Background: This study aimed to determine the relationship between nutritional status and systemic inflammation using four validated nutrition indices—Hemoglobin, Albumin, Lymphocyte, and Platelet (HALP) score, Prognostic Nutritional Index (PNI), Controlling Nutritional Status (CONUT) score, and Nutritional Risk Index (NRI)—and three immune–inflammation biomarkers—Systemic Immune–Inflammation Index (SII), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR)—in healthy adults with varying body mass index (BMI) levels. Methods: This retrospective study included 290 clinically healthy adults aged 18–60 years, categorized by BMI. Individuals with chronic diseases, medication use, or morbid obesity (BMI ≥ 40 kg/m2) were excluded. Nutrition scores (HALP, PNI, NRI, CONUT) and systemic immune–inflammation indices (SII, NLR, PLR) were calculated from laboratory data. For the comparisons of SII, PLR, NLR, PNI, HALP, NRI, and CONUT values between groups, age was adjusted for, and an ANCOVA test was performed. Results: Among the systemic immune–inflammation indices, SII and NLR were significantly higher in both the overweight and obesity groups. The CONUT score, a negative indicator of nutritional status, demonstrated positive correlations with SII, NLR, and PLR in the overweight group, and with PLR in the obesity group. Although PNI showed significant inverse correlations with SII, PLR, and NLR in both groups, the mean PNI values remained above 50, indicating overall normal nutritional status in the study population. HALP was inversely correlated with SII, PLR, and NLR in both groups. Conclusions: The HALP score appears to be the most reliable marker, as it reflects the inverse relationship between nutritional status and systemic immune–inflammation indices.

Objectives: HbA1c is the most widely used test as an indicator of glucoregulation in patients with type 2 diabetes mellitus (T2DM). Asprosin and oxidative stress levels can be reduced with good glycemic control (GC) and thus prevented or delayed micro/macro complications in patients with T2DM. The relationship between asprosin, which is thought to affect GC, and oxidative stress parameters such as lipid hydroperoxides (LOOHs), glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (Cu,Zn-SOD), and total antioxidant capacity (TAC) was evaluated in T2DM patients. Materials and Methods: The study was conducted prospectively in 75 healthy people admitted to the hospital for a general health check-up and 150 T2DM patients treated in the diabetes outpatient clinic. The patient’s glycemic status measurements were categorized as good glycemic control group (GGC) is defined as HbA1c < 7 and poor glycemic control (PGC) group is defined as HbA1c ≥ 7. Results: The study found a consistent increase in LOOH and MDA levels across the control, GGC, and PGC groups, while GSH, Cu/Zn-SOD, and TAC levels decreased in these respective groups. Additionally, asprosin levels showed a gradual rise in all groups. Positive correlations were observed between asprosin levels and various metabolic and oxidative stress markers, including BMI, WC, FBG, insulin, homeostasis model assessment for insulin resistance (HOMA-IR), DM duration, LOOH, and MDA, while negative correlations were noted with GSH, Cu/Zn-SOD, and TAC specifically in the PGC group. Furthermore, multivariate regression analysis identified HOMA-IR as the primary influencing factor on asprosin levels in PGC patients. Conclusions: Current glycemic dysregulation may lead to increased circulating asprosin and oxidative stress, which cause complications. Since asprosin levels may be an important hormonal factor in determining GC in T2DM, the use of this hormone may be recommended in the future to accelerate therapeutic approaches in T2DM. Early diagnosis and appropriate treatment may delay the development and progression of diabetic complications.

Objectives: The aim of this study was to investigate the circulating levels of asprosin, clusterin, zinc-alpha-2-glycoprotein (ZAG), nuclear factor-kappa B (NF-κB), and peroxisome proliferator-activated receptor-gamma (PPAR-γ) in patients with T2DM in relation to microvascular and macrovascular complications. Measuring these biomarkers may provide insight into the pathophysiology of T2DM and indicate novel targets for the therapy of diabetes-related complications. Methods: A total of 260 subjects consisting of four groups: healthy controls (Group-1), T2DM patients without complications (Group-2), T2DM patients with microvascular complications (Group-3), and T2DM patients with macrovascular complications (Group-4). Results: The mean age of all subjects was 52.96 ± 6.4, 127 of whom were male. Asprosin, clusterin, and NF-κB levels were significantly higher, while ZAG and PPAR-γ levels were significantly lower in diabetic patients than healthy subjects (p < 0.01, for all). Asprosin (p < 0.01), clusterin (p < 0.01), and NF-κB (p: 0.002) levels were significantly higher and PPAR-γ (p < 0.01) level was significantly lower (p < 0.001) in Group-3 than Group-2. Asprosin (p < 0.01) and NF-κB (p: 0.011) levels were significantly higher while ZAG (p < 0.01) level was significantly lower in Group-4 than Group-2. Serum ZAG level was found lower in Group-4 than in Group-3 (p = 0.037). Further, the biomarkers presented significant correlation with biomarkers like HbA1c and HOMA-IR. It was observed that increasing serum asprosin, clusterin, and NF-κB levels and decreasing serum PPAR-γ levels were effective in the development of microvascular complications while the increased asprosin levels and decreased ZAG levels had a significant effect on the development of macrovascular complications in the binary logistic regression analysis. Conclusions: This study confirms that altered levels of asprosin, clusterin, ZAG, NF-κB, and PPAR-γ are associated with T2DM and its complications. These biomarkers reflect the pathophysiological processes of metabolic disturbance and inflammation in T2DM and, therefore, have the potential for use in targeted interventions to prevent and manage diabetes-related complications.

Objective: Coronavirus disease 2019 (COVID-19) is the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Acute respiratory distress and preterm delivery are the two major complications induced by SARS-CoV-2 infection during pregnancy. In the presence of dyspnea, the use of systemic corticosteroids was recommended in pregnant and non-pregnant groups. Our primary aim was to investigate the effect of early-onset steroid treatment on mortality and adverse effects in pregnant women with COVID-19. Our secondary aim was to investigate the effect of steroid treatment on the length of hospital stay and intensive care unit (ICU) stay, and duration of treatment. The study also investigated infection, preterm birth, and ideal body weight (lbw) in newborns. Methods: In this retrospective study, 253 patients were divided into three groups according to steroid administration. In Group 1 patients (n:112), treatment was started at the time of hospitalization. In Group 2 patients (n:90), treatment was started at least 24 h after hospitalization. Group 3 consisted of patients (n:51) who did not receive steroid treatment. Methylprednisolone (32 mg/day) was given to pregnant patients with a gestational age below 24 weeks or above 34 weeks, and dexametazone (6 mg/day) was given in four doses followed by 32 mg/day methylprednisolone for the others (whose baby was at a gestational age of 24 weeks and above but less than 34 weeks). Result: The hospital stay, ICU stay, and steroid administration time were significantly lower in the Group 1 when compared to the others (p < 0.05). The steroid treatment requirement was 4.4 days in Group 1 and 5.7 days in Group 2 (p < 0.05). While no death was observed in Group 1, one patient died in Group 2 and three patients died in Group 3. There was no difference between the groups in terms of complications, including preterm labor. Conclusions: No death was also observed with early-onset treatment. Early-onset treatment may be beneficial for fewer hospitalizations, fewer ICU stays, and less mechanical ventilation requirement in pregnant women with COVID-19. In addition, with early treatment, the total number of steroid administration days was reduced, which is important in terms of reducing the risk of side effects.

Background and Objectives: Type 1 Diabetes Mellitus (T1DM) is an autoimmune disease with T cell-mediated pathogenesis of pancreatic β-cell destruction, leading to insulin deficiency. MicroRNAs such as miR-223 and miR-106b, along with PTEN, have been reported to participate in the pathophysiology of diabetes and its complications. The current study has explored the expression of miR-223, miR-106b, and PTEN and their association with various clinical and biochemical parameters in subjects diagnosed with T1DM. Materials and Methods: Sixty T1DM patients (two groups as uncomplicated/ with microalbuminuria) and fifty healthy volunteers, age- and sex-matched, were enrolled in this study. The fasting venous blood samples were collected, and PTEN and miRNAs (miR-223 and miR-106b) levels were measured by ELISA and real-time PCR, respectively. Results: The PTEN levels of patients with microalbuminuria were significantly lower than those of patients without microalbuminuria, while those of miR-223 and miR-106b were significantly increased in the T1DM group compared with the healthy control group (p < 0.001). ROC analysis indicated that PTEN, miR-223, and miR-106b could be potential biomarkers for diagnosing T1DM with high specificity but with variable sensitivities. Also, PTEN and miR-223 were negatively correlated with r =−0.398 and p < 0.0001, indicating that they were interrelated in their role within the T1DM pathophysiology. Conclusions: In the current study, it has been shown that the circulating levels of PTEN, miR-223, and miR-106b are significantly changed in T1DM patients and may back their potential to be used as non-invasive biomarkers for the diagnosis and monitoring of T1DM. Low PTEN protein expression was related to high miR-223 expression, indicating involvement of these miRNA in the regulation of PTEN. Further studies should be performed to clarify the exact mechanisms and possible clinical applications of these molecules.

Background: Post-stroke dysphagia is associated with aspiration pneumonia, malnutrition, and poor functional outcomes. Although systemic biochemical abnormalities are common after stroke, their contribution to swallowing recovery and transition to oral feeding remains unclear. This study investigated the association of systemic biochemical markers with oral feeding transition and swallowing-related functional improvement in patients with chronic post-stroke dysphagia. Methods: This retrospective single-center study included 89 patients with chronic post-stroke dysphagia who received enteral nutrition between February 2023 and December 2025. Biochemical parameters and swallowing outcomes, assessed using the Functional Oral Intake Scale (FOIS) and Penetration–Aspiration Scale (PAS), were retrospectively analyzed. Changes between baseline (T0) and follow-up (T1) were calculated (Δ = T1 − T0). Multivariable logistic and linear regression analyses were performed to identify independent predictors of transition to oral feeding and improvement in aspiration severity. Results: Of the 89 patients, 52 (58.4%) achieved oral feeding. Significant improvements in swallowing function were observed following rehabilitation, as reflected by increased FOIS scores and decreased PAS-soft and PAS-liquid scores (all p < 0.001), together with reductions in CRP (C-reactive protein), D-dimer, white blood cell count, and neutrophil count (all p < 0.05). Patients who achieved oral feeding demonstrated greater improvements in PAS scores (both p < 0.001) and a divergent change in vitamin B12 levels (a decrease among those who transitioned versus an increase among those who remained enterally fed) (p = 0.049). In exploratory multivariable analyses, higher NIHSS (National Institutes of Health Stroke Scale) scores and lower baseline 25-hydroxyvitamin D levels were associated with a lower likelihood of transition to oral feeding (NIHSS OR = 0.78, p = 0.031; vitamin D OR (Odds ratio) = 1.12, p = 0.001), whereas baseline PAS-liquid score was not an independent predictor of transition. In the linear regression analysis of aspiration severity, baseline PAS-liquid score was the strongest predictor of ΔPAS-liquid (B = −0.527, p = 0.001), while lower baseline 25-hydroxyvitamin D was associated with less improvement (B = −0.021, p = 0.047). Given the limited sample size and the absence of correction for multiple comparisons, the biochemical associations should be interpreted as exploratory. Conclusions: In patients with chronic post-stroke dysphagia, transition to oral feeding was primarily associated with neurological severity, whereas improvement in aspiration severity was most strongly related to baseline aspiration burden. Lower baseline 25-hydroxyvitamin D showed exploratory associations with both outcomes. Because 25-hydroxyvitamin D did not change significantly during follow-up and the models were underpowered, this association should be regarded as hypothesis-generating rather than clinically established. These biochemical findings require confirmation in larger prospective studies.