Regression of an enchondroma: a case report and proposed etiology.

Enchondromas are common benign bone lesions that are found in the medullary cavity of tubular bones, usually at the metaphysis. Regression is highly unusual, and loss of matrix mineralization in an existing enchondroma should prompt investigation for malignant transformation. We present the case of a 50-year-old woman with an enchondroma of the proximal humeral metadiaphysis, which underwent loss of matrix mineralization that corresponded to replacement with marrow fat on MRI. This transformation of the cartilage tumor matrix into normal bone marrow may occur in a process similar to that seen with endochondral ossification.

Clinical usefulness of adjusted D-dimer cut-off values to exclude pulmonary embolism in a community hospital emergency department patient population.

BACKGROUND: Plasma D-dimer measurement is used in the assessment of the clinical probability of pulmonary embolism (PE), in order to minimize the requirement for pulmonary computed tomography angiography (CTA). PURPOSE: To evaluate whether doubling the threshold value of serum D-dimer from 500 µg/L to 1000 µg/L could safely reduce utilization of pulmonary CTA to exclude PE in our emergency department patient population. MATERIAL AND METHODS: Emergency department patients evaluated for PE with a quantitative D-dimer assay and pulmonary CTA were eligible for inclusion. D-dimer values were retrospectively collected in all included patients. Pulmonary CT angiograms were reviewed and scored as positive or negative for PE. Receiver-operating characteristic (ROC) analysis was used to determine the accuracy of quantitative D-dimer measurements in differentiating between positive and negative PE patients as per CTA. RESULTS: A total of 237 consecutive patients underwent pulmonary CTA and had a D-dimer measurement performed. Median D-dimer level was 1007 µg/L and in 11 (5%) patients the pulmonary CT CTA was positive for PE. The ROC curve showed an area under the curve (AUC) of 0.91 (P < 0.0001). Increasing the D-dimer threshold value of 500 µg/L to 1000 µg/L increased the specificity from 8% to 52% without changing the sensitivity. CONCLUSION: Adjusting the D-dimer cut-off value for the emergency department community population and patient age increases the yield and specificity of the ELISA D-dimer assay for the exclusion of PE without reducing sensitivity.

Neuronal HIF-1 alpha protein and VEGFR-2 immunoreactivity in functionally related motor areas following a focal M1 infarct.

Clinical and experimental data support a role for the intact cortex in recovery of function after stroke, particularly ipsilesional areas interconnected to the infarct. There is, however, little understanding of molecular events in the intact cortex, as most studies focus on the infarct and peri-infarct regions. This study investigated neuronal immunoreactivity for hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2) in remote cortical areas 3 days after a focal ischemic infarct, as both HIF-1alpha and VEGFR-2 have been implicated in peri-infarct neuroprotection. For this study, intracortical microstimulation techniques defined primary motor (M1) and premotor areas in squirrel monkeys (genus Saimiri). An infarct was induced in the M1 hand representation, and immunohistochemical techniques identified neurons, HIF-1alpha and VEGFR-2. Stereologic techniques quantified the total neuronal populations and the neurons immunoreactive for HIF-1alpha or VEGFR-2. The results indicate that HIF-1alpha upregulation is confined to the infarct and peri-infarct regions. Increases in VEGFR-2 immunoreactivity occurred; however, in two remote regions: the ventral premotor hand representation and the M1 hindlimb representation. Neurons in these representations were previously shown to undergo significant increases in VEGF protein immunoreactivity, and comparison of the two data sets showed a significant correlation between levels of VEGF and VEGFR-2 immunoreactivity. Thus, while remote areas undergo a molecular response to the infarct, we hypothesize that there is a delay in the initiation of the response, which ultimately may increase the 'window of opportunity' for neuroprotective interventions in the intact cortex.