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)

ESR is a time-honored, simple, inexpensive test, but unfortunately it lacks sensitivity and specificity. Clinicians need to be aware of appropriate uses, because any test is expensive when ordered often, and evaluation of false-positive results may incur substantial costs and place the patient at risk from additional procedures. ESR should not be used to screen asymptomatic persons for disease. If an increased ESR is encountered and no explanation is immediately apparent, clinicians should repeat the test in several months rather than pursue an exhaustive search for occult disease. ESR may be useful in establishing a "sickness index" in elderly persons who have nonspecific changes in health status and a moderate probability of underlying disease; in screening for infection in specific settings (e.g., orthopedic surgery, pediatrics, gynecology); in diagnosing and monitoring temporal arteritis, polymyalgia rheumatica, and possibly other rheumatic diseases; in monitoring patients with treated Hodgkin's disease; and in assessing iron deficiency in anemia of chronic disease (when correlated with serum ferritin level). An ESR value exceeding 100 mm/hr has a 90% predictive value for serious underlying disease, most often infection, collagen vascular disease, or metastatic tumor. In asymptomatic persons with a markedly elevated ESR value, a minimal number of tests usually reveal the cause.
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PMID:The erythrocyte sedimentation rate. Still a helpful test when used judiciously. 959 Sep 99

Fever of unknown origin (FUO) is a common clinical diagnostic dilemma. In the elderly, causes of FUO most commonly include malignancy or infection, and less commonly include collagen vascular diseases. Among the collagen vascular diseases causing FUO in the elderly, polymyalgia rheumatica/temporal arteritis, and adult Still's disease (adult juvenile rheumatoid arthritis) are difficult diagnoses to prove. Among the infectious causes of FUO in the elderly are subacute bacterial endocarditis, intra-abdominal abscesses, and extrapulmonary tuberculosis. In the elderly, neoplastic causes of FUO include lymphomas, hepatomas, renal cell carcinomas, and hepatic or central nervous system metastases. Acute leukemias, particularly during "blast" transformation, may present as acute fevers in the absence of infection, but are rare causes of FUO. Preleukemia/myelodysplastic syndromes are exceedingly rare causes of FUO. We present a case of an elderly man who presented with findings that initially suggested adult Still's disease. Prolonged and profound monocytosis provided the key clue to his subsequent diagnosis of preleukemia/myelodysplastic syndrome. In this patient, a positive Naprosyn test result also suggested a neoplastic cause for his FUO. After months of prolonged fevers, myelocytes/metamyelocytes were eventually demonstrated in his peripheral smear during hospital evaluation. These findings, in concert with the persistent monocytosis, highly elevated ferritin levels, polyclonal gammopathy on serum protein electrophoresis, and eventual presence of myelocytes/metamyelocytes on peripheral smear, prompted a bone marrow test that demonstrated blast cells confirming the diagnosis of preleukemia myelodysplastic syndrome as the cause of this patient's FUO.
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PMID:Fever of unknown origin due to preleukemia/myelodysplastic syndrome: the diagnostic importance of monocytosis with elevated serum ferritin levels. 1686

Fever of unknown origin (FUO) refers to prolonged fevers of > or = 101 degrees F and that persists for > 3 weeks that remain undiagnosed after an intensive in-hospital/outpatient workup. The most common FUO categories of are infectious, neoplastic, rheumatic/inflammatory, and miscellaneous causes. Malignancies have supplanted infectious diseases as the most common cause of FUOs in the adult population. Rheumatic/inflammatory causes of FUO are relatively less common than previously because of the introduction over the years of sophisticated diagnostic tests for most rheumatic diseases. The rheumatic/inflammatory disorders that remain important causes of FUO today are those that cannot be readily diagnosed by readily available/noninvasive tests, for example, adult Still's disease and temporal arteritis (TA). In older patients with FUO, TA can be a difficult diagnosis when the characteristic findings (ie, scalp tenderness, jaw claudication) are not present. Patients with TA presenting as FUO often have only headaches that may be accompanied by bilateral jaw discomfort. Endocrine causes of FUOs are rare. The most common endocrine disorder rarely presenting as an FUO is de Quervain's subacute thyroiditis. As in TA, subacute thyroiditis may present with headache and pain at the angle of the jaw. Both TA and subacute thyroiditis may be accompanied by fatigue, weight loss, and night sweats. We present a case of 55-year-old woman who presented with an FUO with clinical and laboratory findings suggesting TA. However, the absence of thrombocytosis and a normal alkaline phosphatase argued against the diagnosis of TA. Also against the diagnosis of TA was weight loss without loss of appetite and a slightly increased pulse. After nonspecific laboratory test results suggested that TA was not the cause of her FUO, additional tests were ordered. Thyroid function test results suggested the possibility of de Quervain's subacute thyroiditis as the cause of her FUO. To the best of our knowledge, this is the first case of de Quervain's subacute thyroiditis presenting as an FUO with elevated ferritin levels.
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PMID:Fever of unknown origin (FUO): de Quervain's subacute thyroiditis with highly elevated ferritin levels mimicking temporal arteritis (TA). 2010 88

Giant cell arteritis still results in high morbidity related to systemic complications involving the eyes, the central nervous system, the heart and the aorta. Therefore, reliable diagnostic criteria are required in giant cell arteritis and polymyalgia rheumatica (PMR), to detect and manage at early stages patients with giant cell arteritis and PMR. Indeed, diagnostic criteria of giant cell arteritis and PMR have been validated. Taken together, first we propose to review the diagnostic criteria of giant cell arteritis (ACR, GRACG) and PMR (Bird, Jones-Hazleman, Chuang-Hunder, Dasgupta). Second, more recent diagnostic criteria of GCA and PMR are further reviewed, including biochemical/immunological data (especially anti-ferritin antibodies), temporal artery biopsy and imaging findings (artery ultrasonography, angio-CT-scan, angio-MRI, PET-scan, joint echography, and MRI).
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PMID:[Giant cell arteritis and polymyalgia rheumatica: diagnostic criteria]. 2349 14

Giant cell arteritis (GCA) is considered to be a T cell-dependent disease. Autoantibodies have not consistently been found in GCA. The exception is antiphospholipid antibodies (APLA), which were found in 30-80% of GCA cases. Recently, efforts have been made to seek autoantibodies in GCA using newer methods of detection: serological identification of antigens by recombinant cDNA expression cloning, and a proteomic approach. In these studies, lamin C (a nuclear envelope antigen) was recognized by antibodies in 32% of GCA sera and none of the controls. Other autoantigenic proteins were also identified: lamin A, vinculin (a cytoskeleton antigen), and annexin 5 (an endothelial protein). In a recent study, 92% of 36 patients with GCA and/or polymyalgia rheumatica (PMR) had autoantibodies to a human ferritin peptide (the heavy chain N-terminal); 89% had antibodies to bacterial ferritin peptide of Staphylococcus epidermidis. The significance of these findings needs to be studied further. GCA may be a part of the newly described ASIA syndrome (autoimmune syndrome induced by adjuvants). A recent study from Italy reported 10 cases of GCA/PMR within 3 months of influenza vaccination. These comprised 50% of all cases of GCA/PMR diagnosed during the 6 year period of the study. Another 11 cases of GCA following influenza vaccinations were reported. GCA pathogenesis involves all branches of the immune system, including antigen-presenting cells, T cells and B cells, and autoantibody formation is not uncommon. GCA etiology remains unknown, but may be associated with exposure to bacterial or viral antigens.
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PMID:Autoimmune aspects of giant cell arteritis. 2516 95

Takayasu arteritis (TA) is difficult to diagnose because diagnostic biomarkers have not yet been established. In a previous study, we detected autoantibodies against the human ferritin heavy chain protein (HFC) in the sera of patients with giant cell arteritis (GCA) and/or polymyalgia rheumatica (PMR). The aim of this study is to evaluate the frequency of autoantibodies against HFC in TA. We established seven ELISA assays for the detection of autoantibodies against HFC. We used the full-length recombinant HFC expressed in Escherichia coli or one of six different HFC peptides as autoantigens: 1-18Aa (98.8 % purity), 19-45Aa (98.8 % purity), 52-78Aa (98.3 % purity), 79-104Aa (98.8 % purity), 105-143Aa (98.4 % purity) and 145-183Aa (98.5 % purity). We collected sera from 48 patients with TA, 36 patients with systemic lupus erythematosus (SLE), 35 patients with arteriosclerosis, 133 patients with febrile diseases, which are known to generate unspecific autoantibodies, and 50 blood donors, which served as controls. The best results were obtained using the ferritin peptides as antigens. By combining the results from the different ELISAs that detect autoantibodies against the HFC peptides 19-44A, 79-104A and 105-144A, we were able to detect ferritin peptide antibodies in 30/48 (62 %) of the TA patients. The frequency was lower than in early GCA and PMR (previous study showed up to 92 %). Positive results were observed in 0/50 (0 %) of the control blood donors, 10/36 (28 %) of the SLE patients, 4/35 (11 %) of the arteriosclerosis patients and 27/133 (20 %) of the fever patients. Considering the lack of biomarkers for TA, autoantibodies against HFC peptides could act as useful markers for TA.
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PMID:Association of ferritin antibodies with Takayasu arteritis. 2517 78

In patients with giant cell arteritis (GCA), autoantibodies against cytoskeletal elements, cardiolipin, neutrophil cytoplasmic antigens, ferritin, endothelial and smooth muscle cells have been reported, however no updated reviews are available evaluating their clinical utility. Methodology of detection is important, especially for quantitative assays, e.g. enzyme-linked immunoassays and multiplex beadbased immunoassays, while semiquantitative assays contribute valuable data on isoforms, epitope mapping and cellular localization. Most studies to date reporting on antiphospholipid antibodies in GCA have focused on anti-cardiolipin antibodies (aCL), while the highest prevalence of autoantibodies in GCA patients was reported for the anti-N-terminal peptides of the ferritin heavy chain (92%). Antineutrophil cytoplasmic antibodies were shown to be present in only a small percentage of GCA patients, decreasing after therapy, however in combination with aCL and antibodies against peptides of N-terminal ferritin heavy chain, they could represent an added value in detecting relapse in GCA patients.
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PMID:Evaluating the utility of autoantibodies for disease activity and relapse in giant cell arteritis. 2968 12