Purpose: To retrospectively assess endoleak shapes and locations within aneurysms to differentiate type II from type I and type III endoleaks.
Materials And Methods: The institutional review board granted an exemption for this HIPAA-compliant study; patient informed consent was not required. A retrospective review of arterial phase helical computed tomographic (CT) studies and medical records was performed for 39 patients (29 men, 10 women; age range, 60-89 years; mean, 78.5 years) who had an endoleak after endoaortic graft implantation for treatment of abdominal aortic aneurysm and who subsequently underwent angiography (n = 25), surgery (n = 8), or long-term follow-up (n = 6) to classify their endoleak into a specific type. At CT, endoleak shape (tubular or nontubular) and location (central or peripheral) were recorded. An endoleak was classified as type II if it contained a peripheral tubular component (PTC) near the aortic wall, with or without an identifiable feeding vessel. Endoleaks without these features were classified as type I or III. The Fisher exact test was used to assess associations between CT findings and endoleak type.
Results: There were 22 type II and 17 type I or III endoleaks. CT enabled correct identification of 22 (100%) of 22 type II endoleaks, all of which contained a PTC. Of 17 type I or III endoleaks, only two (12%) contained a PTC and were misclassified as type II endoleaks; the remaining 15 (88%) were correctly classified. Overall, CT enabled correct identification of endoleaks as type II or type I or III in 37 (95%) of 39 patients. PTCs were significantly more common (P < .001) in type II than in type I or III endoleaks, with a sensitivity, specificity, accuracy, negative predictive value, and positive predictive value of 100%, 88.2%, 94.9%, 100%, and 91.7%, respectively.
Conclusion: A PTC is a statistically significant predictor of type II endoleak in most patients.
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http://dx.doi.org/10.1148/radiol.2403051013 | DOI Listing |
Knee Surg Sports Traumatol Arthrosc
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Department of Molecular Medicine & Surgery, Stockholm Sports Trauma Research Center, Karolinska Institute, Stockholm, Sweden.
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Lysosomal storage disorders characterized by defective heparan sulfate (HS) degradation, such as Mucopolysaccharidosis type IIIA-D (MPS-IIIA-D), result in neurodegeneration and dementia in children. However, dementia is preceded by severe autistic-like behaviours (ALBs), presenting as hyperactivity, stereotypies, social interaction deficits, and sleep disturbances. The absence of experimental studies on ALBs' mechanisms in MPS-III has led clinicians to adopt symptomatic treatments, such as antipsychotics, which are used for non-genetic neuropsychiatric disorders.
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