Changes in CT utilization between 1981 and 1984: implications for Medicare payment for MR imaging under the prospective payment system

In the absence of data on current or likely patterns of use of magnetic resonance (MR) imaging, use of computed tomography (CT) at one institution in 1981 and 1984 was analyzed to provide data relevant to current federal deliberations regarding Medicare payment for inpatient MR imaging. Between 1981 and 1984 inpatient CT utilization increased 59%, primarily due to a 265% increase in body CT. In 1984 inpatients who underwent at least one CT procedure were as likely to undergo more than one procedure as to undergo only one. CT procedures were performed in a high proportion of diagnosis-related groups (DRGs), with more than one-half of head CT procedures performed in non-neurologic DRGs. Given the similarities between clinical applications of CT and MR imaging, these findings regarding CT utilization have the following implications: (a) a delay in recalibration of DRG payment rates may not take account of expected growth in utilization of MR imaging, (b) a DRG "add-on" for MR imaging should reflect the likelihood that more than one MR imaging procedure will be performed in many hospitalizations, and (c) adjustments in DRG payments for MR imaging should not be limited to the 35 neurologic DRGs.     

Quality assessment of randomized controlled trials of contrast media

Numerous randomized controlled trials (RCTs) have been conducted to define the relative benefits of low-osmolality contrast media (LOM) and high-osmolality contrast media (HOM). Because of the clinical and economic significance of the conclusions drawn from these RCTs, the authors used a standardized instrument to evaluate the quality of study design and data analysis of 100 RCTs published between 1982 and 1987 that compared LOM and HOM. The mean quality score (+/- standard deviation) was 39 +/- 12 (maximum possible score, 100). The largest number of patients studied in any RCT was 435; the smallest was five. A majority of the RCTs received high scores on three attributes of quality, intermediate scores on seven, and low scores on nine. These results underscore the difficulty of designing, performing, analyzing, and reporting high-quality RCTs. Nevertheless, limitations in study design and data analysis need to be considered when interpreting results of these RCTs. Future RCTs comparing LOM and HOM should be performed with greater attention to basic elements of good study design and data analysis.     

Utilization of a mutagenesis screen to generate mouse models of hyperaldosteronism

Primary aldosteronism is considered to be responsible for almost 10% of all cases of arterial hypertension. The genetic background of this common disease, however, has been elucidated only for the rare familial types, whereas in the large majority of sporadic cases, underlying mechanisms still remain unclear. In an attempt to define novel genetic loci involved in the pathophysiology of primary aldosteronism, a mutagenesis screen after treatment of mice with the alkylating agent N-ethyl-N-nitrosourea was established for the parameter aldosterone. As the detection method we used a time-resolved fluorescence immunoassay that allows the measurement of aldosterone in very small murine sample volumes. Based on this assay, we first determined the normal aldosterone values for wild-type C3HeB/FeJ mice under baseline conditions [92 ± 6 pg/ml for females (n = 69) and 173 ± 16 pg/ml for males (n = 55)]. Subsequently, aldosterone measurement was carried out in more than 2800 F(1) offspring of chemically mutagenized C3HeB/FeJ mice, and values were compared with aldosterone levels from untreated animals. Persistent hyperaldosteronism (defined as levels +3 sd above the mean of untreated animals) upon repeated measurements was present in seven female and two male F(1) offspring. Further breeding of these founders gave rise to F(2) pedigrees from which eight lines with different patterns of inheritance of hyperaldosteronism could be established. These animals will serve for detailed phenotypic and genetic characterization in the future. Taken together, our data demonstrate the feasibility of a phenotype-driven mutagenesis screen to detect and establish mutant mouse lines with a phenotype of chronic hyperaldosteronism.