Sabrina Scilletta

Objective: Automated insulin delivery (AID) systems have significantly improved the management of type 1 diabetes (T1D), leading to better glycemic control and reduced hypoglycemia. However, older adults (≥ 65 years) remain underrepresented in clinical trials, and evidence specific to this population is limited. Design and patients: This narrative review synthesizes current evidence on the efficacy, safety, and usability of AID systems in older adults (≥ 65 years) with T1D. A comprehensive literature search of MEDLINE/PubMed was conducted using the PICO framework to identify relevant RCTs, observational studies, and systematic reviews, supplemented by literature studies on cognitive, functional, and psychosocial factors impacting technology adoption. Results: While data from randomized trials and meta-analyses in the general population consistently demonstrate improvements in time in range (TIR, 70–180 mg/dL) and reductions in hypoglycemia, evidence in older adults is still emerging. Frail individuals and those with multiple comorbidities are often underrepresented or excluded from current studies. Nevertheless, the available evidence suggests that many of these benefits are also maintained in older populations, particularly regarding hypoglycemia reduction. At the same time, factors such as cognitive impairment, functional limitations, caregiver dependence, and reduced digital literacy may affect the adoption and effective use of these technologies. Conclusions: AID systems appear effective and generally safe in selected older adults, with benefits in glycemic control and hypoglycemia reduction. However, given the marked heterogeneity of this population, further studies are needed to better define their role and applicability in routine clinical practice.

Diabetic gastroparesis (DGP) is a chronic and frequently underrecognized complication of diabetes mellitus, characterized by delayed gastric emptying in the absence of mechanical obstruction. It represents a clinically significant manifestation of diabetic autonomic neuropathy and arises from a complex interplay of sustained hyperglycemia, oxidative and nitrosative stress, advanced glycation end-product accumulation, impaired insulin/IGF-1 signaling, lipid dysmetabolism, and inflammatory activation. These mechanisms converge to damage autonomic and enteric neurons, reduce interstitial cells of Cajal density, and disrupt gastric smooth muscle function, ultimately leading to impaired and unpredictable gastric motility. Beyond gastrointestinal symptoms, DGP profoundly affects metabolic control. The altered timing and variability of gastric emptying disturb the physiological coordination between nutrient absorption and insulin pharmacokinetics, generating a temporal mismatch that predisposes patients to early postprandial hypoglycemia followed by late hyperglycemia. This pattern increases glycemic variability, complicates insulin dose adjustment, and contributes to oxidative stress and vascular risk. In this narrative review, we examine the current understanding of DGP pathophysiology and its clinical implications for insulin therapy. We discuss diagnostic strategies, nutritional interventions, and pharmacological treatments, with particular attention to insulin timing modulation. We also analyze the emerging role of diabetes technologies, including continuous glucose monitoring and automated insulin delivery systems, as well as future perspectives such as glucose-responsive insulins and regenerative approaches targeting gastric neuromuscular dysfunction. A mechanism-based, personalized therapeutic strategy may improve metabolic stability and patient outcomes.

Background/Objectives: An intensive lipid-lowering therapy is needed in familial hypercholesterolemia (FH) subjects; however, the adherence to the Mediterranean diet (MD) and its effects have not been fully evaluated in FH subjects. This study aimed to evaluate the impact of the MD on metabolic and vascular profiles in FH subjects. Methods: In this cross-sectional study 253 genetically confirmed FH subjects were included. Adherence to MD was assessed by the validated Pyramid-based MD Score (PyrMDS) and FH subjects were stratified according to the tertiles of PyrMDSs (low, intermediate, and high), with a higher score indicating higher adherence to MD. The lipid profile as well as the subendocardial viability ratio (SEVR), an indirect measure of myocardial perfusion, were assessed in all FH subjects. Results: Compared to the low-PyrMDS group, FH subjects with a high MD adherence showed lower levels of low-density lipoprotein cholesterol (LDL-C) (149.7 ± 71.4 vs. 176.7 ± 77.4 mg/dL, p = 0.006). After accounting for lipid-lowering therapies, smoking habit, and arterial hypertension, individuals in the high-PyrMDS group showed higher SEVR than those in the intermediate- and low-PyrMDS groups (167 ± 3.51 [standard error—SE] vs. 150 ± 5.03 [SE] vs. 148 ± 3.75 [SE], all p < 0.01). After adjusting for age, sex, and lipid-lowering therapies, PyrMDS was independently associated with LDL-C (β = −0.11, p = 0.03). Conclusions: Greater adherence to the MD was associated with more favorable metabolic and vascular profiles in FH subjects independent of lipid-lowering therapies. This suggests that MD adherence should be actively promoted in clinical practice alongside pharmacological interventions.

Background: Familial hypercholesterolemia (FH) is a genetic disorder characterized by elevated low-density lipoprotein-cholesterol (LDL-C) and increased cardiovascular risk. While the role of LDL-C in atherogenesis is well established, the contribution of inflammatory activation in FH, particularly in relation to genotype, remains poorly defined. We aimed to evaluate the impact of genotype on neutrophil-to-lymphocyte ratio (NLR) and on subclinical atherosclerosis in a cohort of FH subjects. Methods: We conducted a cross-sectional study on 423 FH subjects not on lipid-lowering therapy and free from atherosclerotic cardiovascular disease. Biochemical, genetic, and vascular assessments were performed in all participants. The population was divided into 2 groups based on genotype: low-density lipoprotein receptor (LDLR; n = 273) and non-LDLR (NLDLR, n = 150). Vascular profile was assessed by coronary artery calcium score and carotid/femoral plaque presence. NLR was calculated from peripheral blood counts. Results: The LDLR group exhibited an higher NLR (2.27 ± 0.86 vs 2.05 ± 0.68, P < .05) than the NLDLR group. LDL-C levels and LDLR genotype were significantly associated with NLR (both P < .05). Multiterritorial plaque involvement was more frequent in the LDLR group than the NLDLR group (P for trend <.05). Age (P < .001), LDL-C (P < .001), smoking status (P < .05), and NLR (P < .05) were independently associated with subclinical atherosclerosis. Conclusion: FH subjects with LDLR mutations had a higher NLR and a more severe atherosclerosis distribution. Our findings support the role of NLR as a noninvasive biomarker of early immune activation and highlights the importance of lipoinflammatory status evaluation in FH subjects.

Fatty liver disease has been identified as a marker of malnutrition in different clinical settings. Recently, the COntrolling NUTritional status score (CONUT score) emerged as a promising tool for malnutrition assessment. Our aim was to evaluate short-term outcomes among patients with malnutrition-related liver steatosis in an Internal Medicine department. Furthermore, we evaluated the association of the CONUT score with malnutrition-related liver steatosis. Data from 247 patients hospitalized in an Internal Medicine department were retrospectively collected. The study population was stratified into three groups based on hepatic radiodensity assessed with computed tomography: mild steatosis (≥56.1 HU), moderate steatosis (between 49.7 and 56 HU), and severe steatosis (≤49.6 HU). We then calculated the CONUT score. Severe steatosis patients had higher in-hospital mortality (18.2 vs. 15.5%) and longer in-hospital stays compared with the mild steatosis group (length of in-hospital stay longer than 12 days: 45% vs. 40%). Logistic regression analysis showed that severe steatosis was not significantly associated with in-hospital all-cause death, while a high CONUT score was an independent risk factor for sepsis. We found an independent relationship between malnutrition-associated liver steatosis and the CONUT score. These results identified the CONUT score as a tool for nutritional assessment of hospitalized patients.

The increasing utilization of Glucagon-like Peptide-1 receptor agonists (GLP-1 RAs) in managing type 2 diabetes mellitus has raised interest regarding their impact on thyroid function. In fact, while these agents are well known for their efficacy in glycemic control and weight management, their association with thyroid disorders requires clarification due to the complex interplay between thyroid hormones and metabolic pathways. Thyroid dysfunction commonly co-occurs with metabolic conditions such as diabetes and obesity, suggesting a profound interconnection between these systems. This review aims to contribute to a deeper understanding of the interaction between GLP-1 RAs and thyroid dysfunction and to clarify the safety of GLP-1 RAs in diabetic patients with thyroid disorders. By synthesizing existing evidence, this review highlights that, despite various studies exploring this topic, current evidence is inconclusive, with conflicting results. It is important to note that these drugs are relatively recent, and longer-term studies with larger sample sizes are likely needed to draw clearer conclusions. Currently, no existing guidelines provide definitive directions on this clinical issue; however, it is advisable to include thyroid function tests in the routine screening of diabetic patients, particularly those treated with GLP-1 Ras, with the goal of optimizing patient care and management.

The coronavirus disease 19 (COVID-19) emergency led to rearrangements of healthcare systems with a significant impact on those internal medicine departments that had not been converted to COVID-19 wards. A reduced number of departments, indeed, had to cope with the same number of patients along with a lack of management of patients’ chronic diseases. We conducted a retrospective study aimed at examiningthe consequences of the COVID-19 pandemic on internal medicine departments that were not directly managing COVID-19 patients. Data from 619 patients were collected: 247 subjects hospitalized in 2019 (pre-COVID-19 era), 178 in 2020 (COVID-19 outbreak era) and 194 in 2021 (COVID-19 ongoing era). We found that in 2020 in-hospital mortality was significantly higher than in 2019 (17.4% vs. 5.3%, p = 0.009) as well as length of in-hospital stay (LOS) (12.7 ± 6.8 vs. 11 ± 6.2, p = 0.04). Finally, we performed a logistic regression analysis of the major determinants of mortality in the entire study population, which highlighted an association between mortality, being bedridden (β = 1.4, p = 0.004), respiratory failure (β = 1.5, p = 0.001), glomerular filtration rate (β = −0.16, p = 0.03) and hospitalization in the COVID-19 outbreak era (β = 1.6, p = 0.005). Our study highlights how the COVID-19 epidemic may have caused an increase in mortality and LOS even in patients not directly suffering from this infection.