Background: To evaluate the association between glaucomatous visual field loss and self-reported driving limitation, and to explore potential threshold ranges of visual field loss associated with an increased likelihood of driving restriction. Methods: In this cross-sectional study, 100 patients with primary open-angle glaucoma underwent standard automated perimetry. Visual function was assessed using Mean Deviation (MD) and Visual Field Index (VFI) from the better eye. Driving status, driving limitation, and self-reported driving difficulties were assessed using a structured questionnaire. Multivariable logistic regression was performed to determine independent associations between visual field parameters and driving limitation, adjusting for age, sex, cataract status, and systemic comorbidities. Because MD and VFI are closely related indices of visual field loss, separate multivariable models were constructed for each parameter. Receiver operating characteristic (ROC) analysis was used to explore threshold values associated with driving limitation. Results: Driving limitation increased progressively with worsening functional severity, affecting 17% of participants with preserved function, 48% of those with borderline impairment, and 72% of those with definite impairment (p < 0.001). Reduced VFI was independently associated with driving limitation (OR = 0.972, 95% CI: 0.948–0.996; p = 0.021). In a separate model, more negative MD was also independently associated with driving limitation (OR = 0.924, 95% CI: 0.875–0.976; p = 0.004). Male sex was associated with a lower likelihood of driving limitation. ROC analysis identified threshold values of VFI ≤ 71% (AUC = 0.663) and MD ≤ −13.36 dB (AUC = 0.650), both characterized by high specificity but limited sensitivity. Participants who had ceased driving demonstrated worse visual field indices than active drivers, whereas never-drivers showed no consistent association with visual field loss. Conclusions: Glaucomatous visual field loss was significantly associated with self-reported driving limitation and behavioural self-regulation. Objective perimetric parameters, particularly VFI and MD in the better eye, may help identify patients more likely to report driving difficulties. The reported threshold values should be interpreted as exploratory reference points rather than clinically actionable criteria and require further validation before clinical application.

Acute lymphoblastic leukemia. According to the publication, the patient received a CODPL regimen followed by methotrexate, vindesine, and idarubicin (22 consolidation cycles). Two and a half years later, the boy developed a full-blown relapse treated with CD19-and CD22-targeted CAR-T cells. The second relapse, with extramedullary (non-CNS) involvement, occurred seven years after diagnosis. Treatment with inotuzumab ozogamicin followed by belimumab led to molecular remission, after which allogeneic hematopoietic stem cell transplantation (HSCT) from a 10/10 matched unrelated donor was performed using myeloablative TBI-containing (10 Gy) conditioning. In the post-transplant period, viral infections were noted (ADV, HHV-6, and H1N1). Against this background, on day +160 PLR developed. It significantly improved after injections of a drug referred to as "lezumab" in both eyes. On day +194 transplant-associated thrombotic microangiopathy (TA-TMA) was diagnosed.Throughout the post-transplant period, the patient demonstrated full donor chimerism.The presented case is well documented and clinically complex. At the same time, the interpretation proposed by the authors raises questions.The pathophysiology of PLR is currently still not well defined. The condition was described more than a hundred years ago; however, a unified concept of its development is lacking [2,3]. It is considered an ischemic injury of the retinal nerve fiber layer due to occlusion of peripapillary terminal arterioles caused by various factors, such as thrombosis or microembolization by fat emboli, leukocyte aggregation induced by different factors. PLR has been associated with numerous conditions, notably trauma (complement activation), acute pancreatitis (systemic release of proteases and lipase), and systemic lupus erythematosus (immune complexes), as well as numerous other disorders. They are often regarded as related comorbidities rather than a direct relationship, with at most a potential causal link, as the putative "triggers" are heterogeneous [4,5].In the present case, there are multiple factors previously associated with the development of PLR in the post-transplant setting. These include intensive multi-agent chemotherapy, radiation therapy, HSCT, immunotherapy, immunosuppressive treatment, viral infections. Under such conditions, it is difficult to identify a single causal factor, especially in the absence of a unified etiology, a well-defined pathogenetic mechanism, and the presence of only clinical diagnostic criteria.As indicated by the title, the primary focus of this article is CAR-T cell therapy. CAR-T cells were administered approximately 3 years prior to the onset of ophthalmologic symptoms. After subsequent allo-HSCT, complete donor chimerism in blood and bone marrow was achieved. Li et al. provided no evidence for persistence of CAR-T cells at the time of PLR onset, as no CAR-T-specific monitoring data were reported. Thus, there is no evidence of a cellular substrate for the hypothesized interaction. Therefore, the available evidence does not sufficiently support an association between prior CAR-T therapy and the development of PLR.At the same time, the authors estimated another mechanism of PLR development, in which a key role is assigned to complement activation. Complement may contribute to endothelial injury in PLR [6,7,8] but is not a direct mediator of CAR-T cytotoxicity [9],and its rise during cytokine release syndrome (absent in this patient) is limited to the early post-infusion period [10]. In the presented case PLR was diagnosed The only reported measurement of the terminal complement complex C5b-9 (298 ng/mL) was obtained in peripheral blood 34 days after PLR onset. This assessment was performed in the setting of clinically apparent TA-TMA, characterized by thrombocytopenia, proteinuria, renal dysfunction, and other manifestations of systemic endothelial injury. No serial measurements of complement activation markers or other complement components were reported.TA-TMA is characterized by endothelial injury, microvascular dysfunction, and thrombosis of small vessels. The retina is part of the microvascular bed and is susceptible to ischemic injury, similarly to the kidneys, brain, lungs, and gastrointestinal tract. In this context, the ophthalmologic findings warrant consideration within the broader spectrum of microangiopathic processes. Ocular involvement interpreted as PLR has been reported in primary thrombotic microangiopathies [11] and, although uncommon, also in association with TA-TMA. Notably, previously reported cases usually share several clinical features with the present patient, including young age, acute lymphoblastic leukemia or lymphoma, exposure to intensive multi-agent chemotherapy, HSCT, myeloablative conditioning, total body irradiation, and infectious complications [12,13,14,15]. Nevertheless, the available evidence remains limited, and the relationship between PLR and subsequent TA-TMA in the present case cannot be established with certainty.Therefore, the available data do not permit assessment of whether complement activation contributed to the development of PLR in this case and do not provide sufficient evidence to support complement activation as a leading mechanism underlying the retinal manifestations observed.A separate comment concerns the role of the TTC37 variant. Biallelic loss-of-function mutations in TTC37 cause autosomal recessive trichohepatoenteric syndrome (THES1, OMIM #222470)[16] often associated with antibody deficiency. In the present report, the patient was described as carrying a class II TTC37 variant associated with predominantly antibody deficiencies. No further information regarding the specific variant was provided. To date, no established association has been reported between heterozygous TTC37 variants and endothelial injury, complement activation, Purtscher-like retinopathy, transplant-associated thrombotic microangiopathy, or HSCT...

Circulating histones are increasingly recognised as biologically relevant components of extracellular chromatin, but their composition and treatment-associated dynamics in acute myeloid leukaemia (AML) remain poorly defined. In this prospective single-centre observational study, we profiled 13 histone measures by ImageStream imaging flow cy-tometry in 31 plasma samples from 15 newly diagnosed AML patients at diagnosis/day 7/day 28 (n=15/10/6), with 30 healthy controls and 12 patients with myelodysplastic neoplasms with increased blasts. At diagnosis, nine of 13 measures differed from controls after false discovery rate (FDR) correction, defining a bidirectional profile with higher H2A-, H2B- and macroH2A1-associated measures and lower H3, H4 and H3/H4; the largest differences included in-creased macroH2A1.1 (7.07% vs. 0.47%; δ=0.98) and reduced H4 (0.14% vs. 3.25%; δ=−0.87). By day 7, five measures remained FDR-significant, all decreasing: H4, H3/H4 and the three tetrameric complexes. At day 28, no paired comparison remained FDR-significant; however, H3/H4 showed a significant overall temporal change across the six complete serial trajectories (q = 0.0334). Exploratory day-28 trajectories showed concordant decreases in all three tetrameric complexes in complete remission, with opposite changes in residual disease. MDS with increased blasts showed higher macroH2A1-containing tetrameric complexes than controls and AML. These findings support disease- and treatment-associated redistribution of circulating histone populations across myeloid neoplasia.