[¹⁸F]FDG PET/CT enables in vivo quantification of cerebral glucose metabolism, revealing functional abnormalities before morphological changes on CT or MRI. This review summarizes major clinical indications, methodological aspects, and key metabolic patterns. In cognitive impairment, [¹⁸F]FDG PET is a core biomarker within the amyloid/tau/neurodegeneration (A/T/N) framework, predicting conversion from mild cognitive impairment (MCI) to Alzheimer’s disease (AD) and differentiating AD, dementia with Lewy bodies (DLB), frontotemporal lobar degeneration (FTLD), vascular dementia, and atypical parkinsonian syndromes (APS). In movement disorders, it distinguishes Parkinson’s disease (PD) from APS – including multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS) – and supports prognosis in amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD). In epilepsy, interictal hypometabolism aids localization of the epileptogenic zone, especially in MRI- negative cases, while in neuro-oncology, [¹⁸F]FDG PET assists in primary central nervous system lymphoma (PCNSL), glioma grading, and recurrence assessment. The review also highlights roles in inflammatory and infectious diseases, such as autoimmune encephalitis, neurosarcoidosis, and post-coronavirus disease 2019 (COVID-19) sequelae. Standardized preparation, glucose control, and statistical comparison with normal databases remain essential for accurate interpretation.
(1) Background: The aim of this retrospective observational study was to evaluate the effects of sodium–glucose cotransporter-2 inhibitors (SGLT2i) therapy in patients with chronic kidney disease (CKD) who had been receiving renin–angiotensin– aldosterone system (RAAS) inhibitor (RAASi) treatment for at least one year. (2) Methods: The medical records of 73 patients with CKD, staged according to the KDIGO 2012 guidelines, were reviewed at the start of combined therapy (RAASi and SGLT2i), marked as T0, and again after six months (T1). Biochemical parameters assessed at both time points included urinary albumin-to-creatinine ratio (UACR), estimated glomerular filtration rate (eGFR), urinary albumin, urinary proteinuria, serum creatinine, and hemoglobin. (3) Results: A significant reduction in UACR (p < 0.001) and 24-hour urine albumin excretion (p = 0.050) was observed. Urine protein/24h (p = 0.074) and serum creatinine (p = 0.391) showed decreasing trends, while eGFR increased (p = 0.154), although these changes did not reach statistical significance. Regarding UACR category migration, 25% of patients improved, 74% remained stable, and only 1% worsened. (4) Conclusions: After six months of combined SGLT2i and RAASi therapy, most patients showed stable or improved renal status, suggesting a nephroprotective effect of dual therapy in CKD.
Background: Patent foramen ovale (PFO) is an anatomical variant in which the normal fetal interatrial passage persists after birth. It is estimated to be present in approximately 25% of adults. Furthermore, it appears to be involved in 50% of cryptogenic strokes. A cryptogenic stroke means the etiology remains unknown despite a thorough assessment (including arterial imaging, echocardiography, rhythm monitoring, and relevant laboratory testing, such as lipid profile and hemoglobin A1c). Secondary prevention options after a PFO-associated stroke consist of antiplatelet therapy, anticoagulant therapy, or percutaneous closure of the PFO, and it is still debatable which option is better. Objective: To critically review the available evidence regarding PFO closure vs. medical therapy as the optimal therapeutic option for secondary prevention after PFO-associated cryptogenic stroke, and to discuss relevant factors for patient selection. Methods: We conducted a focused review and searched the PubMed database for relevant literature on the subject. We included records about patients with PFO and a history of stroke. We chose to include only the free full-text sources. On the other hand, studies regarding children, studies comparing different devices or techniques, and observational studies on long-term complications and recurrence predictors were excluded. Results: Eight records were included, comprising 3750 participants, all diagnosed with PFO and stroke, to compare different therapeutic strategies for preventing stroke recurrence (PFO closure versus medical therapy). Conclusions: The results indicated that closure of PFO may provide greater protection against recurrent stroke than medical therapy alone in adequately selected patients with PFO-associated cryptogenic stroke. Additionally, given the lack of recent studies, further research is warranted to improve patient selection and evaluation of medium- and long-term prognosis.
