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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Temporal artery biopsy specimens from 26 patients of various ages with and without giant cell arteritis afforded an opportunity to examine several ultrastructural features of these human muscular arteries, including senescent and atherosclerotic alterations and the fine structural pathology of temporal arteritis. The unusual pathologic features of temporal arteritis were found superimposed on the progressive accumulation of smooth muscle cells, collagen and occasional discrete intimal atherosclerotic plaques in the intima of aging arteries. Two features of giant cell arteritis were conspicuous: first, the accumulation of large numbers of histiocytes and epitheloid and giant cells at the intimal-medial junction and second, fragmentation, degeneration and dissolution of the internal elastic lamina. The close proximity of the granulomatous reaction to the degenerating lamina suggests that these two aspects of the pathologic picture are in some way related, and possible immunologic mechanisms of this relationship are discussed on the basis of the ultrastructural findings.
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PMID:Light and electron microscopic studies on human temporal arteries with special reference to alterations related to senescence, atherosclerosis and giant cell arteritis. 16 78

Thirty consecutive patients with severe scleritis or episcleritis were admitted as in-patients to the Medical Ophthalmology Unit and assessed for systemic disease. There were seventeen women and thirteen men. The mean age was 53 with a median of 57 (range 23-83). Eighteen of the patients had scleritis: eleven of these had evidence of connective tissue disease and three of them had temporal arteritis. Twelve patients had episcleritis: six of them had a collagen disease and one of them developed temporal arteritis. This high incidence of temporal arteritis in association with scleritis has not been previously reported. It is important to diagnose and treat overt temporal arteritis early with parenteral steroids so that ischaemic papillopathy can be avoided. A higher incidence of collagen diseases than previously described is reported in episcleritis. It is thought that this is secondary to selection since patients with the usual self-limiting episcleritis are not normally referred for further in-patient investigation. In no patient was more than one significant diagnosis made. There was no significant medical illness in only 11% of patients with scleritis and 33% of patients with episcleritis. The majority of the non-collagen diseases (e.g. hypertension) were not previously recognized. In none of the patients with temporal arteritis was the diagnosis made before admission. It is concluded that full examination and investigation for underlying disease is indicated in both scleritis and severe episcleritis.
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PMID:Scleritis and temporal arteritis. 101 96

Seven patients of temporal arteritis with eye involvement have been presented. These cases represent a spectrum of disease from intermittent diplopia with minimal 6th nerve weakness through mild retinal ischemia with recovery to permanent bilateral blindness. Temporal arteritis should be suspected when any form of ocular ischemia is suspected by history or found on examination of an elderly person. An early diagnosis may protect the vision in both eyes if vision is normal at the time of diagnosis. If vision in one eye is decreased because of ischemia, the vision in the other eye can usually be retained if proper therapy is instituted. Furthermore, adequate therapy may even result in improvement in vision in the involved eye. Patients with biopsy proven temporal arteritis should be continued on steroid therapy until the active disease is quiescent. Inactivity should be determined by carefully monitoring the ESR while steroids are being tapered. If the ESR rises, it is indicative of continued inflammation and if steroids are not continued, the eyes remain at risk as seen in Case 5. If the ESR remains elevated for a year or more despite continuation of high steroid levels, consideration should be given to repeating the temporal artery biopsy. Temporal arteritis should be considered in the differential diagnosis of any multisystem disease in older patients. Even central nervous system involvement may occur concomitantly, since the intracranial vessels are not immune from the disease process. Tuberculosis, systemic syphilis and more recently the collagen vascular diseases have been dubbed the "great imitators" and "the protean diseases." We suggest that the same terminology can be applied to temporal arteritis. Temporal arteritis can affect any organ. Moreover, there is a wide spectrum of variation in the degree of involvement of any particular tissue as illustrated by these 7 cases of ocular involvement.
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PMID:Temporal arteritis: a spectrum of ophthalmic complications. 118 Apr 60

The presence of circulating immunocomplexes (CIC) was evaluated in several collagen diseases and in a control group of 100 healthy individuals. Three methods were used for their detection: binding to C1q in solid phase, binding to conglutinin in solid phase, and measurement of the serum capacity to solubilize an experimental immunocomplex. In the group of patients with systemic lupus erythematosus (SLE) significant differences were found for the three techniques (p less than 0.001) and also for activity (p less than 0.001). The most sensitive method was binding to C1q. The sensitivity of the three techniques for CIC was very low in the group of patients with systemic sclerosis, and the highest rate of positive results was found with binding to C1q (10%). In the group with hypersensitivity vasculitis and polyarteritis nodosa CIC were found in 71% of cases, more than one method being positive in 50%. The highest sensitivity was obtained with the conglutinin method (48%). In patients with temporal arteritis, significant differences were only found for conglutinin binding method (p less than 0.001), with low rates of positivity.
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PMID:[Evaluation and significance of circulating immunocomplexes and their correlation with other immunologic parameters in connective tissue diseases]. 228 96

Coronary artery disease is overwhelmingly atherosclerotic in nature, but inflammatory disease of the coronary arteries can be just as life-threatening a cause of ischemic heart disease in all age groups. Coronary vasculitis is not short in variety; as a clinicopathologic entity it spans the entire spectrum of systemic vasculitides. Coronary vasculitis is most closely associated with the polyarteritis group of necrotizing angiitis, vasculitis of collagen-vascular disease, and granulomatous giant cell arteritis. This article provides an overview of coronary vasculitis as an independent entity as well as a manifestation of systemic vasculitis, both the common and the uncommon varieties.
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PMID:Coronary vasculitis. A review in the current scheme of classification of vasculitis. 354 44

Temporal arteritis is a systmic disease with a predilecation for the cranio-temporal vascular area. Histologically it is a panarteritis. Diagnosis is based on the presence of lymphocytes, histiocytes and foci of epitheloid cells in the media of the temporal artery. The presence of giant cells is, however not obligatory. The present study emphasizes the value of biopsy of the temporal artery in diagnosing this disease. It, furthermore, also points out the 10-percent possibility of false negative biopsy results based on patchy vascular lesions. Tenderness to touch of the temporal artery, characteristic of temporal arteriitis, can be explained by perineural inflammatory infiltration of nerves in the adventitia of this artery. Examination under the electron microscope reveals almost complete destruction of the smooth muscles of the media by epitheloid cell granulomas. Massive neogenesis of collagen ensues. Furthermore, numerous myofibroblasts, macrophages and histiocytes are observed. Several macrophages close to each other create the impression of giant cells in the light microscope. The electron microscope image allows for clear differentiation between temporal arteritis on one hand and of arteriosclerosis on the other. Using the immunoperoxidase method in temporal arteritis, immune globulines are found intracellularly in plasma cells. Extracellularly, however, neither immune golbulins nor complement deposits are found in the vascular wall. Thus, the assumption that temporal arteritis represents a immune complex disorder cannot be maintained. The most frequent ophthalmologic complication in temporal arteritis is ischemic optic neuropathy. Histologic examination of a bulbus presenting anterior ischemic optic neuropathy in a case of temporal arteritis revealed predominantly lymphocytic infiltrations of the short and long ciliary arteries. No inflammatory infiltration was found in the central retinal artery. The development of anterior ischemic optic neuropathy can be explained by impaired perfusion or by occlusion of the short posterior ciliary arteries. In 60% of patients suffering from temporal arteritis, we found anticollagen antibodies in the serum. Collagenization of the vascular wall as observed in our electron-microscopic examinations must, therefore, be considered the paradoxical consequence of an immune reaction caused by collagen auto-antibodies. Collagen auto-antibodies play a decisive role in the maintenance and chronicity of the inflammatory process in temporal arteritis. In therapy, corticosteroids should not be administered according to rule but rather in doses adjusted to individual requirements.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Electron microscopic and immunohistologic studies of patients with Horton's temporal arteritis]. 638 7

The occurrence of acute leukemia in patients receiving chemotherapeutic agents for malignant disease has been well established. Recent reports have suggested that chemotherapeutic drugs used to treat inflammatory conditions may have an oncogenic potential. From 1969 to 1977, 11 patients with a variety of collagen-vascular diseases who developed acute nonlymphocytic leukemia were seen at the Cleveland Clinic. Rheumatoid arthritis was the most common underlying disease, in addition to giant cell arteritis, polyarteritis nodosa, chronic glomerulonephritis, and scleroderma. All patients were treated with alkylating agents, and 10 of the 11 received multiple cytotoxic agents. According to the French-American-British classification there were six examples of M4 (myelomonocytic leukemia), with single examples of M1 (myeloblastic leukemia without maturation), M2 (myeloblastic leukemia with maturation), M5a (monocytic leukemia, poorly differentiated), M5b (monocytic leukemia, differentiated), and M6 (erythroleukemia). Cytogenetic studies were abnormal in five patients studied, showing varying degrees of aneuploidy. All patients died, and the mean duration of time from the diagnosis of leukemia to death was four and one-half months, with only one complete remission.
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PMID:Acute nonlymphocytic leukemia in patients receiving chemotherapy for nonmalignant diseases. 677 41

Out of 110 cases of fever of unknown origin (FUO) that met Petersdorf and Beeson's criteria 15 patients were selected because of prolonged FUO with more than six months elapsed between admission and the final diagnosis. In this group of chronic FUO an etiological diagnosis was reached in 11 cases, distributed as follows: four cases with infections (two with toxoplasmosis, one with brucellosis, and another with a brain abscess); one with colon carcinoma; two with collagen-vascular diseases (systemic lupus erythematosus, temporal arteritis); and four with different diseases (two with familial mediterranean fever, one with idiopathic granulomatous disease, and another with factitious fever). In four cases no cause for the FUO could be determined. The procedures used to obtain the diagnosis were non-invasive in five cases (clinical course and serological tests), and invasive in another five (angiography, biopsies, and exploratory laparotomy). In one case the ethology could only be ascertained at autopsy. In the FUO with a prolonged course the peculiar etiological spectrum, the lesser yield of invasive procedures, and a mortality inferior to that of FUO in general all deserve special emphasis.
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PMID:[Fever of unknown origin with a prolonged course (author's transl)]. 724 70

Circulatory disorders of the optic nerve may be classified into acute and chronic lesions as well as into anterior and posterior ones. In general, anterior lesions clinically prevail; they are located around the lamina cribrosa and are pathogenetically explained as a consequence of decreased blood flow in the posterior ciliary arteries as well as in the perilaminar capillaries. The symptoms of the acute anterior lesions are described. The nerve head infarction may be induced by various circulatory disorders such as arteriosclerosis, diabetes, elevated blood pressure, giant cell arteritis or other collagen diseases, but also by others. The particular importance of giant cell arteritis is stressed. The prognosis of acute anterior ischemic optic neuropathy is poor, possibilities of treatment are discussed. The chronic anterior lesion is considered to be caused by an imbalance between intraocular pressure and the perfusion pressure in the posterior ciliary arteries and consequently in the perilaminar capillaries. The clinical signs ('low tension glaucoma') are described, the therapeutic measures, although limited, are outlined. The ischemic lesions of the posterior part of the optic nerve are less well defined. However, theoretical considerations as well as clinical experience suggest that such lesions occasionally occur taking either an acute or a chronic course.
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PMID:Circulatory disorders of the optic nerve. 745 23

The mechanism for central nervous system (CNS) involvement in connective tissue diseases is variable. Although CNS vasculitis does occur in some connective tissue diseases, it is rare in many others, including systemic lupus erythematosus. Overall, the most common pathogenetic mechanism for CNS dysfunction in patients with connective tissue disease is probably secondary CNS involvement, due either to multiple systemic organ dysfunction (including hypercoagulable or hypofibrinolytic states) or due to CNS and systemic infections. The pathogenetic role of antineuronal antibodies is yet to be defined. Generally, nervous system complications of those collagen diseases that classically produce necrotizing vasculitis should be treated with cytotoxic agents. The less severe vasculitides, particularly temporal arteritis, respond well to steroids, as does sarcoidosis. There are a variety of mechanisms for nervous system disorders in complex multiple system diseases. The etiology is often outside of the nervous system, and results of therapy are highly variable.
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PMID:Connective tissue disease and sarcoidosis of the central nervous system. 808 13


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