Background: Previous studies reported mitochondrial and endoplasmic reticulum redox stress in peripheral blood mononucleated cells (PBMCs) of treatment-naïve Hodgkin lymphoma (HL) patients. Here, we assessed whether this response also applies to non-HL (NHL) patients, and whether the oxidative damage is a selective feature of PBMCs or, rather, also affects tissues not directly involved in the inflammatory response. Methods: Isolated PBMCs of 28 HL, 9 diffuse large B cell lymphoma, 8 less aggressive-NHL, and 45 controls underwent flow cytometry to evaluate redox stress and uptake of the glucose analogue 2-NBDG. This analysis was complemented with the assay of malondialdehyde (MDA) levels and enzymatic activity of glucose-6P-dehydrogenase and hexose-6P-dehydrogenase (H6PD). In all lymphoma patients, ¹⁸F-fluoro-deoxyglucose uptake was estimated in the myocardium and skeletal muscles. Results: Mitochondrial reactive oxygen species generation and MDA levels were increased only in HL patients as well as H6PD activity and 2-NBDG uptake. Similarly, myocardial FDG retention was higher in HL than in other groups as opposed to a similar tracer uptake in the skeletal muscle. Conclusions: Redox stress of PBMCs is more pronounced in HL with respect to both NHL groups. This phenomenon is coherent with an increased activity of H6PD that also extends to the myocardium.

Prostate cancer still represents one of the most frequent cancers and causes of death worldwide, despite the huge therapeutic advances in the last decades. The introduction into clinical practice of prostate-specific membrane antigen positron emission tomography/computed tomography (PSMA PET/CT) has significantly improved diagnostic capacity, allowing for the identification of lesions previously undetectable. The case we are presenting is about a 90-year-old man affected by metastatic prostate cancer and treated with hormonal therapies. At the second progression, the restaging with PSMA PET/CT pointed out a millimetric cardiac intra-atrial metastasis, on which little/scarce literature data are still available. On one hand, this finding confirms the high sensitivity of this technique, which should be preferred over traditional imaging. On the other hand, it suggests that introducing next-generation imaging into clinical practice may provide novel insights about prostate cancer metastatic spread.

Background: Iatrogenic cerebral amyloid angiopathy (iCAA) is a rare form of CAA occurring decades after neurosurgical procedures involving cadaveric dural grafts. While typically associated with recurrent lobar intracerebral hemorrhages, recent reports suggest a possible overlap with CAA-related inflammation (CAAri). We report a case of iCAA with features indicative of active neuroinflammation that demonstrated a positive response to immunosuppressive therapy. Methods: Over a 12-year natural history, the patient underwent a comprehensive work-up, including serial clinical assessments, brain MRIs, core CSF biomarker analysis, amyloid PET imaging, and next-generation sequencing panel testing. Results: Previous clinical charts confirmed the use of cadaveric graft (Lyodura) in a neurosurgical intervention thirty years before. During hospitalization for seizures, brain MRI revealed, along with a severe form of CAA, an area of vasogenic edema. Given the suspicion of an active inflammatory process, corticosteroid and subsequent methotrexate maintenance therapy were introduced, leading to clinical and radiological improvement. Over 30 months of follow-up, the patient has remained clinically and radiologically stable, with no new hemorrhagic or inflammatory events. Conclusions: This case highlights the potential interplay between iCAA and neuroinflammation. The absence of new hemorrhages following immunosuppression suggests a possible disease-modifying effect, warranting further investigation into the role of neuroinflammation in iCAA and its therapeutic implications.