Background/Objectives: Type 2 diabetes mellitus (T2DM), is a rapidly growing global health concern, often accompanied by chronic kidney disease (CKD) and metabolic disturbances. Obesity-related indices, such as the visceral adiposity index (VAI) and body adiposity index (BAI), have been linked to cardiovascular and renal complications in diabetic patients. However, studies integrating both the atherogenic coefficient (AC) and prognostic nutritional index (PNI) for evaluating diabetic nephropathy (DN) remain limited. This study aimed to assess the associations of obesity-related indices with immunological and nutritional factors in patients with T2DM and prediabetes (PreDM). Methods: A retrospective, cross-sectional study was conducted over six months at a university clinical hospital in Dolj County, Romania. The study enrolled 268 newly diagnosed T2DM patients and 150 PreDM patients. Anthropometric parameters, laboratory tests, and demographic data were collected. AC and PNI were calculated using standard formulas, and statistical analyses were performed to determine their associations with metabolic and inflammatory markers. Results: Our study found that T2DM patients had significantly lower PNI values, indicating mild malnutrition, while PreDM patients maintained a normal nutritional status. AC was significantly higher in T2DM patients, correlating with lipid profile alterations and systemic inflammation. Obesity indices, particularly VAI, were significantly elevated in T2DM patients with higher AC values. Statistically significant differences in total cholesterol, low-density lipoprotein cholesterol (LDL-c), and triglycerides were observed between AC subgroups, reinforcing its role in cardiovascular risk assessment. Conclusions: The findings highlight the potential of AC and PNI as biomarkers for assessing nutritional, inflammatory, and lipemic status in diabetic patients. The significant associations between obesity-related indices, lipid profiles, and inflammation markers suggest that early assessment of these parameters may potentially aid in predicting diabetic complications. Further studies are needed to explore the clinical utility of AC and PNI in managing T2DM and CKD progression. Future research should investigate how the lipidic spectrum alters the progression of DN across various patient groups with diabetes and prediabetes

Chronic kidney disease (CKD) is a multifactorial disorder increasingly recognized as a systemic condition marked by persistent inflammation, oxidative stress, dyslipidemia, and endothelial dysfunction. Diabetic nephropathy, a leading cause of CKD, amplifies cardiovascular risk through intertwined mechanisms beyond traditional risk factors. This review synthesizes current evidence on the interplay between inflammation, oxidative stress, and atherosclerosis in CKD, with a special focus on emerging molecular biomarkers—PCSK9, EPHX2, AOPPs, and TBARSs—and their integration with clinical indices. These markers illuminate pathophysiological networks underlying CKD progression and cardiovascular complications, offering novel insights into risk stratification, disease monitoring, and targeted therapy. By exploring molecular and clinical intersections, this review underscores the potential of a personalized, biomarker-driven approach to CKD management.

We compared oxidative markers and their links to inflammation in diabetic nephropathy and hemodialysis to identify independent determinants. We studied 180 adults, 90 patients with type 2 diabetes and diabetic nephropathy and 90 patients on hemodialysis. We measured serum advanced oxidation protein products (AOPP) and thiobarbituric acid reactive substances (TBARS) by enzyme-linked immunosorbent assay (ELISA). Partial correlations were adjusted for age, sex, and albumin with false discovery rate (FDR) control. Principal component analysis (PCA) summarized inflammatory indices and linear models tested predictors of AOPP and TBARS. Oxidative damage was higher in hemodialysis, with AOPP median 25.80 versus 5.06 and TBARS 8.49 versus 1.89, p less than 0.0001. C reactive protein (CRP) and mean corpuscular volume-to-lymphocyte ratio (MCVL) were higher in patients ongoing hemodialysis; systemic immune-inflammation index (SII) was higher in diabetic nephropathy. PCA yielded a dominant inflammation axis in both cohorts, 74.73 percent in hemodialysis and 85.20 percent in diabetic nephropathy. In regression, creatinine (β = 2.47, p = 0.026) predicted AOPP in hemodialysis. Dialysis vintage inversely predicted TBARS, β = −0.2305, p = 0.0209. In diabetic nephropathy, the PCA inflammation score predicted AOPP, β = 1.134, p = 0.0003. Protein oxidation tracked systemic inflammation in diabetic nephropathy, but not in hemodialysis. AOPP outperformed TBARS as an inflammatory partner and a practical monitoring candidate in diabetic kidney disease. Prospective studies should test for prognostic value and therapy sensitivity.

In patients diagnosed with multiple myeloma (MM), the primary complaints at the time of diagnosis are often related to bone involvement, significantly impacting quality of life and increasing both morbidity and mortality. Obesity is associated with a chronic inflammatory state that results in the production of various cytokines and adipokines, which may promote bone destruction. Adiponectin, an adipokine predominantly secreted by adipocytes, is notably diminished in circulation among individuals with obesity, a phenomenon that has also been observed in MM. This reduction may contribute to the disruption of an already compromised bone architecture. The increase in adipose tissue is associated with heightened leptin production, a key adipokine, which can play a significant role in the pathophysiology of MM and its related bone complications. Obesity is associated with hyperinsulinemia and increased levels of free IGF-1. In MM, IGF-1 plays a critical role as a growth factor, produced by both myeloma cells and osteoclasts within the bone marrow microenvironment. Our gathered data indicates a significant relationship between the adipokines produced by adipose tissue and the bone matrix, particularly in the context of obesity and MM. However, it is important to note that the existing body of research on this topic is relatively sparse, with the majority of studies conducted on murine models rather than human subjects. This limitation highlights a critical need for further investigation to elucidate the precise mechanisms that contribute to bone destruction under these conditions.

Atopic dermatitis (AD) has been linked to osteoporosis and fractures, but the strength, mechanisms, treatment implications, and clinical significance of this relationship remain uncertain. This review critically assesses epidemiological and osteoimmunological evidence connecting AD with skeletal fragility and proposes a lifespan-based, risk-adapted screening framework. A recent cohort-based meta-analysis found associations between AD and osteoporosis (odds ratio [OR], 1.56) and any fracture (OR, 1.08), although heterogeneity was substantial. Risk appeared higher with severe or long-standing disease and reflected interactions among inflammatory, therapeutic, nutritional, behavioral, and age-related factors. Systemic glucocorticoids were the clearest modifiable treatment-related risk, but did not fully account for the association. The RANK–RANKL–osteoprotegerin system and IL-4, IL-13, IL-31, and IL-33 offer biological plausibility, although their skeletal effects are context-dependent and supported primarily by indirect or preclinical evidence. Available data do not show that dupilumab causes osteoporosis. Emerging pediatric findings suggest improvements in growth and bone-related biomarkers, but provide no evidence of fracture prevention. AD alone does not warrant universal DXA screening. Assessment should be individualized based on age, history of fragility fractures, disease severity and duration, cumulative systemic glucocorticoid exposure, nutritional status, physical activity, muscle function, and falls. Prospective studies combining standardized AD phenotyping with longitudinal imaging, biomarkers, and adjudicated fractures are needed.

Background/Objectives: Inflammatory and hematologic indices derived from routine blood tests have been increasingly investigated as prognostic biomarkers in multiple myeloma (MM). However, their clinical utility remains inconsistent, and data on novel composite indices, such as the mean corpuscular volume-to-lymphocyte ratio (MCVL) and the cumulative inflammatory index (IIC), are lacking in MM. Methods: We conducted a retrospective study including 122 patients with newly diagnosed MM. Hematologic and inflammatory indices were evaluated at baseline and after four cycles of induction therapy. Associations with progression-free survival (PFS) and overall survival (OS) were assessed using Kaplan–Meier analysis, Cox regression models, and receiver operating characteristic (ROC) curve analysis. Results: Baseline inflammatory biomarkers, including NLR, PLR, MLR, SII, as well as MCVL and IIC, were not significantly associated with PFS or OS. ROC analysis demonstrated poor discriminative ability for all evaluated markers at both baseline and post-induction timepoints (AUC values close to or below 0.50). In contrast, post-induction inflammatory indices, particularly PLR, MLR, AISI, and SIRI, were significantly associated with PFS in both univariable and multivariable Cox regression analyses. Neither baseline nor post-induction MCVL and IIC showed independent prognostic value. Conclusions: Baseline inflammatory and erythrocyte-derived indices, including the novel composite markers MCVL and IIC, have limited prognostic utility in MM. In contrast, dynamic changes in inflammatory biomarkers during treatment may provide more clinically relevant information regarding disease progression. These findings support the integration of longitudinal biomarker assessment into future risk stratification models in MM.