PubMed HealthSearch

PubMed · 9023693

Thyroid autonomy with color-coded image-directed Doppler sonography: internal hypervascularization for the recognition of autonomous adenomas.

Abstract

In a prospective study, we assessed the possibility of recognizing autonomous adenomas of the thyroid with color-coded image-directed Doppler sonography using internal hypervascularization in thyroid nodules for identification. Fifty-three patients with thyroid nodules underwent additional CCDS examination and nuclear scintigraphy (reference). Of 29 patients having autonomous adenomas, 28 patients presented internal hypervascularization in their nodules resulting in a sensitivity of 96% and a specificity was 75%. Interestingly CCDS detected six adenomas in patients showing normal laboratory data (bTSH, TT3, FT4). CCDS could be used to exclude focal adenomas with a negative predictive value of 94%. The positive predictive value for adenoma was 82%.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D Becker, H J Bair, W Becker, E Günter, W Lohner, S Lerch, E G Hahn. 1997. Thyroid autonomy with color-coded image-directed Doppler sonography: internal hypervascularization for the recognition of autonomous adenomas.. https://doi.org/10.1002/(sici)1097-0096(199702)25%3A2%3C63%3A%3Aaid-jcu3%3E3.0.co%3B2-h

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

HMGA proteins up-regulate CCNB2 gene in mouse and human pituitary adenomas.

The high mobility group As (HMGAs) belong to a family of nonhistone nuclear proteins that orchestrate the assembly of nucleoprotein complexes. Through a complex network of protein-DNA and protein-protein interaction, they play important roles in gene transcription, recombination, and chromatin structure. This protein family is involved, through different mechanisms, in both benign and malignant neoplasias. We have recently reported that transgenic mice carrying the Hmga1 or Hmga2 genes under transcriptional control of the cytomegalovirus promoter develop pituitary adenomas secreting prolactin and growth hormone. We have shown that the mechanism of the HMGA2-induced pituitary adenoma is based on the increased E2F1 activity. The expression profile of mouse normal pituitary glands and adenomas induced in HMGA transgenic mice revealed an increased expression of the ccnb2 gene, coding for the cyclin B2 protein, in the neoplastic tissues compared with the normal pituitary gland. Here, we show, by electrophoretic mobility shift assay and chromatin immunoprecipitation, a direct binding of HMGA proteins to the promoter of ccnb2 gene, whereas luciferase assays showed that HMGAs are able to up-regulate ccnb2 promoter activity. Finally, we report an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression. Because cyclin B2 is involved in the regulation of the cell cycle, these results taken together indicate that HMGA-induced cyclin B2 overexpression gives an important contribution to experimental and human pituitary tumorigenesis.

Adenoma

Forced expression of Id-1 in the adult mouse small intestinal epithelium is associated with development of adenomas.

Ids are dominant-negative helix-loop-helix (HLH) proteins that play overlapping yet distinct roles in antagonizing basic HLH transcription factors. Although Ids affect myogenesis, neurogenesis, and B-cell development, little is known about their in vivo functions in epithelia. We have examined the effects of forced expression of Id-1 in the small intestinal epithelium of adult chimeric mice. 129/Sv embryonic stem cells, transfected with DNA containing Id-1 under the control of transcriptional regulatory elements that function in all intestinal epithelial cell lineages, were introduced into C57Bl/6 (B6) blastocysts heterozygous for the ROSA26 marker. The B6 ROSA26/+ intestinal epithelium of the resulting adult chimeras produces Escherichia coli beta-galactosidase, allowing identification of this internal control cell population. Chimeras produced from nontransfected embryonic stem cells served as additional controls. Immunohistochemical studies of the control chimeras indicated that the small intestinal epithelium supports a complex pattern of endogenous Id expression. Id-1 is restricted to the cytoplasm; levels do not decrease as descendants of multipotent intestinal stem cells differentiate. Id-2 and Id-3 are only detectable in nuclei; levels increase markedly as epithelial cells differentiate. Forced expression of Id-1 in the 129/Sv epithelium results in a decline in Id-2 and Id-3 to below the limits of immunodetection. A subset of chimeric-transgenic mice lacked growth factor- and defensin-producing Paneth cells in their 129/Sv epithelium and also developed intestinal adenomas. These changes were not present in normal control chimeras. Adenomas were composed of proliferating beta-Gal-positive and -negative epithelial cells, suggesting that they arose through cooperative interactions between 129/Sv(Id-1) and B6 ROSA26/+ cells. These chimeras provide a model for studying how perturbations in Id expression affect tumorigenesis.

Adenoma

Pathophysiological relationships between lower urinary tract symptoms and the prostate do not strengthen over time.

BACKGROUND: The aim of this survey was to examine the relationships among baseline prostate gland volume and changes in urinary symptomatology 3 years later. METHODS: A Scottish community-based cohort of 193 men aged 40-79 years who had prostate volume measured by transrectal ultrasound (TRUS) were followed-up at 3 years. RESULTS: Only baseline nocturia correlated with prostate volume (r = 0.202, P = 0.0057), although some relationships existed for the antero-posterior dimension of the prostate gland. More statistically significant relationships were evident for adenoma volume rather than prostate volume, but they still had relatively low correlations (range, 0.19-0.31). CONCLUSIONS: This study demonstrates the lack of relationships between prostate gland variables and lower urinary tract symptoms (LUTS). Those relationships that are statistically significant (at the P < 0.01 level) are weak, and only explain at most 9% of the total variation of prostate or adenoma volume or their dimensions.

Adenoma