appropriate and reliable site for ultrasound study: the pterygo-maxillary fossa. The velocimetric data thus collected confirm that the internal maxillary artery is affected and define the etiopathogenesis of intermittent jaw claudication during temporal arteritis. This sign is observed on average in one patient in three suffering from temporal arteritis. While several cases of intermittent jaw claudication have been described in severe atheromatous stenosis of the common carotid or external carotid arteries, or in relation to other causes (rheumatological, neoplastic, psychological ...), the observation of this syndrome in a suspicious clinical and paraclinical context constitutes an excellent orientation sign in favor of temporal arteritis.
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PMID:[Intermittent claudication of the jaw in temporal arteritis]. 269 73

Ophthalmoplegia from ischemia to peripheral ocular motor nerves or muscles may complicate the course of giant cell arteritis (GCA). Although brainstem ischemia is known to occur in GCA, internuclear ophthalmoplegia has not been described. Two cases of biopsy-proven GCA are described in which internuclear ophthalmoplegia resulted from brainstem ischemia. Embolization from thrombosed extradural segments of inflammed vertebral arteries, or arteritis of brainstem perforating vessels may account for brainstem infarction. Rapid tapering of steroids was temporally related to brainstem infarction in both cases.
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PMID:Internuclear ophthalmoplegia in giant cell arteritis. 275 73

Tonic pupil is usually an idiopathic condition. In some cases, the cause of the ciliary ganglion lesion leading to tonic pupils is obvious. Rarely ischemia causes a lesion of the ciliary ganglion or the short ciliary nerves due to the good blood supply of the ciliary ganglion. Only two cases of tonic pupils in the course of giant cell arteritis are mentioned in the literature, but tonic pupils are probably much more common with this disease. Five cases are demonstrated here. All had associated ischemic optic neuropathy, and stagnation of the blood flow in the supratrochlear artery could be demonstrated in two cases by Doppler sonography. Tonic pupils may also occur when an oclusion of the internal carotid artery resolves, probably because of transient stasis of the orbital blood flow. In another case, tonic pupils were associated with choroidal ischemia (proved by video fluorescent angiography) of unknown origin. The diagnosis of tonic pupils was made by pharmacological testing for cholinergic hypersensitivity with 0.1% pilocarpine.
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PMID:[Tonic pupil caused by ischemia]. 279 12

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

Patients with severe ischemic symptoms that fail to respond to steroid therapy, despite a dramatic and continuous drop in the erythrocyte sedimentation rate, may require arterial bypass surgery to overcome arterial ischemia caused by arteritis. We report the case of a patient with bilateral subclavian artery occlusion secondary to giant cell arteritis who responded well to steroid therapy and arterial reconstructive surgery. The patient has remained well for five years.
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PMID:Arm ischemia secondary to giant cell arteritis. 322 72

Circulatory disturbances of the tongue are extremely rare because of its rich blood supply. Based on five case reports and a review of the literature we show that lingual circulatory disturbances may be due to impairment of venous drainage resulting in a large acute swelling of the tongue, or to ischemia carrying a painful tongue swelling, and possibly ulceration or partial tongue necrosis. The impairment of venous drainage appears to develop only as a consequence of an extensive posttraumatic or inflammatory edema of the floor of the mouth and tongue base. Ischemic lingual necrosis is most often due to giant cell arteritis and mostly occurs in elderly women. The correct diagnosis should be established as soon as possible because high-dose cortisone therapy both relieves the patient's complaints and prevents life-threatening complications such as myocardial infarction and apoplexy.
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PMID:[Acute circulatory disorders of the tongue]. 336 Jun 28

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 rarely presents as clinically advanced extra-ocular ischemia or gangrene. Clinically isolated leg involvement with amputation is even more unusual. A 69-year-old woman is described who had giant cell arteritis necessitating bilateral leg amputations. No other clinical sequelae have ensued during a four-year follow-up period. Temporal artery biopsy subsequent to the amputations revealed no arteritis. Disparities between the usual patterns of clinical and anatomic involvement in giant cell arteritis underlie the potential diagnostic difficulties in this disease. Although typically diagnostic, temporal artery biopsy does not always bridge the clinical and anatomic disparities.
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PMID:Giant cell arteritis of the legs. Clinical isolation of severe disease with gangrene and amputations. 376 4

A 78-year-old white woman had catastrophic visual loss in one eye due to temporal arteritis. Despite treatment with doses of oral corticosteroids high enough to normalize the Westergren erythrocyte sedimentation rate, she experienced progressive retinal ischemia with visual loss in the second eye. The use of 1,000 mg of pulsed intravenous methylprednisolone every 12 hours restored her vision. Brief hospitalization of patients with arteritic ischemic optic neuropathy for treatment with intravenous methylprednisolone may offer a significant chance of visual recovery of the involved eye and provide optimal protection to the uninvolved eye.
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PMID:Treatment of temporal arteritis with ocular involvement. 394 48


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