Excess adiposity has been associated with Hodgkin lymphoma (HL) development, but its implications remain unclear. Bone marrow (BM), a frequent extranodal involvement site, contains both red and fatty yellow marrow. We investigated whether obesity influences HL outcomes and characterized the BM and cytokine profiles. In this retrospective study, HL patients were analyzed to assess the association between obesity with relapse and mortality. Yellow and red marrow composition were evaluated using CT imaging and correlated with HL outcomes. A nested study analyzed cytokines in the interstitial marrow fluid (IMF) and in circulation of HL patients, in comparison to a control group of healthy blood donors. Further, in vitro functional analyses were performed. Overweight/obesity in HL patients was associated with lower rates of BM involvement, disease relapse, and mortality. Moreover, dense yellow marrow was related to increased risk of death. HL subjects had elevated levels of adiponectin in IMF compared to marrow donors, whereas higher insulin, interleukin 8, and osteoprotegerin levels in IMF were associated with shorter time to relapse. At the molecular level in BM, HL patients had overexpression of LEPR and IGFBP3 in adipocytes, while stromal cells overexpressed IGF-axis receptors. In in vitro studies, human recombinant IGF-1 significantly induced the L428 HL cell line proliferation, which when combined with IGFBP-3 modified apoptosis. The current findings suggest that obesity is associated with a lower incidence of BM involvement and mortality in patients with HL. The obesity together with HL mechanistically influences systemic and local BM cytokine production, thereby impacting HL fate.

Despite advancements in cancer immunotherapy, most lymphomas remain unresponsive to checkpoint inhibitors. P-selectin glycoprotein ligand-1 (PSGL-1), recently identified as a promoter of T-cell exhaustion in murine melanoma models, has emerged as a novel immune checkpoint protein and promising immunotherapeutic target. In this study, we investigated the potential of PSGL-1 antibody targeting in B-cell lymphoma. Using allogeneic co-culture systems, we demonstrated that targeted antibody interventions against human PSGL-1 enhanced T-cell activation and effector cytokine production in response to lymphoma cells. Moreover, in vitro treatment of primary lymphoma cell suspensions with PSGL-1 antibody resulted in increased activation of autologous lymphoma-infiltrating T cells. Using the A20 syngeneic B-cell lymphoma mouse model, we found that PSGL-1 antibody treatment significantly slowed tumor development and reduced the endpoint tumor burden. This antitumoral effect was accompanied by augmented tumor infiltration of CD4+ and CD8+ T cells and reduced infiltration of regulatory T cells. Finally, anti-PSGL-1 administration enhanced the expansion of CAR T cells previously transferred to mice bearing the aggressive Eμ-Myc lymphoma cells and improved disease control. These results demonstrate that PSGL-1 antibody blockade bolsters T-cell activity against B-cell lymphoma, suggesting a potential novel immunotherapeutic approach for treating these malignancies.

BackgroundThe importance of Cervicovaginal Microbiota in protecting against infections (such as HPV) is already well established, namely through Lactobacillus spp., as well as the mechanism through which HPV leads to Cervical Neoplasia. However, it is not possible to classify HPV as a complete carcinogen. Thus, the importance of exploring Cervicovaginal dysbiosis with the intention of deciphering this interaction with HPV, takes on greater relevance. The main objectives of this study were: 1) Comparison of the MCV composition of women with or without HPV and women with ASCUS or LSIL; 2) Characterization of cytokines present in the vaginal microenvironment; 3) Evaluation of the blood count ratios as prognostic systemic inflammatory biomarkers; 4) Correlation between MCV, HPV serotypes and cytokines.MethodsThis was a retrospective, observational, multicenter, cross-sectional study. CVM analysis was performed by isolation RNA and sequencing on a NGS platform. Cytokine concentrations of CVM were obtained through Multiplex platform. Statistical analysis was performed in SPSS v 26.0. An α of 0.05 was considered statistically significant.ResultsHighlighting the core of the study, CVM types of CST I and CST IV were found to influence the emergence of cervical lesions. Neutrophil-to-Lymphocyte ratio was found to impact the prognosis of ASCUS. Within CVM, Lactobacillus prevent the growth of other CST IV species, while the latter express symbiotic relationships with each other and show affinity for specific HPV serotypes. At last, RANTES chemokine is significantly elevated in cervicovaginal infections.ConclusionThe importance of using vaginal cytokine profiles and CVM is highlighted in the hypothesis of prevention of Cervical Neoplasia development, as well as in its use as a prognostic biomarker. Taken together, these insights are one step closer to personalized medicine.

Aims: In heart failure patients renal dysfunction represents impaired tissue perfusion. We investigated the association of customarily used renal function parameters with short-term prognosis in patients admitted with acute decompensated heart failure in class III or IV of New York Heart Association. Material and Methods: Univariate Cox proportional hazard model was used to assess the relationship between variables and outcomes. Survival curves were designed using the Kaplan -Meier method. Results: We followed 65 patients for a median of 13.7 (01-03 6.7-18.9) months. Variables associated with an increased risk for short-term rehospitalization were baseline urea (HR: 1.098, 95% Cl: 1.022-1.179, P-value=0.01), admission urea (HR: 1.048, 95% Cl: 1.013-1.084, P-value=0.006), baseline creatinine (HR: 1.111, 95% Cl: 1.004-1.229, P-value=0.041), admission creatinine (HR: 1.047, 95% CI: 1.005-1.092, P-value=0.027) and admission glomerular filtration rate <30 mUmin (HR: 3.535, 95% CI: 1.467-8.518, P-value=0.005). Increased risk for short-term mortality was associated with baseline urea (HR: 1.145, 95% CI: 1.032-1.270, P-value=0.010), admission urea (HR: 1.076, 95% CI: 1.021-1.135, P-value=0.006), baseline creatinine (HR: 1.157, 95% CI: 1.009-1.328, P value -0.037), admission creatinine (HR: 1.127, 95% Cl: 1.055-1.204, P-value<0.001) and admission glomerular filtration rate <30 mUmin (HR: 9.791, 95% Cl: 2.855-33.580, P-value<0.001). Variables associated with an increased risk for end of follow-up mortality were admission urea (HR: 1.056, 95% CI: 1.019-1.094, P-value=0.003), admission creatinine (HR: 1.104, 95% CI: 1.054-1.156, P- value<0.001) and admission glomerular filtration rate <30 mUmin (HR: 3.906, 95% Cl: 1.7208.871, P- value=0.001). Conclusion: Renal dysfunction was a reliable predictor of worse prognosis as several parameters correlated with short-term prognosis.

Abstract Background Excessive adiposity, or obesity, has been associated with cancer promotion, including an increased risk for developing Hodgkin Lymphoma (HL). However, the association between obesity and survival in HL can be somewhat paradoxical and may indeed influence prognosis. Examining the bone marrow (BM) cytokine profile in HL patients could provide insights into the mechanisms underlying the altered association between excess adiposity and HL. The BM is an important site for hematopoiesis and can be influenced by various factors, including disease processes and systemic metabolic changes associated with obesity. Methods From our cohort, we analyzed interstitial marrow fluid (IMF) from BM aspirates of 16 HL patients at diagnosis and 11 control subjects. Participants were then matched by sex, age, and Body mass index (BMI) for inclusion in our discovery protein array analysis (n = 8 HL and n = 8 donors). We validated our findings in the total sample by measuring adipokine-related molecules using ELISA. Adiposity was measured through abdominal circumference measurement and BMI. Gene expression analysis was conducted through RT-qPCR. Activated signaling pathways were analyzed using HL cell line (L428 cells). Statistical analyses were performed using SPSS and GraphPad. Results The IMF of HL patients presented downregulation of interleukins (IL-1α/β, IL-6sR, IL-12), chemokines (CCL2, CCL3, CCL16), IGF-axis mediators (IGFBP-1, IGFBP-2, IGFBP-3, IGF-1sR), sTNFRII, TGFβ1, leptin, osteoprotegerin (OPG), and Fas compared to healthy donors and after controlling for adiposity status. Interestingly, HL overweight/obese subjects showed up-regulation of OPG and lymphotactin in IMF. The results were confirmed by quantification of cytokines, where we observed lower levels of insulin growth factor binding protein IGFBP-3 and higher levels of OPG levels in HL patients. The high-molecular weight (HMW) and total of adiponectin levels were high in HL BM. We further demonstrate that LEPR , TGFβ1 , and IGFBP3 transcripts were upregulated in fractionated BMAd from HL compared to controls, while IFG2R was upregulated in SC. Finally, we observed a possible modulation of L428 cells through IGFBP-3 in an IGF-1-dependent manner, which could be reflected in the BM TME of HL disease. Conclusions Our data supports a role for the insulin axis in the BM microenvironment of obese HL patients, particularly through the regulation of insulin ligand-binding proteins.

Abstract Background Excessive adiposity, or obesity, has been associated with cancer promotion, including an increased risk for developing Hodgkin Lymphoma (HL). However, the association between obesity and survival in HL can be somewhat paradoxical and may indeed influence prognosis. Examining the bone marrow (BM) cytokine profile in HL patients could provide insights into the mechanisms underlying the altered association between excess adiposity and HL. The BM is an important site for hematopoiesis and can be influenced by various factors, including disease processes and systemic metabolic changes associated with obesity. Methods From our cohort, we analyzed interstitial marrow fluid (IMF) from BM aspirates of 16 HL patients at diagnosis and 11 control subjects. Participants were then matched by sex, age, and Body mass index (BMI) for inclusion in our discovery protein array analysis (n = 8 HL and n = 8 donors). We validated our findings in the total sample by measuring adipokine-related molecules using ELISA. Adiposity was measured through abdominal circumference measurement and BMI. Gene expression analysis was conducted through RT-qPCR. Activated signaling pathways were analyzed using HL cell line (L428 cells). Statistical analyses were performed using SPSS and GraphPad. Results The IMF of HL patients presented downregulation of interleukins (IL-1α/β, IL-6sR, IL-12), chemokines (CCL2, CCL3, CCL16), IGF-axis mediators (IGFBP-1, IGFBP-2, IGFBP-3, IGF-1sR), sTNFRII, TGFβ1, leptin, osteoprotegerin (OPG), and Fas compared to healthy donors and after controlling for adiposity status. Interestingly, HL overweight/obese subjects showed up-regulation of OPG and lymphotactin in IMF. The results were confirmed by quantification of cytokines, where we observed lower levels of insulin growth factor binding protein IGFBP-3 and higher levels of OPG levels in HL patients. The high-molecular weight (HMW) and total of adiponectin levels were high in HL BM. We further demonstrate that LEPR, TGFβ1, and IGFBP3 transcripts were upregulated in fractionated BMAd from HL compared to controls, while IFG2R was upregulated in SC. Finally, we observed a possible modulation of L428 cells through IGFBP-3 in an IGF-1-dependent manner, which could be reflected in the BM TME of HL disease. Conclusions Our data supports a role for the insulin axis in the BM microenvironment of obese HL patients, particularly through the regulation of insulin ligand-binding proteins.

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Human papillomavirus (HPV) infection is a necessary but not sufficient factor for the development of invasive cervical cancer (ICC) and high-grade intraepithelial lesion (HSIL). Oxidative stress is known to play a crucial role in HPV infection and carcinogenesis. In this study, we comprehensively investigate the modulation of HPV infection, HSIL and ICC, and ICC through an exploration of oxidative stress-related genes: CβS, MTHFR, NOS3, ACE1, CYBA, HAP, ACP1, GSTT1, GSTM1, and CYP1A1. Notably, the ACE1 gene emerges as a prominent factor with the presence of the I allele offering protection against HPV infection. The association of NOS3 with HPV infection is perceived with the 4a allele showing a protective effect. The presence of the GSTT1 null mutant correlates with increased susceptibility to HPV infection, HSIL and ICC, and ICC. This study also uncovers intriguing epistatic interactions among some of the genes that further accentuate their roles in disease modulation. Indeed, the epistatic interactions between the BB genotype (ACP1) and DD genotype (ECA1) were shown to increase the risk of HPV infection, and the interaction between BB (ACP1) and 0.0 (GSTT1) was associated with HPV infection and cervical lesions. These findings underscore the pivotal role of four oxidative stress-related genes in HPV-associated cervical lesions and cancer development, enriching our clinical understanding of the genetic influences on disease manifestation. The awareness of these genetic variations holds potential clinical implications.

Aims: In heart failure patients renal dysfunction represents impaired tissue perfusion.We investigated the association of customarily used renal function parameters with short-term prognosis in patients admitted with acute decompensated heart failure in class III or IV of New York Heart Association.Material and Methods: Univariate Cox proportional hazard model was used to assess the relationship between variables and outcomes.Survival curves were designed using the Kaplan-Meier method.Results: We followed 65 patients for a median of 13.7 (Q1-Q3 6.7-18.9)months.Variables associated with an increased risk for short-term rehospitalization were baseline urea (HR: 1.098, 95% CI: 1.022-1.179,P-value=0.01),admission urea (HR: 1.048, 95% CI: 1.013-1.084,P-value=0.006),baseline creatinine (HR: 1.111, 95% CI: 1.004-1.229,P-value=0.041),admission creatinine (HR: 1.047, 95% CI: 1.005-1.092,P-value=0.027)and admission glomerular filtration rate <30 mL/min (HR: 3.535, 95% CI: 1.467-8.518,P-val-ue=0.005).Increased risk for short-term mortality was associated with baseline urea (HR: 1.145, 95% CI: 1.032-1.270,P-value=0.010),admission urea (HR: 1.076, 95% CI: 1.021-1.135,P-value=0.006),baseline creatinine (HR: 1.157, 95% CI: 1.009-1.328,P value=0.037),admission creatinine (HR: 1.127, 95% CI: 1.055-1.204,P-value<0.001)and admission glomerular filtration rate <30 mL/min (HR: 9.791, 95% CI: 2.855-33.580,P-value<0.001).Variables associated with an increased risk for end of follow-up mortality were admission urea (HR: 1.056, 95% CI: 1.019-1.094,P-val-ue=0.003), admission creatinine (HR: 1.104, 95% CI: 1.054-1.156,P-value<0.001)and admission glomerular filtration rate <30 mL/min (HR: 3.906, 95% CI: 1.7208.871,P-value=0.001).Conclusion: Renal dysfunction was a reliable predictor of worse prognosis as several parameters correlated with short-term prognosis.

Aims: In heart failure patients, anemia and iron deficiency are predictors of poor outcome.We studied the association of anemia, iron deficiency and related hematological parameters with short-term rehospitalization, short-term all-cause mortality and end of follow-up all-cause mortality in heart failure patients.Material and Methods: Anemia, iron deficiency, red cell distribution width and erythropoietin were assessed in patients hospitalized with acute decompensated heart failure.Univariate Cox proportional hazard model was used to assess the relationship between variables and outcomes.Results: 65 patients were followed for a median of 13.7 (Q1-Q3 6.7-18.9)months.Mean age was 79.2 (SD 10.8) years.The mean left ventricular ejection fraction was 50.38 ± 19.07 %.Variables associated with an increased risk for short-term rehospitalization were red cell distribution width (HR 1.35; 95% CI 1.16-1.58),anemia (HR 3.81; 95% CI 1.29-11.28)and anemia with iron deficiency (HR 3.50; 95% CI 1.30-9.38).Increased risk for short-term mortality was associated with red cell distribution width (HR 1.83; 95% CI 1.29-2.59),erythropoietin (HR 1.38; 95% CI 1.04-1.82),absolute iron deficiency (HR 7.22; 95% CI 1.50-34.81)and anemia with iron deficiency (HR 4.48; 95% CI 1.26-15.88).Variables associated with increased risk for end of follow-up mortality were red cell distribution width (HR 1.31; 95% CI 1.12-1.54)and erythropoietin (HR 1.29; 95% CI 1.11-1.49).Conclusions: Conclusions: Anemia and red cell distribution width correlated with higher risk for short-term rehospitalization.Absolute iron deficiency, red cell distribution width and erythropoietin were associated with higher risk for short-term mortality.Red cell distribution width and erythropoietin were associated with higher risk for end of follow-up mortality.

Aims: In heart failure patients, anemia and iron deficiency are predictors of poor outcome. We studied the association of anemia, iron deficiency and related hematological parameters with short-term rehospitalization, short-term all-cause mortality and end of follow-up all-cause mortality in heart failure patients. Material and Methods: Anemia, iron deficiency, red cell distribution width and erythropoietin were assessed in patients hospitalized with acute decompensated heart failure. Univariate Cox proportional hazard model was used to assess the relationship between variables and outcomes. Results: 65 patients were followed for a median of 13.7 (Q1-Q3 6.7-18.9) months. Mean age was 79.2 (SD 10.8) years. The mean left ventricular ejection fraction was 50.38 +/- 19.07 %. Variables associated with an increased risk for short-term rehospitalization were red cell distribution width (HR 1.35; 95% CI 1.16-1.58), anemia (HR 3.81; 95% CI 1.29-11.28) and anemia with iron deficiency (HR 3.50; 95% CI 1.30-9.38). Increased risk for short-term mortality was associated with red cell distribution width (HR 1.83; 95% CI 1.29-2.59), erythropoietin (HR 1.38; 95% CI 1.04-1.82), absolute iron deficiency (HR 7.22; 95% CI 1.50-34.81) and anemia with iron deficiency (HR 4.48; 95% CI 1.26-15.88). Variables associated with increased risk for end of follow-up mortality were red cell distribution width (HR 1.31; 95% CI 1.12-1.54) and erythropoietin (HR 1.29; 95% CI 1.11-1.49). Conclusions: Conclusions: Anemia and red cell distribution width correlated with higher risk for short-term rehospitalization. Absolute iron deficiency, red cell distribution width and erythropoietin were associated with higher risk for short-term mortality. Red cell distribution width and erythropoietin were associated with higher risk for end of follow-up mortality.

The AQP3 polymorphism is a promising biomarker for HT. HPSE polymorphism predicts PE-associated variations in the intermediate phenotype.

Abstract Aims In heart failure patients renal dysfunction represents impaired tissue perfusion. We investigated the association of customarily used renal function parameters with short-term prognosis in patients admitted with acute decompensated heart failure in class III or IV of New York Heart Association. Material and Methods Univariate Cox proportional hazard model was used to assess the relationship between variables and outcomes. Survival curves were designed using the Kaplan-Meier method. Results We followed 65 patients for a median of 13.7 (Q1-Q3 6.7-18.9) months. Variables associated with an increased risk for short-term rehospitalization were baseline urea (HR: 1.098, 95% CI: 1.022-1.179, P-value=0.01), admission urea (HR: 1.048, 95% CI: 1.013-1.084, P-value=0.006), baseline creatinine (HR: 1.111, 95% CI: 1.004-1.229, P-value=0.041), admission creatinine (HR: 1.047, 95% CI: 1.005-1.092, P-value=0.027) and admission glomerular filtration rate <30 mL/min (HR: 3.535, 95% CI: 1.467-8.518, P-value=0.005). Increased risk for short-term mortality was associated with baseline urea (HR: 1.145, 95% CI: 1.032-1.270, P-value=0.010), admission urea (HR: 1.076, 95% CI: 1.021-1.135, P-value=0.006), baseline creatinine (HR: 1.157, 95% CI: 1.009-1.328, P value=0.037), admission creatinine (HR: 1.127, 95% CI: 1.055-1.204, P-value<0.001) and admission glomerular filtration rate <30 mL/min (HR: 9.791, 95% CI: 2.855-33.580, P-value<0.001). Variables associated with an increased risk for end of follow-up mortality were admission urea (HR: 1.056, 95% CI: 1.019-1.094, P-value=0.003), admission creatinine (HR: 1.104, 95% CI: 1.054-1.156, P- value<0.001) and admission glomerular filtration rate <30 mL/min (HR: 3.906, 95% CI: 1.7208.871, P- value=0.001). Conclusion Renal dysfunction was a reliable predictor of worse prognosis as several parameters correlated with short-term prognosis. Resumen Introducción En la insuficiencia cardíaca, la disfunción renal representa hipoperfusión tejidual. Investigamos la asociación entre parámetros utilizados en el cotidiano y el pronóstico precoz de enfermos ingresados por insuficiencia cardíaca descompensada en classe III o IV de New York Heart Association. Material y métodos Aplicamos el modelo de riesgo proporcional de Univariante Cox y curvas de supervivencia de Kaplan-Meier. Resultados La mediana de seguimiento de los 65 enfermos fue de 13.7 (Q1-Q3 6.7-18.9) meses. Se correlacionarón con el reingreso precoz la urea basal (HR: 1.098, 95% CI: 1.022-1.179, P-value=0.01), urea al ingreso (HR: 1.048, 95% CI: 1.013-1.084, P-value=0.006), creatinina basal (HR: 1.111, 95% CI: 1.004-1.229, P-value=0.041), creatinina al ingreso (HR: 1.047, 95% CI: 1.005-1.092, P-value=0.027) y tasa de filtración glomerular <30 mL/min al ingreso <30 mL/min (HR: 3.535, 95% CI: 1.467-8.518, P-value=0.005). El riesgo de mortalidad precoz se correlacionó con la urea basal (HR: 1.145, 95% CI: 1.032-1.270, P-value=0.010), urea al ingreso (HR: 1.076, 95% CI: 1.021-1.135, P-value=0.006), creatinina basal (HR: 1.157, 95% CI: 1.009-1.328, P value=0.037), creatinina al ingreso (HR: 1.127, 95% CI: 1.055-1.204, P-value<0.001) y tasa de filtración glomerular <30 mL/min al ingreso <30 mL/min (HR: 9.791, 95% CI: 2.855-33.580, P-value<0.001). Se correlacionarón con la mortalidad al final del seguimento la urea al ingreso (HR: 1.056, 95% CI: 1.019-1.094, P-value=0.003), creatinina al ingreso (HR: 1.104, 95% CI: 1.054-1.156, P- value<0.001) y tasa de filtración glomerular <30 mL/min al ingreso (HR: 3.906, 95% CI: 1.7208.871, P- value=0.001). Conclusiones La disfunción renal fue un predictor de peor pronóstico precoz.

Abstract BACKGROUND AND AIMS Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disease characterized by the formation and growth of renal cysts, affecting the decrease of renal function, which may lead to end-stage renal disease (ESRD). Due to the enormous intrafamilial phenotypic variability of ADPKD and since serum creatinine and glomerular filtration rate (GFR) have a limited ability to assess the disease and predict its progression at earlier stages, there is a need to find new biomarkers to predict disease progression. The α-glutathione s-transferase (GST-α) and haptoglobin (Hp) are produced mainly by the proximal convoluted tubule, and these enzymes are released into the urinary lumen in direct response to tubular damage. This study aims to evaluate the urine concentration of α-GST and Hp biomarkers at different stages of ADPKD progression and correlate the levels of urinary biomarkers α-GST and Hp with traditional markers of renal dysfunction. METHOD Twenty-five patients with ADPKD, mean age of 41.57 ± 14.43 years, mostly female (56.0%), diagnosed according to the Ravine criteria and with a follow-up of at least 60 months. Demographic, hemodynamic, urinary creatinine (UCr) and serum creatinine (SCr) data were collected in baseline (T0) and at the end of the follow-up period (T1). GFR was determined using the CKD-EPI formula, grouping patients into early stages (CKD1 and CKD2) and advanced stages (CKD3 to CKD5). Biomarkers were determined by the ELISA method and indexed to UCr in T1. In addition, α-GST was determinate in a control sample composed of 17 individuals without diagnosed kidney disease. Statistical analysis was performed by SPSS version 26 with a significant value of P < 0.05. RESULTS Comparing the means of SCr and GFR between T0 and T1 were observed a decrease of renal function during the follow-up period (P = 0.013 and P = .017, respectively). About 14.4% of patients were in an advanced stage of kidney disease in T1, compared with 4.8% in T0. ADPKD patients had increased values of α-GST in relation to the control group (P < 0.001), but no difference in the SCr was found. We also found a trend for higher levels of HP in advanced stages of CKD (P = 0.071). In ADPKD patients, direct correlations were observed between the variation of SCr during the follow-up with α-GST and Hp (r = 0.606, P = 0.048 and r = 0.738, P = 0.037, respectively). A trend to correlation was found between the levels of Hp and the Scr in T1 (r = P = 0.058). CONCLUSION The levels of α-GST and Hp are associated with renal damage and may be helpful in the early identification of the decline in renal function in ADPKD patients.

The studied polymorphisms seem to directly impact and/or modulate levels of some biomarkers associated with progression and stage of CKD in ADPKD patients.

Objective: Apparently healthy young adults may have risk factors associated with arterial hypertension (HBP) and atherosclerosis. The objective was to evaluate the presence of HBP, obesity and other anthropometric or metabolic cardiovascular (CV) risk parameters in young adults and their association to inflammation connected blood count parameters, as possible earlier determinants for the path of CV future disease. Design and method: A sample of 250 students (76 men, 174 women; aged 22.1 ± 2.79 years; 94.8% Caucasians; 82.3% eutrophic) was studied. Body Mass Index (BMI Kg/m2), waist circumference (WC cm) and blood pressure (BP mmHg) were measured according to standard methods. Blood count parameters, glucose, cholesterol, HDL and triglycerides (mmol/L) determined according to standard hospital laboratory. Statistics: t-student, ANOVA or equivalent non-parametric, Chi-square and Pearson/Spearman correlations according normality distribution. Results: Most subjects (91.5%) had normal BP (mean ± SD systolic 116.7 ± 14.0; diastolic 69.6 ± 9.4). HBP frequency showed no differences between gender (p = 0.154), but an association between BMI (p < 0.000) with HBP was observed, as 92.9% of hypertensive patients were also obese or overweight. In male compared to women, higher glucose values (p = 0.000), BMI (p = 0.011) and WC (p = 0.000) but lower HDL values (p = 0.000) were observed. BMI and WC were also higher (respectively p = 0.005 and p = 0.004) in hypertensive subjects. WC adjusted for BMI was a risk factor for HBP (p = 0.043; OR = 1.059; 95% CI = 1.002–1.119). Regarding BMI classes (<18.5, 18.5–25, > 25) values were higher in overweight/obese subjects for the following ratios to HDL: monocytes (p = 0.045), monocytes X LDL (p = 0.006), platelets X LDL (p = 0.002), monocytes X platelets X LDL (p = 0.005), monocytes X platelets (0.032). In hypertensive subjects, monocyte X platelet to HDL ratio was higher (p = 0.03) compared to normotensive and a correlation was also observed between glucose and the following ratios to HDL: monocytes X LDL (p = 0.033), monocytes X platelets (p = 0.045) and monocytes X platelets X LDL (p = 0.034). Conclusions: Even in younger age groups a major impact prediction cardiovascular risk is possible. Anthropometric, metabolic and blood count parameters and its association could be early biomarkers associated with hypertension and should be considered as indicators of present and/or future cardiovascular disease.