Incidental Coronary Artery Calcification Seen on Low-Dose Computed Tomography Is a Risk Factor for Obstructive Coronary Artery Disease in Patients Undergoing Liver Transplant.

Incidental arterial calcification (Ca) on low-dose computed tomography (CT) prior to liver transplant (LT) may help identify those at risk for obstructive coronary artery disease (CAD). A single-center retrospective study of 358 consecutive patients who had undergone LT was performed. Of the 296 patients who met inclusion criteria, 193 patients (65.2%) had CT Ca. Aortic Ca was seen in 116 (39.2%), coronary Ca in 141 (47.6%), and peripheral Ca in 8 patients (2.7%). Patients with coronary Ca were assigned ordinal coronary artery Ca scores and classified as mild, moderate, and severe. All-cause mortality was higher in patients with Ca in any location (14.5% vs 6.8%, P = .05). Of the patients who underwent coronary angiography, those with obstructive CAD were more likely to have aortic and coronary Ca than patients with nonobstructive or no CAD (85.7% vs 50.0%, P = .02 and 92.9% vs 37.9%, P = < .001, respectively). Severe coronary artery Ca scores were more frequent in patients with obstructive CAD (35.7% vs 0%, P < .001). Any severity coronary Ca had an odds ratio of 11.57 (95% CI, 1.61-244.92; P = .04) for obstructive CAD. In conclusion, incidental coronary Ca seen on low-dose CT is a risk factor for obstructive CAD in patients undergoing LT.

Differences in PTH (1-84) release in response to ambient calcium concentrations of parathyroid adenoma fragments and dispersed parathyroid adenoma cells in culture.

In a previous study we observed that during perfusion of normal human parathyroid tissue, the release of PTH (1-84) was modulated by ambient extracellular calcium (Ca++) and lithium (Li+) concentrations in the media and preliminary studies indicated that this stimulus-response coupling was absent in human parathyroid adenoma fragments. The present study compares the responsiveness of parathyroid adenoma fragments and isolated parathyroid adenoma cells from the same adenoma and their response to Ca++ changes and Li+ presence in culture media. The data indicate that parathyroid adenoma tissue fragments fail to respond to ambient changes in Ca++ and Li+. In contrast, dispersed parathyroid cells preparations responded with a significant increase of PTH (1-84) release (50%) under the influence of low ambient calcium concentrations. Six of the dispersed cell preparations also responded with a 45% decrease in PTH release under the influence of a high Ca concentration in the medium. Isolated parathyroid cells obtained from the same adenoma's did not respond to the presence of Li++ in the medium. These data suggest tat human parathyroid adenoma tissue functions autonomously and is not sensitive to calcium regulation in the tissue configuration as opposed to the isolated cell suspensions. The nature of this difference remains elusive.

Effects of 13 cis-retinoic acid on growth and differentiation of human follicular carcinoma cells (UCLA R0 82 W-1) in vitro.

Dedifferentiation of human thyroid tumors is frequently found in humans. The effect of retinoids (13 cis-RA) was studied on the proliferation and differentiation of a human follicular cell line in vitro (UCLA R0 82 W-1). A significant and dose-dependent reduction (P less than 0.001) in cell number and [3H] thymidine uptake was found in cells exposed to 13 cis-RA up to 10 microM. Higher concentrations of 13 cis-RA, however, led to a dose-dependent restoration of cell proliferation. Various parameters of differentiation increased under the influence of 13 cis-RA (10 microM) over nonexposed cells. The 125I uptake increased 4-fold over that in control nonexposed cells (P less than 0.05). [125I] Epidermal growth factor binding increased 5-fold, and [125I] human TSH binding increased significantly after exposure to 13 cis-RA (P less than 0.02). Deiodinase activity, however, was significantly lower in 13 cis-RA exposed cells than in control cells. The present study shows that 13 cis-RA (10 microM) drives the tumor cells toward a more normal state of proliferation and differentiation.