WHAT'S KNOWN ON THIS SUBJECT: Previous studies have confirmed feasibility of MRI for diagnosis of appendicitis in adults and children. No study has assessed clinical end points when using ultrasound and MRI compared with computed tomography for diagnosis of appendicitis in children.WHAT THIS STUDY ADDS: Radiation-free imaging with ultrasound selectively followed by MRI does not change clinical endpoints compared with CT for diagnosing appendicitis in children, with no difference in time to antibiotic administration, time to appendectomy, negative appendectomy rate, perforation rate, or length of stay. abstract BACKGROUND: Cross-sectional imaging increases accuracy in diagnosing appendicitis. We hypothesized that a radiation-free imaging pathway of ultrasonography selectively followed by MRI would not change clinical end points compared with computed tomography (CT) for diagnosis of acute appendicitis in children. METHODS:We retrospectively reviewed children (,18 years old) who had diagnostic imaging for suspected acute appendicitis between November 2008 and October 2012. Before November 2010 CT was used as the primary imaging modality (group A); subsequently, ultrasonography was the primary imaging modality followed by MRI for equivocal findings (group B). Data collected included time from triage to imaging and treatment and results of imaging and pathology.RESULTS: Six hundred sixty-two patients had imaging for suspected appendicitis (group A = 265; group B = 397, of which 136 [51%] and 161 [41%], respectively, had positive imaging for appendicitis). Negative appendectomy rate was 2.5% for group A and 1.4% for group B. Perforation rate was similar for both groups. Time from triage to antibiotic administration and operation did not differ between groups A and B. There was higher proportion of positive imaging and appendectomies in group A and thus more negative imaging tests in group B (ultrasonography and MRI), but diagnostic accuracy of the 2 imaging pathways was similar. CONCLUSIONS:In children with suspected acute appendicitis, a radiationfree diagnostic imaging of ultrasonography selectively followed by MRI is feasible and comparable to CT, with no difference in time to antibiotic administration, time to appendectomy, negative appendectomy rate, perforation rate, or length of stay.
Lymphatic malformations (LMs) are vascular anomalies thought to arise from dysregulated lymphangiogenesis. These lesions impose a significant burden of disease on affected individuals. LM pathobiology is poorly understood, hindering the development of effective treatments. In the present studies, immunostaining of LM tissues revealed that endothelial cells lining aberrant lymphatic vessels and cells in the surrounding stroma expressed the stem cell marker, CD133, and the lymphatic endothelial protein, podoplanin. Isolated patient-derived CD133+ LM cells expressed stem cell genes (NANOG, Oct4), circulating endothelial cell precursor proteins (CD90, CD146, c-Kit, VEGFR-2), and lymphatic endothelial proteins (podoplanin, VEGFR-3). Consistent with a progenitor cell identity, CD133+ LM cells were multipotent and could be differentiated into fat, bone, smooth muscle, and lymphatic endothelial cells in vitro. CD133+ cells were compared to CD133− cells isolated from LM fluids. CD133− LM cells had lower expression of stem cell genes, but expressed circulating endothelial precursor proteins and high levels of lymphatic endothelial proteins, VE-cadherin, CD31, podoplanin, VEGFR-3 and Prox1. CD133− LM cells were not multipotent, consistent with a differentiated lymphatic endothelial cell phenotype. In a mouse xenograft model, CD133+ LM cells differentiated into lymphatic endothelial cells that formed irregularly dilated lymphatic channels, phenocopying human LMs. In vivo, CD133+ LM cells acquired expression of differentiated lymphatic endothelial cell proteins, podoplanin, LYVE1, Prox1, and VEGFR-3, comparable to expression found in LM patient tissues. Taken together, these data identify a novel LM progenitor cell population that differentiates to form the abnormal lymphatic structures characteristic of these lesions, recapitulating the human LM phenotype. This LM progenitor cell population may contribute to the clinically refractory behavior of LMs.
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