The standard treatment for breast cancer typically includes surgery, often followed by systemic therapy and individualized treatment regimens. However, there is growing interest in identifying pre-therapeutic biomarkers that can predict tumor response to neoadjuvant chemotherapy (NACT). This study systematically evaluated various analytical parameters, including age, TNM stage, histological type, molecular subtype, and several biomarker ratios, such as the platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammatory index (SII), and prognostic nutritional index (PNI). We aimed to assess the predictive value of these parameters regarding the tumor’s response rate to NACT. The analysis revealed a statistically significant association between the pathological complete response—pCR (absence of any detectable cancer cells in the tissue following neoadjuvant chemotherapy (NACT))—rate and NLR in the subgroup with values between 1 and 3 (p = 0.001). The optimal cut-off for PLR was determined to be 120.45, with 80.55% of patients achieving pCR showing PLR values below this threshold (p = 0.000). Similarly, the LMR cut-off was found to be 12.34, with 77.77% of patients with pCR having LMR values below this threshold (p = 0.002). Additionally, lower pre-therapeutic values of NLR (p < 0.001), PLR (p = 0.002), SII (p = 0.001), and LMR (p = 0.001) were significantly correlated with pCR compared to the non-pCR subgroup (p < 0.005). These findings highlight the predictive potential of these biomarkers for achieving pCR following NACT. Our study supports the hypothesis that pre-therapeutic values of NLR, PLR, SII, and LMR can serve as predictive biomarkers for pCR in breast cancer patients undergoing NACT. However, the PNI did not demonstrate predictive potential in relation to pCR. These biomarkers may provide valuable insights into patient prognosis and guide personalized treatment strategies.

Acute pancreatitis (AP) is the most common gastrointestinal indication requiring hospitalisation. Severe hypertriglyceridaemia (HTG) is the third most common aetiology of AP (HTGAP), with a complication rate and severity that are higher than those of other aetiologies (non-HTGAP). The aim of this study was to evaluate the supposedly higher complication rate of HTGAP compared to non-HTGAP. The secondary objectives were to find different biomarkers for predicting a severe form. This was a retrospective study that included patients admitted with AP in a tertiary department of gastroenterology and hepatology. The patients were divided into two groups: HTGAP and non-HTGAP. We searched for differences regarding age, gender, the presence of diabetes mellitus (DM), the severity of the disease, the types of complications and predictive biomarkers for severity, hospital stay and mortality. A total of 262 patients were included, and 11% (30/262) of the patients had HTGAP. The mean ages were 44.4 ± 9.2 in the HTGAP group and 58.2 ± 17.1 in the non-HTGAP group, p < 0.0001. Male gender was predominant in both groups, at 76% (23/30) in the HTGAP group vs. 54% (126/232) in non-HTGAP, p = 0.02; 53% (16/30) presented with DM vs. 18% (42/232), p < 0.0001. The patients with HTG presented higher CRP 48 h after admission: 207 mg/dL ± 3 mg/dL vs. non-HTGAP 103 mg/dL ± 107 mg/dL, p < 0.0001. Among the patients with HTGAP, there were 60% (18/30) with moderately severe forms vs. 30% (71/232), p = 0.001, and 16% (5/30) SAP vs. 11% (27/232) in non-HTGAP, p = 0.4 Among the predictive markers, only haematocrit (HT) and blood urea nitrogen (BUN) had AUCs > 0.8. According to a multiple regression analysis, only BUN 48 h was independently associated with the development of SAP (p = 0.05). Diabetes mellitus increased the risk of developing severe acute pancreatitis (OR: 1.3; 95% CI: 0.1963–9.7682; p = 0.7). In our cohort, HTGAP more frequently had local complications compared with non-HTGAP. A more severe inflammatory syndrome seemed to be associated with this aetiology; the best predictive markers for complicated forms of HTGAP were BUN 48 h and HT 48 h.

Type 2 diabetes mellitus (DM) is a chronic metabolic disorder posing multifaceted challenges to global public health. Among its numerous complications, infected diabetic foot ulcers (IDFUs) represent a particularly debilitating consequence. Beyond cardiovascular implications, there is an emerging understanding of the interconnectedness among IDFUs, neuropathy, atherosclerosis, and dyslipidemia. IDFUs, peripheral neuropathy, and atherosclerosis share common risk factors and mechanistic pathways. The primary objective of this study was to characterize the lipid profiles in DM patients with IDFUs, comparing them with DM patients without foot ulcers, and with a control group of healthy subjects. The secondary objectives included evaluating apolipoprotein E (ApoE) levels across these study groups and comparing lipid profiles within IDFU subgroups. A total of 160 patients were assessed for this study. After applying exclusion criteria, 140 participants were included, divided into three groups: Group IDFU (80 patients with IDFUs), Group DM (32 patients with DM but no foot ulcers), and Group Controls (28 healthy controls). Compared to Group DM, Group IDFU demonstrated lower levels of high-density lipoprotein cholesterol (HDL-C) (30.9 ± 12.6 mg/dL vs. 40.8 ± 16.6 mg/dL, p = 0.002), but improved levels of ApoE (160.9 ± 68.4 mg/dL vs. 197.2 ± 69.6 mg/dL, p = 0.01), triglycerides (TG) (126.9 ± 56.2 mg/dL vs. 165.8 ± 79.0 mg/dL, p = 0.004), low-density lipoprotein cholesterol (LDL-C) (84.2 ± 32.3 mg/dL vs. 92.3 ± 39.3 mg/dL, p = 0.1), and total cholesterol (133.6 ± 43 mg/dL vs. 164.6 ± 44.4 mg/dL, p = 0.002). The IDFU patients exhibit improved lipid profiles, excepting HDL-C, which is unusual because IDFU follows complications related to dyslipidemia for DM patients. Anemia, impaired renal function, and elevated TG levels were identified as biomarkers for mortality among patients with IDFUs. The data suggest that a lower level of HDL-C and an improved lipid profile may indicate a systemic end-stage disease manifestation in DM patients with IDFUs.