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The Breast Imaging Reporting and Data System (BI-RADS) lexicon for ultrasonography (US) is based on the established lexicon used successfully in mammography and attempts to provide a common language to avoid ambiguity in interpreting, reporting, and teaching breast US. Proper and consistent use of the BI-RADS US lexicon has numerous advantages, including facilitating (a) communication of final assessment categories that clearly indicate management recommendations, (b) data tracking for self-audits, and (c) clinical review of outcome summaries. However, the literature to date does not include sufficient data on outcomes to validate clinical use of the BI-RADS US lexicon. In this article, a pictorial review of the BI-RADS US lexicon descriptors is provided, and specific cases from a retrospective review are used to highlight the challenges in using the BI-RADS US lexicon. With these examples, suggestions are offered for greater clarity in the use of this lexicon. The technical challenges in follow-up US imaging are described. The challenges in assigning final assessment categories are detailed, as well as the clinical factors that may influence decision making and the management of certain lesions.

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For patients with a palpable breast mass and a mTTS score of 3-4, no further assessment is necessary. Those with a mTTS of 8-9 can proceed to definitive therapy. Patients with a mTTS of 5-7 require further assessment. US and/or core biopsy added little to the accuracy or predictive value of the original TTS.

Our goal was to further define the role of LPL gene polymorphisms in coronary heart disease (CHD) risk. We determined the frequencies of three LPL polymorphisms (D9N, N291S, and S447X) in 899 men from the Veterans Affairs HDL Intervention Trial (VA-HIT), a study that examined the potential benefits of increasing HDL with gemfibrozil in men with established CHD and low high density lipoprotein cholesterol (HDL-C; р 40 mg/dl), and compared them with those of men without CHD from the Framingham Offspring Study (FOS). In VA-HIT, genotype frequencies for LPL D9N, N291S, and S447X were 5.3, 4.5, and 13.0%, respectively. These values differed from those for men in FOS having an HDL-C of Ͼ 40, who had corresponding values of 3.2% ( P ‫؍‬ 0.06), 1.5% ( P Ͻ 0.01), and 18.2% ( P Ͻ 0.01). On gemfibrozil, carriers of the LPL N9 allele in VA-HIT had lower levels of large LDL ( ؊ 32%; P Ͻ 0.01) but higher levels of small, dense LDL ( ؉ 59%; P Ͻ 0.003) than did noncarriers. Consequently, mean LDL particle diameter was smaller in LPL N9 carriers than in noncarriers (20.14 ؎ 0.87 vs. 20.63 ؎ 0.80 nm; P Ͻ 0.003). In men with low HDL-C and CHD: 1 ) the LPL N9 and S291 alleles are more frequent than in CHD-free men with normal HDL-C, whereas the X447 allele is less frequent, and 2 ) the LPL N9 allele is associated with the LDL subclass response to gemfibrozil. -Brousseau,

Objective. To determine whether sonography can be used to categorize some solid breast masses as probably benign so that biopsy can be deferred. Methods. We prospectively characterized 844 sonographically visible solid breast masses referred for biopsy. Mammographic and sonographic features of the masses were recorded, and all masses were categorized by American College of Radiology Breast Imaging Reporting and Data System classification before biopsy. Of the 844 masses, 148 were categorized as probably benign (Breast Imaging Reporting and Data System category 3). Sonographically guided biopsy (n = 804) or fine-needle aspiration (n = 40) was performed for pathologic correlation. Results. Of the 148 masses that met the sonographic criteria for probably benign masses, there was 1 malignancy, for a negative predictive value of 99.3%. Conclusions. Follow-up can be an acceptable alternative to biopsy for sonographically probably benign solid masses.

Tangier disease (TD), caused by mutations in the ATP-binding cassette 1 (ABC-1) gene, is a rare genetic disorder characterized by severe deficiency of high density lipoproteins (HDL) in the plasma, hypercatabolism of HDL, and defective apolipoprotein (apo)-mediated cellular cholesterol efflux. In the present study, we assessed plasma lipid concentrations, HDL particle size and subspecies, and cellular cholesterol efflux in 9 TD heterozygotes from a kindred in which the proband was homozygous for an A ¨ C missense mutation at nucleotide 5338 of the ABC-1 transcript. Relative to age-and gender-matched controls from the Framingham Offspring Study (FOS), TD heterozygotes had significant reductions ( P Ͻ 0.000) in HDL-C ( ؊ 54% female; ؊ 40% male) and apoA-I ( ؊ 33% female; ؊ 37% male) concentrations, as well as significantly less cholesterol ( ؊ 68% female; ؊ 58% male) distributed in the largest HDL subclasses, H5 and H4. Consequently, HDL particle size (nm) was significantly smaller ( P Ͻ 0.000) in TD heterozygotes (8.6 ؎ 0.6 female; 8.7 ؎ 0.1 male) relative to FOS controls (9.4 ؎ 0.4 female; 9.0 ؎ 0.3 male). Further studies demonstrated that apoA-I-mediated cellular cholesterol efflux in TD heterozygotes was essentially half that of controls (11 ؎ 2 vs. 20 ؎ 3% of total [ 3 H]cholesterol, P Ͻ 0.001), with strong correlations observed between cholesterol efflux and both HDL-C level (r ‫؍‬ 0.600) and particle size (r ‫؍‬ 0.680). In summary, our data demonstrate that apolipoprotein-mediated cholesterol efflux is aberrant in TD heterozygotes, as it is in homozygotes. This finding, along with the associations observed between HDL-C concentration, HDL particle size, and cholesterol efflux, supports the concept that plasma HDL-C levels are regulated, in part, by cholesterol efflux, which in turn influences HDL particle size and, ultimately, HDL apoA-I catabolism.

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