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)

A female with recurrent thrombosis was found to have a functional abnormality of antithrombin, with a ratio of functional to immunological activity in plasma of approximately 50%. Crossed immunoelectrophoresis in the presence of heparin was normal, indicating an abnormality of the reactive site, rather than the heparin binding domain. Accordingly, the antithrombin was isolated by heparin-Sepharose chromatography: this produced a mixture of normal and variant antithrombin, as the patient was heterozygous for the abnormality. To remove the normal component, the antithrombin was passed through a column of thrombin-Sepharose. On sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), prior to its application to thrombin-Sepharose, the antithrombin migrated as a single band with identical mobility to that of normal antithrombin. After thrombin-Sepharose, the purified variant component was proteolysed, and migrated as two components, one with a reduced and one with enhanced mobility under non-reducing conditions. This demonstrated that the variant was unable to form stable inhibitor-thrombin complexes and was cleaved in a substrate reaction with thrombin. One site of cleavage was unambiguously ascertained to be the Arg 393-Ser 394 reactive site bond, by NH2 terminal sequencing of the cleaved variant antithrombin: 10 steps beginning at the P1' position, Ser-Leu-Asn-Pro-Asn-Arg,..., were clearly identified. The mutation responsible for this defect was studied by polymerase chain reaction (PCR) amplification of exon 6 of the antithrombin gene and direct sequencing of the amplified product. The presence of both a G and A in the first position of codon 382, identified the mutation GCA to ACA, which results in the substitution of Ala 382 to Thr. This is identical to that reported for antithrombin Hamilton (Devraj-Kizuk et al, 1988), although antithrombin gene polymorphism analysis suggests that the antithrombin Glasgow II mutation has arisen independently. We have recently shown (Caso et al, 1991) that mutation at a nearby position, Ala 384 to Pro, also transforms another variant, antithrombin Vicenza/Charleville, into a substrate for thrombin. The present results with antithrombin Glasgow II suggest that all the alanine residues at the base of the reactive site loop in positions P12-10 may be important for the formation of a stabilized inhibitor-thrombin complex.
Br J Haematol 1991 Sep
PMID:Antithrombin Glasgow II: alanine 382 to threonine mutation in the serpin P12 position, resulting in a substrate reaction with thrombin. 191 89

Temporal artery biopsy is performed to confirm the diagnosis of giant cell arteritis. The technique is described together with the anatomy of the superficial temporal artery.
Br J Hosp Med 1991 Sep
PMID:How to perform a temporal artery biopsy. 193 1

A positive temporal artery biopsy is required to conclusively establish the diagnosis of temporal arteritis. The temporal artery biopsy technique we describe is based on the anatomical branching patterns of the superficial temporal artery, the various fascial layers, and the location of the temporal branches of the facial nerve. Special emphasis is placed on avoiding facial nerve trauma during a biopsy of the frontal branch of the superficial temporal artery. Proper surgical technique combined with a working knowledge of the anatomy of the temporalis region enhances the safety of a temporal artery biopsy procedure.
Ophthalmic Surg 1991 Sep
PMID:Temporal artery biopsy technique: a clinico-anatomical approach. 194 77

Rapidly developing mental confusion and concomitant physical deterioration are reported as presenting symptoms in a case of giant cell arteritis (GCA). Systemic glucocorticoid therapy was followed by partial remission of neuropsychiatric symptoms and complete physical recovery. GCA should be considered as a cause of treatable dementia in the elderly. Temporal artery biopsy is recommended in dement elderly persons with elevated ESR of unknown cause.
Ugeskr Laeger 1991 Sep 09
PMID:[Reversible dementia caused by giant cell arteritis]. 194 62

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.
Med Clin (Barc) 1990 Sep 08
PMID:[Evaluation and significance of circulating immunocomplexes and their correlation with other immunologic parameters in connective tissue diseases]. 228 96

Biopsies from the temporal artery of 32 patients suspected of giant-cell arteritis were evaluated retrospectively by light microscopy, histochemical, and immunohistochemical methods, as well as by transmission electron microscopy (TEM). At the clinical follow-up the 32 patients included four clinical groups: temporal arteritis (8 patients), polymyalgia rheumatica (10 patients), rheumatoid arthritis (4 patients), and a group of miscellaneous diseases unrelated to inflammatory rheumatic diseases (10 patients). There were a number of similarities between age-related alterations in the arteries and the changes in giant-cell arteritis. The most important differences were the inflammatory cellular infiltration of the media, the perifocal accumulation of fibronectin, and the occurrence of deposits of fibrin/fibrinogen and fibrin/fibrinogen degradation products. In addition, alpha-2 macroglobulin, lysozyme and factor VIII were also noted in giant-cell arteritis. The alterations in giant-cell arteritis show a number of similarities to the changes following experimental vascular injury of the rabbit aorta. The nature of the findings in human giant-cell arteritis, as well as the similarity to the experimental arteritis, indicate that giant-cell arteritis may reflect a non-specific reaction to injury, independent of the cause of the disease.
Acta Pathol Microbiol Immunol Scand A 1987 Sep
PMID:Giant-cell arteritis. Histological, immunohistochemical and electronmicroscopic studies. 244 62

A prospective clinical study (1974-1988) was carried out in 33 patients with several types of systemic vasculitis (SV) presenting as fever of unknown origin (FUO) according to the 1961 Petersdorf and Beeson's criteria. Histological confirmation, either from biopsy or necropsy, was available in all cases. The types of SV with FUO were: panarteritis nodosa (PAN) (14 cases), giant cell arteritis (GCA) (13 cases), and overlapping polyangiitic syndrome (OPS) (6 cases). In PAN, the clinical features associated with fever at the onset of the disease were remarkably nonspecific: constitutional symptoms (85%), arthromyalgia (50%), nonspecific abdominal pain (28%), and irritative cough (28%). In the whole course of the cases of GCA a significantly smaller frequency of presentation of local arterial symptoms and polymyalgia rheumatica (p less than 0.01) was found in the subgroup of patients with FUO than in those without it. As regard laboratory data, a higher increase of serum alkaline phosphatase (p less than 0.05) was found in the cases of PAN and OPS with FUO. Striated muscle biopsy and arteriography were the most useful investigations in the diagnosis of PAN. The study that gave the diagnosis in the cases of GCA was temporal artery biopsy.
Med Clin (Barc) 1989 Sep 09
PMID:[Systemic vasculitis as a cause of fever of unknown origin]. 260 77

We describe a series of 7 patients with temporal arteritis (TA), 5 of whom had undoubted TA and 2 almost certainly had TA. All presented with considerable morbidity but responded dramatically to treatment.
J Assoc Physicians India 1989 Sep
PMID:Temporal arteritis. The Indian scene. 263 65

The authors present three cases of AION with suspected temporal arteritis to show why a Doppler sonographic examination should be performed prior to a biopsy of the temporal artery. In Case 1, with stenosis of the internal carotid artery, the cerebral perfusion depended, entirely on collateral circulation, the nutritive vessel of which was the temporal artery. Cases 2 and 3 illustrate a proximal stenosis of the ophthalmic artery. In these two cases the temporal artery maintained the blood supply to the eye. All these findings were obtained by Doppler sonographic examinations. Biopsy of the temporal artery, which could otherwise have caused sudden death in Case 1, or blindness in Cases 2 or 3, was therefore dispensed with.
Klin Monbl Augenheilkd 1989 Sep
PMID:[Why perform Doppler sonography before every biopsy of the temporal artery?]. 268 57

We report a case of temporal arteritis associated with anicteric cholestasis. Serial sections of a transthoracic needle biopsy of the liver revealed giant-cell arteritis in medium-sized hepatic arteries and cholangitis in adjacent bile ducts. The literature reveals that similar pathologic features have only exceptionally been observed in liver biopsies. These lesions may account for liver function disturbances commonly seen in temporal arteritis or polymyalgia rheumatica.
Pathol Res Pract 1989 Sep
PMID:A case of temporal arteritis with intrahepatic arterial involvement. 268 74


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