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)

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.
HNO 1988 Feb
PMID:[Acute circulatory disorders of the tongue]. 336 Jun 28

A 79 year old woman is reported who has suffered pain in the jaws and mouth for several years. Giant cell arteritis was diagnosed by temporal artery biopsy after the appearance of severe temporal and frontal headache. Despite treatment with cortisone, sudden pain in the tongue appeared preventing speaking and swallowing and leading to ischemic necrosis of the anterior two thirds of the tongue. At the same time she had a transitory ischemic cerebral attack. Six almost identical case histories could be found in the literature: in three tongue necrosis was caused by histologically proven giant cell arteritis. From the clinical picture, giant cell arteritis could have been the cause of tongue necrosis in the other three cases.
HNO 1984 Mar
PMID:[Giant cell arteritis as a cause of tongue necrosis]. 670 9

Two inflammatory vascular diseases often show multinucleated macrophages: Takayasu's disease and Horton's disease. Takayasu's disease is a segmentary panarteritis most prominent in the adventitia. Lesions show an inflammatory infiltrate close to the external elastic lamina. Progressive stenosis of the artery, sometimes complicated by calcifying atheroma is the typical course. Horton's disease or temporal arteritis is another segmentary arteritis. Lesions show a mixed inflammatory infiltrate partly localized in the adventitia where there are T CD4+ lymphocytes secreting II-2 and IFN-gamma and also macrophages expressing TGF beta 1, IL-6 and IL-1 beta, and partly situated in the interior part of the wall, around the internal elastic lamina, and mostly made of macrophages and giant cells which produce TNF, collagenase and nitric oxide that are responsible for destruction of the wall. The variety and subtleness of some lesions do not always make a precise diagnosis possible. But any inflammatory vascular lesion, even slight, can reveal a systemic vasculitis.
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PMID:[Pathology of giant cell arteritis]. 992 94

Otorhinolaryngological findings of a temporal arteritis frequently occur in the beginning and/or course of the disease. A purulent sinusitis can be a sign of recurrence of the arteritis and was diagnosed in a 77-year-old woman with known disease that had been biopsied 6 years earlier. Puncture of the maxillary sinus was considered necessary, but no bacteria were found in purulent sinus discharge. When antibiotic treatment failed to bring about a resolution of the inflammatory condition, steroid therapy was begun and the patient recovered within a few days in response to this treatment. The clinical findings in this case show that early diagnosis and treatment by the otorhinolaryngologist are necessary in order to prevent severe complications of the disease.
HNO 1999 Mar
PMID:[Otorhinolaryngologic findings in Horton temporal arteritis. Review of the literature and case report]. 1023 1

Arterial wall damage in giant cell arteritis (GCA) is mediated by several different macrophage effector functions, including the production of metalloproteinases and lipid peroxidation. Tissue-invading macrophages also express nitric oxide synthase (NOS)-2, but it is not known whether nitric oxide-related mechanisms contribute to the disease process. Nitric oxide can form nitrating agents, including peroxynitrite, a nitric oxide congener formed in the presence of reactive oxygen intermediates. Protein nitration selectively targets tyrosine residues and can result in a gain, as well as a loss, of protein function. Nitrated tyrosine residues in GCA arteries were detected almost exclusively on endothelial cells of newly formed microcapillaries in the media, whereas microvessels in the adventitia and the intima were spared. Nitration correlated with endothelial NOS-3 expression and not with NOS-2-producing macrophages, which preferentially homed to the hyperplastic intima. The restriction of nitration to the media coincided with the production of reactive oxygen intermediates as demonstrated by the presence of the toxic aldehyde, 4-hydroxynonenal. Depletion of tissue-infiltrating macrophages in human temporal artery-SCID mouse chimeras disrupted nitrotyrosine generation, demonstrating a critical role of macrophages in the nitration process that targeted medial microvessels. Thus, protein nitration in GCA is highly compartmentalized, reflecting the production of reactive oxygen and reactive nitrogen intermediates in the inflamed arterial wall. Heterogeneity of microvessels in NOS-3 regulation may be an additional determinant contributing to this compartmentalization and could explain the preferential targeting of newly generated capillary beds.
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PMID:Reactive nitrogen intermediates in giant cell arteritis: selective nitration of neocapillaries. 1210 96

Giant cell arteritis (GCA) and Takayasu's arteritis (TA) are the two primary large-vessel arteritides. Recent advances in cellular immunology have allowed better understanding of pathogenesis of these diseases. In GCA and TA, resident adventitial dendritic cells are activated by unidentified stimuli. This activation induces chemokine synthesis which enhances recruitment of inflammatory cells. T-cells infiltrate the vascular wall and specifically recognize one or a few antigens presented by shared epitopes associated with specific HLA molecules on dendritic cells. Activated T-cells produce IFNgamma stimulating two distinct populations of macrophages. Macrophages located in the intima produce pro-inflammatory cytokines (IL-1, IL-6). Macrophages located in the media differentiate into giant cells and/or produce reactive oxygen species, nitric oxide and matrix metallo-proteinases. Macrophages of the media also produce VEGF, which leads to neovascularization and PDGF, which induces intimal hyperplasia and vascular occlusion. In TA, cytotoxic T cells infiltrate the vascular wall and induce apoptosis of the vascular cells. Better understanding of the pathogenesis of large-vessel arteritis may lead to development of immunosuppressive drugs specifically targeting the immunological mechanisms implicated in GCA and TA.
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PMID:[Pathogenesis of primary large vessel arteritis]. 1880 14

A 76-year-old woman presented with fever, redness, swelling, and pain under the chin. Some submental lymph nodes were detected by ultrasound and computed tomography. The diagnosis was a submental phlegmon, for which surgery was performed. The lymph nodes were removed, and antibiotic therapy with daily lavage was done. The histology of the lymph nodes suggested giant cell arteritis.
HNO 2009 Jun
PMID:[Fever, redness, swelling, and pain in the submental region]. 1951 87