Fibroid calcification after uterine artery embolization: Ultrasonographic appearance and pathology

Citation
Ta. Nicholson et al., Fibroid calcification after uterine artery embolization: Ultrasonographic appearance and pathology, J VAS INT R, 12(4), 2001, pp. 443-446
Citations number
10
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging
Journal title
JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
ISSN journal
10510443 → ACNP
Volume
12
Issue
4
Year of publication
2001
Pages
443 - 446
Database
ISI
SICI code
1051-0443(200104)12:4<443:FCAUAE>2.0.ZU;2-B
Abstract
PURPOSE: To describe the ultrasonographic (US) appearance of fibroid calcif ication occurring after uterine artery embolization (UAE) and discuss its e tiology and pathology. MATERIALS AND METHODS: Twenty-seven of a total of 38 patients were followed up clinically and with duplex US for longer than 6 months after UAE for ut erine fibroids. At US, changes in uterine size, fibroid vascularity, and mo rphology have been recorded. Pathologic studies were performed by one of th e authors on resected specimens from a different cohort of patients, at int ervals ranging from 4 months to 1 year after UAE. RESULTS: Twenty patients reported complete resolution of symptoms. In 16 of these, a reduction in fibroid volume of 70%-85% was recorded and, at US, t he development of a peripheral hyperechoic rim around an increasingly hypoe choic fibroid was noted. Computed tomography in two patients revealed it to be a rim of calcium. Histologic studies in a different cohort of patients who had undergone hysterectomy at variable intervals after UAE demonstrated early aggregation of polyvinyl alcohol (PVA) particles, an intermediate gi ant cell inflammatory reaction, and calcification in the periphery of the i nfarcted fibroid at 6-12 months. CONCLUSION: Calcification is the end stage of hyaline degeneration. However , its peripheral location is unlike that of natural fibroid involution and hyaline necrosis. Pathologic studies in resected human fibroids after embol ization suggest that its development is the end result of aggregation of PV A particles in peripheral fibroid arteries.