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Πέμπτη 2 Μαΐου 2019

Nuclear Medicine and Molecular Imaging

68 Ga-DOTANOC and 18 F-DOPA PET/CT: a site-specific approach to the imaging of parangliomas of the head and neck  and of the abdomen

Grade 3 anaphylactic shock after administration of [ 99m Tc]-labeled nanocolloidal albumin (Nanocoll ® ) for sentinel node scintigraphy

The potential for PET-guided revascularization of coronary artery disease

Is the effect of hyperglycemia on liver 18 F-FDG standardized uptake value really clinically significant?

Comment on: Relationship between the expression of PD-1/PD-L1 and 18 F-FDG uptake in bladder cancer

Unconventional immune-related phenomena observed using 18F-FDG PET/CT in Hodgkin lymphoma treated with anti PD-1 monoclonal antibodies

In response to: The validity of 18 F-GE180 as a TSPO imaging agent

The validity of 18 F-GE180 as a TSPO imaging agent

18F-Flurodeoxyglucose positron emission tomography with computed tomography (FDG PET/CT) findings in children with encephalitis and comparison to conventional imaging

Abstract

Purpose

FDG PET/CT is emerging as a new tool for the evaluation of acute encephalitis (AE). However, to date, there are no exclusively pediatric studies on the use of FDG PET for suspected AE. The objective of this study was to compare qualitative and quantitative brain PET to conventional brain imaging in a cohort of children, and to identify patterns of metabolic abnormalities characteristic of AE.

Methods

This retrospective study included 34 children imaged with PET/CT, CT and magnetic resonance imaging (MRI). The positivity rate of all three imaging modalities was measured. Besides visual assessment, quantification of relative regional brain metabolism (RRBM) was performed and compared to a database of normal pediatric brains.

Results

Fourteen subjects had a clinical diagnosis of autoimmune encephalitis (AIE) or encephalitis of unknown origin (EX), six of anti-N-methyl-D-aspartate receptor (anti-NMDAr) encephalitis, three of Hashimoto’s encephalopathy, three of neurolupus and eight had other subtypes of encephalitis.
Quantitative PET was abnormal in 100% of cases, visually assessed PET in 94.1% of subjects, MRI in 41.2% and CT in 6.9%. RRBM quantification demonstrated multiple hyper and hypo metabolic cortical regions in 82.3% of subjects, exclusively hypermetabolic abnormalities in 3%, and exclusively hypometabolic abnormalities in 14.7%. The basal ganglia were hypermetabolic in 26.5% of cases on visual assessment and in 58.8% of subjects using quantification.

Conclusion

In our pediatric population FDG PET was more sensitive than conventional imaging for the detection of AE, and basal ganglia hypermetabolism was frequently encountered.

Clinical significance of amyloid β positivity in patients with probable cerebral amyloid angiopathy markers

Abstract

Purpose

We investigated the frequency and clinical significance of amyloid β (Aβ) positivity on PET in patients with cerebral amyloid angiopathy (CAA).

Methods

We recruited 65 patients who met the modified Boston criteria for probable CAA. All underwent amyloid PET, MRI, APOE genotyping and neuropsychological testing, and we obtained information on MRI markers of CAA and ischemic cerebral small-vessel disease (CSVD). We investigated the CAA/ischemic CSVD burden and APOE genotypes in relation to Aβ positivity and investigated the effect of Aβ positivity on longitudinal cognitive decline.

Results

Among the 65 CAA patients, 43 (66.2%) showed Aβ PET positivity (Aβ+). Patients with Aβ+ CAA had more lobar microbleeds (median 9, interquartile range 2–41, vs. 3, 2–8; P = 0.045) and a higher frequency of cortical superficial siderosis (34.9% vs. 9.1%; P = 0.025), while patients with Aβ− CAA had more lacunes (1, 0–2, vs. 0, 0–1; P = 0.029) and a higher frequency of severe white matter hyperintensities (45.5% vs. 20.9%; P = 0.040). The frequency of ε4 carriers was higher in Aβ+ patients (57.1%) than in Aβ− patients (18.2%; P = 0.003), while the frequency of ε2 carriers did not differ between the two groups. Finally, Aβ positivity was associated with faster decline in multiple cognitive domains including language (P < 0.001), visuospatial function (P < 0.001), and verbal memory (P < 0.001) in linear mixed effects models.

Conclusion

Our findings suggest that a significant proportion of patients with probable CAA in a memory clinic are Aβ− on PET. Aβ positivity in CAA patients is associated with a distinct pattern of CSVD biomarker expression, and a worse cognitive trajectory. Aβ positivity has clinical relevance in CAA and might represent either advanced CAA or additional Alzheimer’s disease neuropathological changes.

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