Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 61-year-old white woman, who had progressive arthritis over a two-year period, developed bilateral peripheral corneal degeneration. The superior cornea thinned to a thickness of approximately two thirds of normal. She died suddenly in the hospital and a primary occlusive vasculitis of the anterior ciliary arteries within the superior rectus muscles was found. There was necrotizing arteritis in the lungs, kidneys, adrenal caps, spleen, fallopian tubes, and skeletal muscle. The observation of an occlusive vasculitis of the anterior ciliary arteries in this patient supports the belief that ischemia may play a major role in peripheral marginal degeneration of the cornea.
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PMID:Peripheral corneal degeneration and occlusive vasculitis in Wegener's granulomatosis. 30 50

A case of acute posterior multifocal placoid pigment epitheliopathy is presented with the unusual feature of the exposure of deep choroidal vessels which filled with dye in the early phase of the fluorescein angiogram in the center of many of the placoid lesions. Visualization of these vessels with surrounding hypofluorescence implies nonperfusion of choriocapillaris presumably due to inflammation, rather than retinal pigment epithelial blockage. The pathology of acute posterior multifocal placoid pigment epitheliopathy is probably a vasculitis of the choriocapillaries, which causes transient occlusion of these vessels and the initial hypofluorescence in the typical lesions during angiography. In many lesions the ischemia is mild enough to cause only temporary disturbance of visual function with subsequent recovery. Only in the center of some of the lesions is the inflammation severe enough to allow for the findings observed in the case presented and to account for the permanent visual defects found in some patients.
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PMID:Evidence for vasculitis in acute posterior multifocal placoid pigment epitheliopathy. 45 51

Nine cases of microemboli of arterial origin to the upper extremity are reported. The source of emboli in five of these cases was in the subclavian artery compressed by osseous anomalies in the thoracic outlet. Three aneurysms, one in a subclavian vein graft and two traumatic false aneurysms in the hand, were also noted to be the sources of distal emboli. One unproved case of emboli from an atherosclerotic plaque of the subclavian artery is also reported. Chronicity of symptoms and delay in operation are often noted and lead to difficulties in surgical management. The compressing osseous structures causing the vascular lesion in the thoracic outlet syndrome must be resected, along with removal of the source of emboli. Cervicodorsal sympathectomy is often needed in cases of extensive thrombosis and/or long-standing ischemia. Embolectomy is usually a futile procedure when the main arterial trunk contains old, organized thrombus. Differential diagnostic problems between collagen vascular disease, vasculitis, vasospastic disease, and microembolic disease in cases of unilateral Raynaud's phenomenon are pointed out.
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PMID:Ischemia of the upper extremity due to noncardiac emboli. 56 Jan 30

From many observations made at autopsy it is apparent that thrombosis in a coronary artery is usually, if not always, associated with rupture of an atheromatous plaque. The sequelae of such rupture include hemorrhage into the plaque with further narrowing of the lumen, formation of an occlusive thrombus or of a non-occlusive thrombus. A developing thrombus in an artery undergoes fragmentation with showering of the distal microcirculation by aggregates of platelets possibly with some admixture of fibrin. In many cases of sudden cardiac death associated with severe atherosclerotic stenosis of the coronary vessels, an occlusive thrombus is not found and the myocardium shows no morphological lesion or else focal patchy early damage in the subendocardial region. One possible mechanism that might explain these findings is microembolism from mural nonobstructing coronary thrombus. Such a mechanism is well established in transient ischemia of the brain and retina related to ulcerated atheroma of the internal carotid artery. Experimental observations indicate that platelet aggregates in the myocardial circulation cause arrhythmias, sudden death, vasculitis, and myocardial ischemic damage. Induction of an occlusive coronary artery thrombus is associated with development of an infarct involving the full thickness of the myocardium. A nonocclusive thrombus is associated with either no myocardial damage or focal subendocardial ischemic injury. It is possible that further aggregation of platelets may facilitate the extension of infarction subsequent to an occlusive event, although there is little evidence on this point. A number of clinical studies show increased platelet reactivity to agents causing aggregation, such as norepinephrine or collagen, in subjects experiencing thromboembolic episodes. It seems unlikely, however, that in vitro tests of platelet function can identify or predict clinical arterial thrombotic disease, although studies of platelet survival and turnover may be more helpful. There is also evidence that platelet survival may be prolonged by drugs having a therapeutic benefit in coronary artery disease and arterial thromboembolism. There is a need for better designed and coordinated clinical trials and for better experimental approaches to explore the relationships among coronary thrombosis, embolsim of the myocardial microcirculation, myocardial ischemia, and sudden death.
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PMID:Platelet aggregation secondary to coronary obstruction. 76 18

Ten patients presenting with a history of the acute onset of hand ischemia have undergone detailed clinical, immunologic, and arteriographic evaluation. The disease is characterized by the acute onset of hand ischemia proceeding to fingertip ulceration, in the absence of recognized systemic disease. None of the patients had any evidence of large artery obstruction. Arteriography showed diffuse obstruction of the palmar and digital arteries. No evidence was found in any patient of any systemic disease process associated with small artery obstruction. These patients are suspected of having a previously unreported variant of hypersensitivity angiitis. Patients are left with permanent obstruction of the palmar and digital arteries. Follow-up suggests the disease in non-recurrent and is characterized by progessive clinical improvement associated with the development of collateral circulation. Conservative management of the condition is recommended.
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PMID:Rapid onset of hand ischemia of unknown etiology: clinical evaluation and follow-up of ten patients. 88 62

An acute intestinal disorder occurred in seven patients soon after renal transplantation. The disorder was characterized initially by massive abdominal distention with progression to multiple bowel perforations in three patients and extensive bowel necrosis in two. Surgical manipulation did not appear to be the cause since the transplants were performed retroperitoneally in the iliac fossa. Ischemia also was not a factor since the mesenteric vessels were patent with no evidence of thrombus formation or vasculitis. The cause appeared to be related to immunosuppressive agents, in particular, high doses of corticosteroids. The disease process appeared to be reversible if immunosuppression was discontinued early, as occurred in two patients.
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PMID:Intestinal necrosis and perforation after renal transplantation. 109 Feb 85

The natural course of Branch Retinal Vein Occlusion is determined by the site and completeness of the occlusion, the integrity of arterial perfusion to the affected sector and the efficiency of the developing collateral circulation. Most patients with tributary vein occlusion have some capillary fall out and microvascular incompetence in the distribution of the affected retina and vision is significantly compromised in over 50% of patients who have either chronic macular oedema or ischemia involving the perifoveolar arcades. Retinal and capillary vasoproliferation with or without intraretinal or preretinal membrane formation are common sequelae, where inner retinal ischemia is extensive and vitreous hemorrhage is often a distinct threat to vision. Treatment of the sequelae of vein occlusion are largely centered on laser photocoagulation to diseased retina to limit fluid accumulation and abolish preretinal and papillary neovascularization. Vitrectomy and retinal detachment procedures are occasionally required in patients with uncontrolled vitreous hemorrhage and retinal membrane formation which threatens the integrity of the macula. A small proportion of patients with vein occlusion subsequent to vasculitis require medical therapy.
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PMID:Branch retinal vein occlusion and its management. 128 82

We examined 8 cases of allergic granulomatous angiitis (AGA). All cases showed peripheral nerve lesion, comprising damage of all myelinated fibers, which was more severe in larger ones. Immunofluorescent deposits of IgE were detected in the peripheral myelin. There was lymphocyte infiltration both around the endoneural capillaries and in the endoneurium, and an increase of endothelial cells. Nerve ischemia due to obstruction of the vasa nervorum, circulation insufficiency of the small vessels, or immunological abnormality through IgE may play a pathogenetic role in the peripheral neuropathy of AGA.
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PMID:Allergic granulomatous angiitis and peripheral nerve lesion. 133 6

Takayasu Arteritis is a vasculitis of the giant cell type which affects young people. Complications of this disease can include myocardial infarction, stroke, limb loss, renal failure, and mesenteric ischemia. A case study demonstrates some of the complexities of diagnosis and treatment for this condition. Nursing care should be directed toward the alteration in tissue perfusion, prevention of infection in a patient on immunosuppressive therapy, and a variety of potential problems with coping.
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PMID:Takayasu arteritis. 134 36

A 73-year-old Japanese man with a history of partial gastrectomy due to gastric cancer 4 years previously was admitted because of intermittent fever. The patient developed abdominal pain, erythema, and myalgia in addition to the fever during the final clinical course, and died of acute heart failure. Autopsy disclosed atrophy of the left lobe of the liver and acute myocardial infarction. Neither metastasis nor recurrence of the cancer was observed. Small- and medium-sized arteries of the visceral organs showed various stages of necrotizing vasculitis with narrowing of the lumina. The vasculitis was most prominent in the left lobe of the liver and in the heart. Narrowing of the portal vein due to portal tract inflammation in addition to vasculitis of the hepatic arteries may have induced ischemia and infarction, which had resulted in atrophy of the left hepatic lobe.
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PMID:Polyarteritis nodosa with atrophy of the left hepatic lobe. 136 33


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