Pregnancy complications associated with thrombophilia represent significant risks for maternal and fetal health, leading to adverse outcomes such as pre-eclampsia, recurrent pregnancy loss, and intra-uterine growth restriction (IUGR). They are caused by disruptions in key physiological processes, including the coagulation cascade, trophoblast invasion, angiogenesis, and immune control. Recent advancements in epigenetics have revealed that non-coding RNAs, especially microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and extracellular vesicles (EVs) carrying these RNAs, play crucial roles in the regulation of these biological processes. This review aims to identify the epigenetic biomarkers that are the best candidates for evaluating thrombophilia-related pregnancy complications and for assessing the efficacy of anticoagulant and antiaggregant therapies. We emphasize their potential integration into personalized treatment plans, aiming to improve the risk assessment and therapy strategies for thrombophilic pregnancies. Future research should focus on validating these epigenetic biomarkers and establishing standardized protocols to enable their integration into clinical practice, paving the way for a precision medicine approach in obstetric care.

Optimal glycemic control without the presence of diabetes-related complications is the primary goal for adequate diabetes management. Recent studies have shown that hemoglobin A1c level cannot fully evaluate diabetes management as glycemic fluctuations are demonstrated to have a major impact on the occurrence of diabetes-related micro- and macroangiopathic comorbidities. The use of continuous glycemic monitoring systems allowed the quantification of glycemic fluctuations, providing valuable information about the patients’ glycemic control through various indicators that evaluate the magnitude of glycemic fluctuations in different time intervals. This review highlights the significance of glycemic variability by describing and providing a better understanding of common and alternative indicators available for use in clinical practice.

Background and Objectives: This retrospective cohort study investigates the role of genetic thrombophilia in pregnant women experiencing early pregnancy loss compared to those with late pregnancy loss. Materials and Methods: Participants were categorized into early and late pregnancy loss groups based on gestational age. A total of 156 patients were included, out of which 103 had early-trimester pregnancy losses and 96 had multiple miscarriages. Results: The study revealed a synergistic effect of Factor V Leiden (FVL G1691A) and Methylenetetrahydrofolate Reductase (MTHFR C677T) mutations (coefficient 3.42). Prothrombin (PT) G20210A and β-Fibrinogen 455 G>A mutations exhibited a significant interaction (coefficient 1.98). Additionally, MTHFR A1298C and Plasminogen Activator Inhibitor-1 (PAI-1 4G/5G) mutations showed a significant interaction (coefficient 1.65). FVL G1691A and Endothelial Protein C Receptor (EPCR) allele A1/A2 mutations also demonstrated a significant association (coefficient 2.10). Lastly, MTHFR C677T and Glycoprotein IIb/IIIa T1565C mutations interacted significantly (coefficient 1.77). Risk factor analysis identified several mutations associated with early pregnancy loss, including PAI-1 4G/5G homozygous (OR 3.01), FVL G1691A heterozygous (OR 1.85), and MTHFR A1298C heterozygous (OR 1.55). Both homozygous and heterozygous MTHFR C677T mutations were significant risk factors (OR 2.38; OR 2.06), as was PT G20210A homozygous mutation (OR 1.92). The PAI-1 4G/4G homozygous variant posed a risk (OR 1.36). Late pregnancy loss was associated with MTHFR A1298C homozygous mutation (OR 3.79), β-Fibrinogen 455 G>A heterozygous mutation (OR 2.20), and MTHFR A1298C heterozygous mutation (OR 2.65). Factor XIII G1002T heterozygous mutation (OR 1.18) and PAI-1 4G/5G homozygous mutation (OR 2.85) were also significant risk factors. EPCR allele A1/A2 (OR 1.60) and A2/A3 (OR 1.73) mutations were identified as significant risk factors for late pregnancy loss. Furthermore, FVL G1691A homozygous mutation, PT G20210A homozygous mutation, MTHFR C677T heterozygous mutation, MTHFR A1298C heterozygous mutation, and EPCR allele A1/A2 were identified as significant risk factors for multiple miscarriage. Conclusions: This study highlights significant interactions and risk factors related to genetic thrombophilia mutations in different types of pregnancy loss, contributing valuable insights for miscarriage management guidelines.

Background: Glycemic variability (GV) is a novel parameter used in evaluating the quality of diabetes management. Current guidelines recommend the use of GV indexes alongside the traditional parameter to evaluate glycemic control: hemoglobin A1c (HbA1c). This study aims to evaluate the extent to which HbA1c explains the GV phenomena in patients with Type 1 diabetes (T1DM). Methods: In 147 patients with T1DM, associations between HbA1c and several GV indexes were analyzed. Results: Patients with an HbA1c < 7% had a lower median standard deviation of glycemia (60 vs. 48; p < 0.001), a lower coefficient of variation (34.1 vs. 38.0; p < 0.001), and a significantly increased median time in range (78 vs. 58; p < 0.001). HbA1c was positively correlated with the coefficient of variation (r = 0.349; p < 0.001) and the standard deviation (r = 0.656; p < 0.001) but reversely correlated with a lower time in range (r = −0.637; p < 0.001). Conclusions: HbA1c only partially explains the GV phenomena in patients with T1DM. The HbA1c value is associated more strongly with the time in range and standard deviation than with the coefficient of variation.

Background/Objectives: Glycemic variability (GV) is a novel concept in the assessment of the quality of glycemic control in patients with diabetes, with its importance emphasized in patients with type 1 diabetes. Its adoption in clinical practice emerged with the increased availability of continuous glycemic monitoring systems. The aim of this study is to evaluate the GV in patients with type 1 diabetes mellitus (T1DM) and to assess its associations with other parameters used to evaluate the glycemic control. Methods: GV indexes and classical glycemic control markers were analyzed for 147 adult patients with T1DM in a multicentric cross-sectional study. Results: Stable glycemia was associated with a higher time in range (TIR) (78% vs. 63%; p < 0.001) and a lower HbA1c (6.8% vs. 7.1%; p = 0.006). The coefficient of variation (CV) was reversely correlated with TIR (Spearman’s r = −0.513; p < 0.001) and positively correlated with hemoglobin A1c (HbA1c) (Spearman’s r = 0.349; p < 0.001), while TIR was reversely correlated with HbA1c (Spearman’s r = −0.637; p < 0.001). The composite GV and metabolic outcome was achieved by 28.6% of the patients. Conclusions: Stable glycemia was associated with a lower HbA1c, average and SD of blood glucose, and a higher TIR. A TIR higher than 70% was associated with a lower HbA1c, and SD and average blood glucose. Only 28.6% of the patients with T1DM achieved the composite GV and metabolic outcome, despite 53.7% of them achieving the HbA1c target, emphasizing thus the role of GV in the assessment of the glycemic control.

Although remarkable progress has been made, colorectal cancer remains a significant global health issue. One of the most challenging aspects of cancer treatment is the resistance of tumor cells to classical chemotherapy. Conventional therapy for colorectal cancer often involves the use of 5-fluorouracil as a chemotherapeutic agent. Aspirin, a drug used primarily to prevent cardiovascular complications, became a focus of attention due to its potential use as an antitumor agent. The purpose of the study was to evaluate the potential synergistic cytotoxic effects of aspirin and 5-fluorouracil on colorectal adenocarcinoma cells. The viability of cells, the impact on the morphology and nuclei of cells, the potential antimigratory effect, and the impact on the expression of the major genes associated with cell apoptosis (Bcl-2, Bax, Bad), as well as caspases 3 and 8, were evaluated. The results indicated that the two compounds exerted a synergistic effect, causing a reduction in cell viability accompanied by changes characteristic of the apoptosis process—the condensation of nuclei and the reorganization of actin filaments in cells, the reduction in the expression of the Bcl-2 gene, and the increase in the expression of Bax and Bad genes, along with caspases 3 and 8. Considering all these findings, it appears that aspirin may be investigated in depth in order to be used in conjunction with 5-fluorouracil to increase antitumor activity.