PurposeThe PET tracer [18F]florbetapir is a specific fibrillar amyloid-beta (Aβ) biomarker. During the late scan phase (> 40 min), it provides pathological information about Aβ status. Early scan phase (0–10 min) can provide FDG-‘like’ information. The current investigation tested the feasibility of using florbetapir as a dual-phase biomarker in behavioural variant frontotemporal dementia (bvFTD).MethodsEight bvFTD patients underwent [18F]florbetapir and [18]FDG-PET scans. Additionally, ten healthy controls and ten AD patients underwent florbetapir-PET only. PET data were acquired dynamically for 60-min post-injection. The bvFTD PET data were used to define an optimal time window, representing blood flow-related pseudo-metabolism (‘pseudo-FDG’), of florbetapir data that maximally correlated with the corresponding real FDG SUVR (40–60 min) in a composite neocortical FTD region.ResultsA 2 to 5-min time window post-injection of the florbetapir-PET data provided the largest correlation (Pearson’s r = 0.79, p = 0.02) to the FDG data. The pseudo-FDG images demonstrated strong internal consistency with actual FDG data and were also visually consistent with the bvFTD patients’ hypometabolic profiles. The ability to identify bvFTD from blind visual rating of pseudo-FDG images was consistent with previous reports using FDG data (sensitivity = 75%, specificity = 85%).ConclusionsThis investigation demonstrates that early phase florbetapir uptake shows a reduction of frontal lobe perfusion in bvFTD, similar to metabolic findings with FDG. Thus, dynamic florbetapir scans can serve as a dual-phase biomarker in dementia patients to distinguish FTD from AD and cognitively normal elderly, removing the need for a separate FDG-PET scan in challenging dementia cases.Electronic supplementary materialThe online version of this article (10.1007/s00259-018-4238-2) contains supplementary material, which is available to authorized users.

Background: ACE angioedema has not been characterized in comparison with angioedema from other causes in acute hospitalized patients. Methods: We retrospectively compared ACE-angioedema and non-ACE angioedema patients from January 2013 to May 2017. Results: Of 855 cases screened, 575 met the inclusion criteria of angioedema diagnosis and an electronic medical record. Of these, 297 (51.7%) had ACE angioedema and 278 had angioedema from other causes, of these 31 who were taking an ACE inhibitor that was not considered to be the cause of angioedema (ACE other cause). At least 80% of cases in all groups were African American. Epinephrine was prescribed in 21% of ACE angioedema cases. One-third of patients in all groups were admitted to the ICU, and about 25% required intubation. Previous history of ACE inhibitor-induced angioedema was found in 63 of 278 non-ACE cause angioedema patients (23%) and in 23 (8%) in the ACE cause group. Conclusion: ACE angioedema was the cause of half of angioedema admissions over a 4.5-year period. Mortality, morbidity, and treatment did not differ between the groups. Patients on ACE inhibitors were often treated with medications known not to be effective for ACE angioedema. Over one-fourth of patients not taking an ACE inhibitor had a previous history of ACE angioedema, and 31 patients taking ACE inhibitors were diagnosed with non-ACE angioedema. Regardless of the etiology of angioedema, 25% of patients required airway protection in the form of intubation.