Central Giant Cell Lesion
Mostrando 13-17 de 17 artigos, teses e dissertações.
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13. Hepatic artery involvement in polymyalgia arteritica.
Disturbances of liver function tests are common in polymyalgia arteritica, but the underlying liver lesion has not been defined. We report a patient who was demonstrated to have a giant cell arteritis involving both the hepatic and temporal arteries, and we discuss the possibility that such an arteritis involving the hepatic arteries is responsible for the a
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14. Aneurysmal bone cyst of the sphenoid with orbital involvement.
We present a case of aneurysmal bone cyst involving the roof of the orbit and sphenoid bone, with plain film, computed tomography, and magnetic resonance imaging findings. The natural history and treatment depend on the presence of associated abnormalities such as fibrous dysplasia or a giant cell tumour. In this case the lesion was solitary and was successf
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15. Fibroma of tendon sheath.
A series of nine cases of fibroma of tendon sheath is described including details of the ultrastructural features of two cases. The series was composed of lesions from six males and three females with a mean age of 38 yr. The most common site of involvement was the hand (including fingers) and the mean greater diameter was 19 mm. Typically the tumours were l
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16. Deposition of eosinophil cationic protein in vascular lesions in temporal arteritis.
The possible role of the eosinophil and its cytotoxic granule proteins in the vascular lesions seen in temporal arteritis was elucidated. Sixteen sections of biopsy specimens from arteria temporalis showing giant cell arteritis were stained for eosinophil cationic protein (ECP) by polyclonal antibodies and the immunoperoxidase method. Activated eosinophils w
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17. PTPN11 Mutations in Noonan Syndrome: Molecular Spectrum, Genotype-Phenotype Correlation, and Phenotypic Heterogeneity
Noonan syndrome (NS) is a developmental disorder characterized by facial dysmorphia, short stature, cardiac defects, and skeletal malformations. We recently demonstrated that mutations in PTPN11, the gene encoding the non–receptor-type protein tyrosine phosphatase SHP-2 (src homology region 2-domain phosphatase–2), cause NS, accounting for ∼50% of case
The American Society of Human Genetics.