Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 248 patients with giant cell arteritis, 34 had evidence that the disease affected the aorta or its major branches. Symptoms suggestive of large artery involvement were intermittent claudication of an extremity, paresthesias, and Raynaud's phenomenon. Physical findings included absent or decreased large artery pulses and bruits over large arteries. Four patients presented with decreased upper extremity pulses as the initial manifestation of their arteritis. Nine other patients under treatment for temporal arteritis or polymyalgia rheumatica first developed evidence of large artery involvement as corticosteroid therapy was tapered or discontinued. Angiography, performed in 10 patients, was helpful in indicating arteritis rather than atherosclerosis as the cause of large artery disease. Three patients died with aortic rupture, and, at autopsy, widespread giant cell arteritis was found. However, when corticosteroids were given in adequate doses, the response was favorable in most patients; intermittent claudication decreased and the pulses improved.
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PMID:Large artery involvement in giant cell (temporal) arteritis. 120 May 25

Solar radiation provokes a lifelong series of destructive changes in the supporting elastic tissues of "exposed" skin. Called actinic elastosis/lysis (or actinic "aging"), the sequence begins in early life as simple elastic hyperplasia, converts in middle life to progressive actinic elastotic degeneration, and, in late life, typically ends with a stage of resorption (elastolysis) and atrophy ("aged" skin). Superficial "exposed" arteries such as the temporal artery participate in the same sequence of degenerative elastotic changes, which, as in the skin, may provoke granulomatous responses in a few of the many subjects affected. In the case of the temporal artery, a contingent outcome may be giant cell (temporal) arteritis and its recognized systemic vascular expression, polymyalgia rheumatica. Actinic commotion at the surface of the body is often massive in degree and extent and may be expected to exert a deleterious autoimmune impact on the essential elastic tissues of the arterial system. For this reason, solar radiation should be recognized as a risk factor for other elastic-related vascular diseases, including atherosclerosis and aneurysms. Man-made radiations may be exacerbating the effects of predominant solar radiation. Of the many radiant bands that make up the actinic (electromagnetic) spectrum, little is known for certain about the identity of those that cause these prevalent disorders of elastic tissue. Until this void is filled, more care should be taken with solar and the other "safe" radiations.
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PMID:A study of elastic tissue and actinic radiation in "aging," temporal arteritis, polymyalgia rheumatica, and atherosclerosis. The actinic storm in the modern world. 186 51

Destruction (elastolysis) of the internal elastic lamina is frequently observed near early atherosclerotic plaques. Elastolysis and plaque formation are also found together in the temporal arteritis/polymyalgia rheumatica syndrome. Could it be that atherosclerosis and the syndrome are more closely akin than usually thought, with elastolysis acting as the pathogenetic link between them? A kinship of this nature is in accord with the growing recognition that elastin-related autoimmunity prevails in both these forms of vascular disease. A case can also be made out for the belief that the autoimmune reactions in internal vessels may be provoked by events in the integument where a slow but ultimately massive turnover of dermal and vascular elastic tissue takes place under the harmful influence of solar and other forms of actinic radiation.
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PMID:Destruction of elastic tissue (elastolysis) as a link between atherosclerosis and the temporal arteritis/polymyalgia rheumatica syndrome. Observations on an actinic factor in vascular disease. 636 8

We utilized a standardized in vitro method which employs transmission electron microscopy to monitor the degree of surface activation (cytoplasmic spreading) and amount of aggregation displayed by platelet populations from 314 patients with one of five distinct rheumatic diseases and from 72 normal subjects. The percentage of patients in each group whose platelet populations were hyperactive was as follows: polymyalgia rheumatica, 75 percent; scleroderma, 65 percent; primary gout, 61 percent; rheumatoid arthritis, 57 percent; and degenerative joint disease, 40 percent. Pair-wise contrasts performed after an analysis of variance suggest the following differences and similarities: (1) the mean differential platelet count of the normal subjects differed from that in each disease state; (2) the platelet responsivity in patients with degenerative joint disease most closely resembled that in normal subjects; (3) the platelet response in polymyalgia rheumatica plus temporal arteritis was the most abnormal; and (4) platelet response in scleroderma, rheumatoid arthritis, and gout closely resembled each other. The increased platelet response in vitro may reflect the in vivo presence of disease-related "risk factors" (hyperuricemia, immune complexes, and atherosclerosis). Those patients with "triggered" platelet populations may be appropriate candidates for antiplatelet therapy.
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PMID:A comparative study of platelet reactivity in arthritis. 694 59

We have reviewed the clinical records and histology of 135 patients who underwent temporal artery biopsy between 1973 and 1978. Biopsies were classified histologically as giant-cell arteritis (17%), atypical arteritis (6%), healed arteritis (2%), arteriosclerosis (67%), atherosclerosis (5%), or normal (3%). Most of the histological diagnoses made at the time of biopsy were confirmed but eight cases which had originally been reported as atypical or healed arteritis were classified as arteriosclerosis when reviewed. All 33 patients with histological evidence of arteritis were accepted as clinical cases of temporal arteritis (31) or polymyalgia rheumatica (2) and treated with steroids. A further 24 patients had negative biopsies (arteriosclerosis or atherosclerosis) but were considered on clinical grounds to have cranial arteritis. They too were treated and made a full recovery. In 43 cases, all of whom had negative biopsies, a final diagnosis was reached which was thought to account for the clinical symptoms (e.g., cerebrovascular accident, rheumatoid disease, migraine, etc.). As less than 60% of patients with clinical temporal arteritis had positive biopsies, we suggest that this procedure could be omitted and replaced by a trial of steroid therapy. Biopsy should be reserved for patients with a strong medical contraindication to steroid therapy, or who fail to respond to treatment promptly.
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PMID:Temporal artery biopsy in giant-cell arteritis. A reappraisal. 727 Jul 80

This study of cutaneous elastic tissue and serum fluorescence supports the hypothesis that widespread destruction and resorption of elastic tissue (elastolysis) occurs in the temporal arteritis/polymyalgia rheumatica syndrome. A systemic elastolysis of this nature may be provoked by actinic (radiant) damage to the "exposed" elastic tissues in the skin and superficial arteries, the archetype of such injury being seen in temporal arteritis. Scattered giant cells are the usual agents of elastolysis but tuberculoid ("sarcoid") infiltrates often take over in the later stages. In acute polymyalgia, the phenomenon probably becomes diffuse and humoral. Elastolysis may be a direct pathogenetic link between polymyalgia and other vascular diseases such as idiopathic aneurysm and atherosclerosis.
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PMID:The role of actinically provoked systemic elastolysis in polymyalgic vascular disease. A study based on serum fluorescence and haptoglobin. 732 40

Giant cell arteritis (GCA) is closely identified with the temporal arteritis-polymyalgia rheumatica syndrome of the elderly. It is also a systemic disease that can cripple and kill. Up to 15% of patients with temporal arteritis may have angiographic evidence of extracranial GCA, and aortic insufficiency, ruptured aortic aneurysm, aortic dissection, stroke, or myocardial infarction may be the initial manifestation of systemic GCA. A review of 72 cases of aortic and extracranial GCA, all with histopathologic verification of the disease, revealed that 25% of patients with aortic and extracranial large-vessel GCA had asymptomatic temporal arteritis; the ascending aorta and aortic arch were most frequently involved (39%), followed by the subclavian and axillary arteries (26%), and the femoropopliteal arteries (18%). Nine patients (12.5%) underwent an upper or lower limb amputation. Of the 18 patients whose death was directly attributable to extracranial GCA the causes were ruptured aortic aneurysm (6), aortic dissection (6), stroke (3), and myocardial infarction (3). The findings of these 72 cases caution against attributing all aortic and large-vessel arterial disease in the elderly to atherosclerosis and emphasize that timely surgical intervention may be necessary for life-saving and limb-salvage in patients with aortic and extracranial GCA.
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PMID:Aortic and extracranial large vessel giant cell arteritis: a review of 72 cases with histopathologic documentation. 766 46

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

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

We examined the usefulness of color duplex ultrasonography in patients suspected of having temporal arteritis. Five patients, who were all aged 70 or older, developed a new onset of localized headache with temporal artery abnormalities, and had an elevated erythrocyte sedimentation rate of > 100 mm/hour. The final diagnoses were temporal arteritis in three patients, polymyalgia rheumatica in one, and probable healed temporal arteritis in one. Color duplex ultrasonography showed stenoses, which were confirmed histologically as well, in the superficial temporal artery of all patients. The characteristic findings of active temporal arteritis were, however, demonstrated in only three biopsy specimens, and in the remaining two the stenoses were thought to be related to previous arteritis. The hypoechoic halo, which has been reported to be a characteristic finding of color duplex ultrasonography in active temporal arteritis, was detected in only one patient with active temporal arteritis and another one with probable healed temporal arteritis. No stenoses were demonstrated in the superficial temporal arteries of 30 control subjects (20 with at least one risk factor of atherosclerosis and 10 without it). Color duplex ultrasonography can therefore be considered a powerful method for detecting stenoses in the superficial temporal artery. Its ability to identify their etiology is, however, unsatisfactory, so that temporal artery biopsy remains undoubtedly the most reliable test for etiological evaluation. We thus recommend color duplex ultrasonography as a supplementary method for the diagnosis of temporal arteritis, because it can provide useful information concerning the appropriate site of temporal artery biopsy.
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PMID:[The significance of color duplex ultrasonography for the diagnosis of temporal arteritis]. 1065 58


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