Stroke is a devastating event that carries a potential for long-term disability. Malnutrition is frequently observed in patients with stroke, and dysphagia contributes to malnutrition risk. During both the acute phase of stroke and rehabilitation, specific nutritional interventions in the context of a multidisciplinary team effort can enhance the recovery of neurocognitive function. Early identification and management of malnutrition with dietary modifications or specific therapeutic strategies to ensure adequate nutritional intake should receive more attention, since poor nutritional status appears to exacerbate brain damage and to contribute to adverse outcome. The main purpose of nutritional intervention should be the prevention or treatment of complications resulting from energy-protein deficit. This paper reviews the evaluation and management of malnutrition and the use of specialized nutrition support in patients with stroke. Emphasis is given to enteral tube and oral feeding and to strategies to wean from tube feeding.

Patients with refractory or relapsed (R/R) B-acute lymphoblastic leukemia (B-ALL) and highly aggressive B-non-Hodgkin lymphoma (B-NHL) have very dismal prognosis and limited treatment options. The advent of chimeric antigen receptor (CAR) T-cells constitutes a milestone in current cell and gene therapies, covering the unmet need of treatment of high-risk patients and bringing immunotherapies one step closer towards cancer therapeutics, including hematological malignancies. CAR T-cells targeting CD19 antigen have shown startling remission rates in heavily pre-treated B-ALL and B-NHL patients, in whom CAR T-cell therapy may sometimes be their last treatment resort. However, a high proportion of these patients evade immune surveillance by CAR T-cells losing their initial deep responses, which leads to disease recurrence either as CD19 positive or CD19 negative relapse. As a result, many investigators have questioned the necessity of a consolidative allogeneic hematopoietic stem cell transplantation (allo-HCT) post-CAR T-cell therapy, once patients have achieved remission. However, there is much controversy about whether CAR T-cells should be a bridge therapy to allo-HCT or a definitive treatment due to the paucity of strong evidence-based data. In this context, we review the existing data regarding the necessity, safety and outcomes of allo-HCT undertaken after autologous anti-CD19 CAR T-cell therapy in B-ALL and B-NHL patients.

Background: Adiponectin, leptin, and resistin are the most well-studied adipokines and play important roles in the regulation of glucose metabolism, subclinical inflammation, and cardiovascular homeostasis. Accordingly, measurement of adipokine levels might be useful in cardiovascular risk stratification. Moreover, the study of single-nucleotide polymorphisms of genes that encode these adipokines might also represent a valuable predictive tool in cardiovascular disease prevention strategies. Aims: To summarize the biologic role of the adipokines adiponectin, leptin, and resistin and the prognostic value of their serum levels regarding the occurrence and outcome of ischemic stroke. We also discuss the relationship of single-nucleotide polymorphisms of the adiponectin, leptin genes, and the −420C > G polymorphism of resistin gene with stroke risk. Summary of review: Several studies in the general population evaluated the association between these adipokines and stroke risk, yielding conflicting results. There are more limited data regarding the effect of these adipokines on stroke severity and outcome. A small number of studies also assessed the predictive role of single-nucleotide polymorphisms of the adiponectin, leptin, and resistin genes regarding stroke risk, but the findings were also controversial. Conclusions: It is unclear whether adiponectin, leptin, and resistin levels or the single-nucleotide polymorphisms of their encoding genes are independently associated with stroke risk. However, given the role of these adipokines in the pathogenesis of atherosclerosis, larger prospective studies, both in the general population and in patients with a history of stroke, are needed to determine whether the measurement of serum levels of these adipokines or the evaluation of single-nucleotide polymorphisms in their encoding genes could improve stroke risk prediction. If this relationship is proven, therapeutic interventions targeting adipokine levels might represent a novel approach to reduce stroke-related mortality and disability.

It is unclear whether prior antidiabetic treatment affects stroke severity and outcome. To evaluate this association, we prospectively studied all patients who were admitted in our Department with acute ischaemic stroke (n = 378, mean age = 78.8 ± 6.5 years). The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale. The outcome was assessed with the modified Rankin Scale at discharge and with in-hospital mortality. A total of 123 patients had type 2 diabetes mellitus. At admission, there was a trend for lower National Institutes of Health Stroke Scale in patients treated with dipeptidyl peptidase 4 inhibitors compared with patients treated with other antidiabetic agents (6.1 ± 7.5 vs 10.0 ± 9.2, respectively; p = 0.079). At discharge, patients treated with dipeptidyl peptidase 4 inhibitors had lower modified Rankin Scale than patients treated with other antidiabetic agents (2.1 ± 1.9 vs 3.2 ± 2.1, respectively; p < 0.05). Patients treated with dipeptidyl peptidase 4 inhibitors also had lower in-hospital mortality than patients treated with other antidiabetic agents (0.0% vs 15.1%, respectively; p < 0.05). In conclusion, prior treatment with dipeptidyl peptidase 4 inhibitors in patients with acute ischaemic stroke appears to be associated with better functional outcome and lower mortality risk.

Chimeric antigen receptor (CAR) T-cell therapies have revolutionised the field of haematological malignancies by achieving impressive remission rates in patients with highly refractory haematological malignancies, improving overall survival. To date, six commercial anti-CD19 and anti-BCMA CAR T-cell products have been approved by the Food and Drug Administration (FDA) for the treatment of relapsed/refractory B-cell haematological malignancies and multiple myeloma. The indications for CAR T-cell therapies are gradually expanding, with these therapies being investigated in a variety of diseases, including non-malignant ones. Despite the great success, there are several challenges surrounding CAR T-cell therapies, such as non-durable responses and high-grade toxicities. In addition, a new safety concern was added by the FDA on 28 November 2023 following reports of T-cell malignancies in patients previously treated with either anti-CD19 or anti-BCMA autologous CAR T-cell therapies both in clinical trials and in the real-world setting. Since then, several reports have been published presenting the incidence and analysing the risks of other secondary malignancies after CAR T-cell therapies. In this opinion article, the current landscape of secondary malignancies after CAR T-cell therapies is presented, along with a proposed strategy for future research aiming at potentially diminishing or abrogating the risk of developing secondary malignancies after CAR T-cell therapies.