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1.
Rev Neurol (Paris) ; 176(3): 194-199, 2020 Mar.
Article in English | MEDLINE | ID: mdl-31987628

ABSTRACT

PURPOSE: Intracranial plaque gadolinium enhancement revealed by high-resolution MRI imaging (HR MRI) is considered as a marker of plaque inflammation, a contributing factor of plaque unstability. The aim of the present study was to assess the distribution of gadolinium enhancement in intracranial atherosclerosis. METHODS: Single center analysis of ischemic stroke patients with intracranial atherosclerotic stenosis of M1 or M2 segments of middle cerebral artery, or terminal internal carotid artery (ICA) based on CT-angio or MR-angio. High-resolution MRI imaging (HRMRI) was performed within 6 first weeks following the index event, with 3DT2 BB (black-blood) and 3D T1 BB MR sequences pre and post-contrast administration. RESULTS: We identified 8 patients with 14 plaques, 4 were deemed non-culprit and 10 culprit. All culprit plaques (10/10 plaques) and 3 out of 4 non-culprit plaques showed a gadolinium enhancement. CONCLUSION: At the acute/subacute stage of stroke, a gadolinium enhancement may affect multiple asymptomatic intracranial plaques and may reflect a global inflammatory state.


Subject(s)
Arteries/diagnostic imaging , Image Enhancement/methods , Ischemic Stroke/diagnostic imaging , Magnetic Resonance Angiography/methods , Systemic Inflammatory Response Syndrome/diagnostic imaging , Aged , Aged, 80 and over , Arteries/metabolism , Arteries/pathology , Brain/blood supply , Brain/diagnostic imaging , Carotid Artery, Internal/diagnostic imaging , Carotid Artery, Internal/metabolism , Carotid Artery, Internal/pathology , Carotid Stenosis/diagnostic imaging , Carotid Stenosis/metabolism , Carotid Stenosis/pathology , Contrast Media/pharmacokinetics , Female , Gadolinium/pharmacokinetics , Humans , Intracranial Arteriosclerosis/diagnostic imaging , Intracranial Arteriosclerosis/metabolism , Ischemic Stroke/metabolism , Male , Middle Aged , Middle Cerebral Artery/diagnostic imaging , Middle Cerebral Artery/metabolism , Middle Cerebral Artery/pathology , Plaque, Atherosclerotic/diagnostic imaging , Plaque, Atherosclerotic/metabolism , Stroke/diagnostic imaging , Stroke/metabolism , Systemic Inflammatory Response Syndrome/metabolism
2.
Rev Neurol (Paris) ; 175(9): 534-543, 2019 Oct.
Article in English | MEDLINE | ID: mdl-31208813

ABSTRACT

INTRODUCTION: Currently, no single diagnostic modality allows the distinction between early progression (EP) and pseudo-progression (Psp) in glioblastoma patients. Herein we aimed to identify the characteristics associated with EP and Psp, and to analyze their diagnostic value alone and in combination. MATERIAL AND METHODS: We reviewed the clinical, conventional magnetic resonance imaging (MRI), and molecular characteristics (MGMT promoter methylation, IDH mutation, and EGFR amplification) of glioblastoma patients who presented an EP (n=59) or a Psp (n=24) within six months after temozolomide radiochemotherapy. We analyzed relative cerebral blood volume (rCBV) and relative vessel permeability on K2 maps (rK2) in a subset of 33 patients using dynamic-susceptibility-contrast MRI. RESULTS: In univariate analysis, EP was associated with neurological deterioration, higher doses of dexamethasone, appearance of a new enhanced lesion, subependymal enhancement, higher rCBV and rK2 values. Psp occurred earlier after radiotherapy completion and was associated with IDH1 R132H mutation, and MGMT methylation. In multivariate analysis, rCBV, rK2, and MGMT methylation status were independently associated with EP and Psp. All patients with a methylated MGMT promoter and a low rCBV (<1.75) were classified as Psp while all patients with an unmethylated MGMT promoter and a high rCBV (≥1.75) were classified as EP. Among patients with discordant MGMT methylation and rCBV characteristics, higher rK2 values tended to be associated with EP. CONCLUSION: Combined analysis of MGMT methylation, rCBV and vessel permeability on K2 maps seems helpful to distinguish EP from Psp. A prospective study is warranted to confirm these results.


Subject(s)
Brain Neoplasms/diagnosis , Brain Neoplasms/therapy , DNA Methylation , DNA Modification Methylases/genetics , DNA Repair Enzymes/genetics , Glioblastoma/diagnosis , Glioblastoma/therapy , Magnetic Resonance Imaging/methods , Tumor Suppressor Proteins/genetics , Adult , Aged , Biomarkers, Tumor/analysis , Biomarkers, Tumor/genetics , Brain Neoplasms/genetics , Brain Neoplasms/pathology , Chemoradiotherapy/adverse effects , Contrast Media , DNA Modification Methylases/analysis , DNA Repair Enzymes/analysis , Diagnosis, Differential , Disease Progression , Female , Follow-Up Studies , Glioblastoma/genetics , Glioblastoma/pathology , Humans , Male , Middle Aged , Predictive Value of Tests , Prognosis , Radiation Injuries/diagnosis , Radiation Injuries/genetics , Retrospective Studies , Time Factors , Treatment Outcome , Tumor Suppressor Proteins/analysis
3.
Ter Arkh ; 84(12): 120-4, 2012.
Article in Russian | MEDLINE | ID: mdl-23480003

ABSTRACT

The paper analyzes the most important clinical studies dealing with the measurement of procalcitonin concentrations in patients with lower respiratory tract infections or sepsis. Procalcitonin is a marker of bacterial infection, which is successfully used for diagnosis and antimicrobial therapy monitoring in patients with pneumonia or in septic states. The review presents the latest algorithms for interpreting the concentrations of procalcitonin in clinical practice.


Subject(s)
Algorithms , Anti-Bacterial Agents/therapeutic use , Calcitonin , Protein Precursors , Respiratory Tract Infections , Sepsis , Biomarkers/analysis , Biomarkers/blood , Calcitonin/analysis , Calcitonin/blood , Calcitonin Gene-Related Peptide , Drug Monitoring/methods , Early Diagnosis , Humans , Protein Precursors/analysis , Protein Precursors/blood , Randomized Controlled Trials as Topic , Respiratory Tract Infections/diagnosis , Respiratory Tract Infections/drug therapy , Respiratory Tract Infections/metabolism , Sepsis/diagnosis , Sepsis/drug therapy , Sepsis/metabolism
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