| 1. |
- Larsson, K, et al.
(författare)
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A Western blot and molecular genetic investigation of the estrogen receptor beta in giant cell arteritis.
- 2006
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Ingår i: Clinical and experimental rheumatology. - 0392-856X. ; 24:2 Suppl 41
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The epidemiology of giant cell arteritis (GCA) may indicate a pathogenetic relationship between GCA and female sex hormone metabolism; GCA is two to four times more common in women compared with men. Our previous analyses gave no support for the hypothesis that the pathogenesis of GCA should be related to somatic mutations in the estrogen receptor alpha (ERalpha) gene. The object of the present study was to investigate the size of the estrogen receptor beta (ERBeta), and the size and nucleotide sequence of the ERBeta gene in temporal arteries in GCA. METHODS: The ERBeta protein was analyzed by Western blot technique and the ERBeta gene by RT-PCR and direct sequencing of the PCR product. RESULTS: Western blot analysis revealed an ERBeta of normal size. There were no aberrations in size or nucleotide sequence in the ERBeta gene in the GCA patients. CONCLUSION: The present observations gave no support for the hypothesis that somatic mutations in the ERBeta gene should be involved in the pathogenesis of GCA.
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| 2. |
- Larsson, K, et al.
(författare)
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Early menopause, low body mass index, and smoking are independent risk factors for developing giant cell arteritis.
- 2006
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Ingår i: Annals of the rheumatic diseases. - : BMJ. - 0003-4967 .- 1468-2060. ; 65:4, s. 529-32
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To assess female sex hormone related variables in a group of women with biopsy positive giant cell arteritis and a control group. METHODS: 49 women with biopsy positive giant cell arteritis, aged 50 to 69 years at the time of diagnosis, answered a questionnaire on hormonal and reproductive factors. The same questions were answered by a large population of women from the same geographical area in connection with routine mammograms. The results were tested statistically, using logistic regression analysis of each variable adjusted for age, and a multivariate logistic regression analysis including age and the variables which differed significantly between giant cell arteritis and controls. RESULTS: From the multivariate logistic regression analysis, three independent variables were associated with an increased risk of having giant cell arteritis: smoking and being an ex-smoker (odds ratio (OR) = 6.324 (95% confidence interval (CI), 3.503 to 11.418), p<0.0001); body mass index (a reduction of 1.0 kg/m2 increased the risk by 10% (OR = 0.898 (0.846 to 0.952), p = 0.0003); and menopause before the age of 43 (OR = 3.521 (1.717 to 7.220), p = 0.0006). CONCLUSIONS: There was a significant association between hormonal and reproduction related factors and the risk of developing giant cell arteritis in women given the diagnosis before the age of 70. The results suggest a possible role of oestrogen deficiency in the pathogenesis of giant cell arteritis. To confirm the results, an extended study will be needed, including women older than 70.
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| 3. |
- Nordborg, Claes, 1946, et al.
(författare)
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Stereological study of neovascularization in temporal arteritis.
- 2006
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Ingår i: The Journal of rheumatology. - 0315-162X. ; 33:10, s. 2020-5
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: As giant cell arteritis (GCA) progresses, newly formed microvessels are one of the main sites of leukocyte-endothelial cell interaction. Our aim was to stereologically map the distribution of microvessels in the temporal arterial wall and to assess their relationship to the degree of inflammation in GCA. METHODS: Inflamed temporal arteries from 21 patients who fulfilled the American College of Rheumatology criteria for GCA were analyzed. Paraffin sections, stained with an antibody directed at vascular endothelium, were analyzed stereologically. The degree of inflammation and the surface of microvascular endothelium per volume (microm2/microm3) were assessed in 4 different layers of the arterial wall. RESULTS: The degree of inflammation and of vascularization was greatest in the adventitia, smaller in the media, and smallest in the intima. A significant positive relationship was observed between the degree of inflammation and the degree of vascularization in the media and in the outer and inner layers of the intima. In 8 biopsies, the microvessels formed a prominent plexus in the intima without apparent connection with microvessels in the adventitia/media, and there were no signs of endothelial budding from the arterial lumen. CONCLUSION: Our results confirm that inflammation is a major determinant in neovascularization in GCA. Some new microvessels are formed by the budding of the adventitial vasa vasorum. The presence of intimal microvascular networks without apparent connection with microvessels in the media might indicate additional influence on neovascularization.
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