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)

Helicobacter pylori is the major cause of chronic gastritis. Unlike bacterial infections in general, H. pylori acquisition causes a chronic, usually life-long infection. After acquisition, chronic inflammation (gastritis) appears and develops slowly into atrophic gastritis (with intestinal metaplasia) in a proportion of affected subjects. Inflammation and atrophy result from a failure of the immune system to eliminate the H. pylori infection. In infected stomach, several cascades of reactions are triggered which may result in impairments of structure and function of the gastric mucosa, some of which lesions also increase the risk of gastric carcinoma (CGA). A sequence of events from an early H. pylori infection into an atrophic gastritis has risen a theory that the H. pylori acquisition is a key issue in the development of GCA. Several aspects in the epidemiology and pathogenesis of GCA can be understood and explained by this infectious background. The H. pylori gastritis is unexpectedly common in patients with GCA of both intestinal or diffuse type, and the infection and gastritis precede the development of cancer. In Finland, 70-80% of the GCA cases seem to develop in connection with an H. pylori-positive gastritis or atrophy, 10-15% develop in a normal stomach (genetically determined GCA cases?), and 10-15% are associated with an H. pylori-negative corpus-limited (autoimmune) gastritis and atrophy. Case control studies suggest that the presence of H. pylori related inflammation raises the risk of GCA twofold, and the appearance of atrophic gastritis (and intestinal metaplasia) raises further this risk 2-3 times, as compared to the risk of GCA in subjects with a normal stomach.
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PMID:Gastric carcinoma: failed adaptation to Helicobacter pylori. 129 56

SPECT of the skull was performed on twelve patients with histologically proven nasopharyngeal carcinoma using newly developed three detectors SPECT system (Toshiba GCA 9300A) mounted with fan-beam collimators, for the purpose of early detection of skull base involvement of the disease. This SPECT system has extremely improved resolution with FWHM of 8 mm in the center, and it provides clear tomographic images of the skull which has anatomically complex structure. SPECT image was taken 3 hours after injection of 740 MBq (20 mCi) of 99mTc-MDP following whole body skeletal survey. In twelve patients with confirmed nasopharyngeal carcinoma, 8 patients showed positive findings on SPECT. Three of SPECT positive patients also showed destructive findings on CT. Other five positive patients did not show destructive findings on CT at their initial examinations, but in three of them CT findings turned to positive later. SPECT was superior to CT in early detection of skull base involvement. We believe that SPECT of the skull is a diagnostic tool for early detection of skull base involvement of nasopharyngeal carcinoma.
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PMID:[Assessment of skull base involvement of nasopharyngeal carcinoma by bone SPECT using three detectors system]. 157 20

The human TP53 gene is a possible tumor suppressor since TP53 gene mutations are observed in greater than 70% of sporadic colorectal carcinoma DNAs. In genomic DNAs from seven colon cancer cell samples, a 405 base pair DNA fragment containing exon 5, intron 5, and exon 6 of the TP53 gene was amplified by polymerase chain reaction and analyzed for mutations. One sample [human colon cancer (HCC) 278] was found to have a TP53 mutation altering the amino acid glutamine 167 in exon 5. A deletion of 2 bases changed glutamine 167 (CAG) to alanine (GCA) and the resulting frame-shift produced an in-frame stop codon at amino acid 179. While the normal TP53 gene gives rise to a 53 kD protein, the estimated size of this mutant TP53 protein if expressed would be approximately 20 kD.
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PMID:Mutation in the TP53 gene in colorectal carcinoma detected by polymerase chain reaction. 195 96

A 58-year-old woman had a unilateral, solitary breast lesion determined by biopsy to be due to giant cell arteritis. Clinical, laboratory, and pathological findings in this patient and in other patients reviewed from the literature revealed that characteristically patients with giant cell arteritis of the breast have (1) tender unilateral or bilateral nodules at times mimicking breast carcinoma; (2) significant constitutional symptoms of anorexia, weight loss, myalgias, fever, and arthralgias; (3) marked elevation of the erythrocyte sedimentation rate; (4) normal or mildly decreased hemoglobin values and normal or slightly elevated leukocyte counts; (5) normal temporal artery biopsy findings; (6) rare organ involvement; and (7) rapid improvement after prednisone therapy or frequent spontaneous resolution. This mode of presentation suggests features of a unique syndrome since many patients had no systemic involvement, require no treatment at all, and had a self-limited clinical course.
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PMID:Giant cell arteritis of the breast. A unique syndrome. 218 37

Recently we experienced a case manifested by a lump in both breast that mimicked carcinoma but was found to be a vasculitis of the giant cell type. Our case was characterized histologically by granulomatous arteritis involving small to medium sized arteries of the breast without involvement of the temporal artery. We described the clinical and pathologic features of a case of giant cell arteritis of the breast and reviewed the eight previously reported cases in foreign literature.
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PMID:Giant cell arteritis of the breast--a case report. 218 74

The breast is an infrequently recognised site of primary giant cell arteritis. Two cases of giant cell arteritis affecting the breast are described and 11 previously described cases are reviewed. All cases presented with single or multiple breast masses, leading to a diagnosis before biopsy of suspected breast carcinoma. Symptoms similar to those of polymyalgia rheumatica occurred in about half of these patients, though the significance of these symptoms was only appreciated in retrospect. Clinical or pathological evidence of giant cell arteritis outside the breast (temporal artery, thyroid artery) was noted in a minority of cases. Seven patients received corticosteroid treatment, and all patients recovered without complications. Two patients had an adenocarcinoma of the breast contiguous with the giant cell arteritis. Giant cell arteritis affecting the breast may be underrecognised and should be considered in older women with polymyalgia rheumatica-like symptoms and tender breast mass(es).
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PMID:Giant cell arteritis (temporal arteritis) affecting the breast: report of two cases and review of published reports. 227 Sep 58

The clinical and pathologic features of a case of giant cell arteritis presenting in the breast and those of seven previously reported similar cases are described. A unique finding in the present case was a coincidental in situ and infiltrating ductal carcinoma in the same biopsy specimen. All the patients were postmenopausal women who presented with a firm mass in one or both breasts that mimicked a carcinoma on physical examination. There was no definite clinical evidence of temporal artery involvement in any patient, and two patients had normal temporal arteries on histologic examination. Five patients, however, had systemic manifestations, arteritis in another site, or both. Giant cell arteritis presenting in the breast may occur as an isolated finding or represent a manifestation of more widespread disease.
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PMID:Giant cell arteritis of the breast: case report and literature review. 282 25

A series of 24 consecutive patients presenting with a fundus picture characterized by a predominance of cotton-wool spots, or a single cotton-wool spot, is reported. Excluded were patients with known diabetes mellitus. Etiologic conditions found included previously undiagnosed diabetes mellitus in five patients, systemic hypertension in five patients, cardiac valvular disease in two patients, radiation retinopathy in two patients, and severe carotid artery obstruction in two patients. Dermatomyositis, systemic lupus erythematosus, polyarteritis nodosa, leukemia, AIDS, Purtscher's retinopathy, metastatic carcinoma, intravenous drug abuse, partial central retinal artery obstruction, and giant cell arteritis were each found in one patient. In only one patient did a systemic workup fail to reveal an underlying cause. The presence of even one cotton-wool spot in an otherwise normal fundus necessitates an investigation to ascertain systemic etiologic factors.
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PMID:Cotton-wool spots. 386 24

Temporal arteritis is still often overlooked in 1982 as shown by the diagnostic delay reported in a retrospective review of 33 patients and in the series previously published in the medical literature. Clinical features to be especially kept in mind are the occasional nature of temporal signs, the pathognomonic value of jaw claudication and the existence of signs which may constitute a premonitory syndrome of blindness. The frequent rise in alkaline phosphatase levels is often misleading. In patients over 65 with an unexplained inflammatory syndrome, biopsy of both temporal arteries should be promptly performed, prior to the unpleasant and costly investigations designed to detect an occult carcinoma. Corticosteroids are still the best treatment of giant cell arteritis but the optimal initial dosage remains unknown as no data from randomized trials are available. Symptomatic relapses have been reported up to 10 years (5 years for ocular symptoms) after onset of the disease. Because of this protracted course, which makes adequate follow-up difficult to ensure, recovery rates from different series are at variance. The main side-effects of maintenance corticosteroid therapy in these elderly patients are osteoporosis, which warrants systematic countermeasures, and probably an increased rate of atheromatosis.
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PMID:[Horton's disease: retrospective study of 33 cases and review of the literature]. 630 48

Two patients with localized polyarteritis nodosa involving the breast are reported. They presented with tender breast masses which were excised because of suspicion of carcinoma. The pathological features were similar with vasculitis of medium-sized and small arteries. The medium-sized arteries showed intimal fibroplasia, fragmentation of internal elastic lamina and inflammatory cellular infiltration. Fibrinoid vasculitis involving small arteries indicated a diagnosis of polyarteritis nodosa rather than giant cell arteritis. Both patients remain well. The differential diagnosis of these two arteritides and of Wegener's granulomatosis involving the breast is reviewed.
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PMID:Localized polyarteritis nodosa of breast--report of two cases and a review of the literature. 790 44


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