(1) The link between periodontal disease (PD) and acute coronary syndromes (ACSs) is predominantly attributed to the atherosclerotic process, mediated by systemic inflammation. However, the correlation between the severity of PD, characterized by the presence of periodontal pathogens, and systemic inflammation in patients with ACS remains inadequately clarified. (2) This study aims to assess the association between the severity of PD and systemic inflammatory biomarkers, along with lipid profiles, in patients with ACS. (3) In total, 42 patients with ACS and concomitant PD were divided into two groups based on the presence of periodontal pathogens belonging to the red or red-orange complexes. Group 1–29 patients displayed pathogens from the red complex (RC) and group 2–13 patients displayed pathogens from the red-orange complex (ROC). All participants underwent a comprehensive dental examination, including DNA sampling from the periodontal pockets for pathogen detection. Systemic inflammation was evaluated alongside assessments of lipid profiles. (4) Inflammatory markers were more pronounced in the RC group compared with the ROC group. Moreover, patients in the RC group showed significantly higher monocyte-to-lymphocyte ratios (0.41 ± 0.20 vs. 0.28 ± 0.12; p = 0.002), platelet-to-lymphocyte ratios (139.50 ± 33.85 vs. 100.90 ± 8.84; p = 0.02), serum C-reactive protein levels (9.34 ± 1.08 mg/L vs. 5.46 ± 1.03 mg/L; p = 0.03), and serum uric acid levels (6.9 ± 0.49 mg/dL vs. 5.4 ± 0.26 mg/dL; p = 0.006). Concerning lipid profiles, the RC group exhibited significantly higher low-density lipoprotein cholesterol (LDL) levels (169.60 ± 12.63 mg/dL vs. 106.70 ± 9.34 mg/dL; p = 0.0007) and significantly lower high-density lipoprotein cholesterol (HDL) levels (29.29 ± 3.50 mg/dL vs. 39.56 ± 2.07 mg/dL; p = 0.002). (5) The severity of PD, indicated by the concomitant presence of pathogens from the red and orange complexes, is associated with an unfavorable lipid profile and elevated inflammatory biomarkers. These findings highlight the potential importance of periodontal intervention in the prevention of ACS.

Acute surgical abdomen is characterized by intense, sudden abdominal pain due to intra-abdominal conditions requiring prompt surgical intervention. The coronavirus disease 2019 (COVID-19) pandemic has led to various complications related to the disease’s complex pathophysiological mechanisms, hence the hypothesis of COVID-19-induced acute abdominal surgical pathologies. The connection between acute surgical abdomen and COVID-19 involves two primary mechanisms. First, there is the presence of angiotensin-converting enzyme 2 (ACE2) receptors in multiple abdominal organs. This facilitates the cytokine storm through direct viral injury and inflammation. Second, the hypercoagulable state induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) increases the thrombotic risk within abdominal vessels, which can subsequently lead to ischemia. ACE2 receptors are notably expressed in the gastric, duodenal, and rectal epithelium, with SARS-CoV-2 viral RNA and nucleocapsid proteins detected in these tissues. The inflammatory response results in significant endothelial damage, activating coagulation pathways that cause monocellular infiltration, lymphocytic inflammation, and uncontrolled coagulation. These findings highlight the need for further research to clarify how COVID-19 leads to acute abdominal pathologies. Understanding these mechanisms is vital for improving clinical management and patient outcomes during future health crises and in the aftermath of the pandemic.

Background and Objectives: The leuko-glycemic index (LGI) is an emerging immunometabolic biomarker that integrates systemic inflammation and stress hyperglycemia and has shown prognostic value in various acute conditions. Its utility in patients with acute surgical abdomen remains unknown. We hypothesized that elevated admission LGI values would be independently associated with higher in-hospital mortality in patients with acute surgical abdomen and would show discriminative performance at least comparable to established inflammation-based indices (NLR, MLR, PLR, SII). Materials and Methods: We conducted a single-center retrospective cohort study including 1927 adults admitted with acute surgical abdomen who underwent emergency surgery between March 2019 and March 2021. Patients were stratified according to in-hospital outcome into survivors (Group 1, n = 1625) and non-survivors (Group 2, n = 302). Demographic, hematological, and biochemical parameters, including inflammation-based ratios (NLR, MLR, PLR, SII) and the LGI, were collected upon admission. Non-parametric tests were used for between-group comparisons, and receiver operating characteristic (ROC) curve analysis assessed the discriminative performance of each index. Multivariable logistic regression was used to assess the independent association of LGI with in-hospital mortality. Results: Non-survivors were older and exhibited more pronounced hematologic and biochemical derangements, including higher leukocyte, neutrophil, glucose, urea, creatinine, and AST levels, along with lower hemoglobin, hematocrit, red blood cell, and lymphocyte counts. All inflammation-based indices were significantly elevated in Group 2 (all p < 0.0001). LGI was markedly higher in non-survivors (median 1986 [IQR 1263–3113] vs. 1568 [980–2083]; p < 0.0001) and showed the highest AUC among the indices tested (0.646, 95% CI 0.607–0.685), significantly higher than MLR, PLR and SII (DeLong p ≤ 0.0002) and nominally higher than NLR (p = 0.042). An LGI cut-off of 1665 yielded a sensitivity of 60.17% and a specificity of 57.73% for in-hospital mortality. In multivariable analysis, log-transformed LGI remained independently associated with in-hospital mortality (OR 1.44 per 1 SD, 95% CI 1.20–1.73; p = 0.0001). Conclusions: Admission LGI was independently associated with in-hospital mortality and outperformed the inflammation-based ratios tested, but its standalone discrimination was modest and its threshold unstable; these findings do not support its use for triage or risk stratification, and external prospective validation would be required before any clinical role could be considered.