ABSTRACT
Glioblastomas are among the most malignant tumors which, despite aggressive treatment, currently have an abysmal prognosis. These lesions are known to cause local and systemic perturbations in the coagulation system, leading to neo-angiogenesis and a high risk of venous thromboembolism. Indeed, there have been multiple proposals of the coagulation system being a possible target for future treatment of these patients. However, non-selective anticoagulant therapy has proven suboptimal and leads to a significant increase of intracranial hemorrhage. Thus, recognizing factors which lead to hyper-coagulation is considered paramount. Hyperglycemia is a well-known pro-thrombotic factor, a fact which has received little attention in neuro-oncology so-far. We previously hypothesized that patients with brain tumors could be highly susceptible to iatrogenic glycemia dysregulation. Here, we analyzed the connection between glycated hemoglobin (HbA1c) and the routine coagulation markers (D-dimers, prothrombin time (PT) and activated partial thromboplastin time (aPTT)) in patients with de novo intracranial glioblastomas. Included in this study were 74 patients, operated on in three hospitals, Clinical Hospital Dubrava, Zagreb, Croatia; University Hospital Center Split, Split, Croatia and University Hospital de la Princesa, Madrid, Spain. We found a significant inverse correlation between HbA1c and aPTT (ρ=-0.379; P=0.0009). We also found a significant inverse correlation between Ki67 immunoreactivity and aPTT (ρ=-0.211; P=0.0082). No connection was found between HbA1c and D-dimers or PT. Our results suggest that hyperglycemic patients, with a more proliferative glioblastoma, could in fact have their coagulation profile significantly disrupted, primarily through the intrinsic coagulation pathway. Such findings could have great clinical importance. Further research in this area could help elucidate the vicious connection between glioblastomas and coagulation, and help combat the deadly disease.
ABSTRACT
AIM: Obesity is a well-known risk factor in the cardiovascular disease continuum. However, its clinical effects are multimodal, perplexed and non-unanimously understood. Our aim was to assess the prevalence and effects of obesity on the cardiometabolic risk factors and systolic function of left ventricle ejection fraction (LVEF) in patients scheduled for cardiovascular rehabilitation. METHODS: A cohort of 302 consecutive patients recently treated for ischaemic or valvular heart disease was matched according to the existence of obesity, defined with body mass index (BMI ≥ 30 kg/m(2) ; n = 90 vs. 212), and the advanced grade of obesity (BMI ≥ 35 kg/m(2) ; n = 19 vs. 283). Nutritional risk screening was performed using the standardised NRS-2002 tool. RESULTS: The mean age of patients was 62.4 ± 11.2 (range 23-86) years; there were more men than women 244 (80.8%) : 58 (19.2%). Group of obese conveyed higher prevalence of ischaemic heart disease than non-obese (OR = 2.69; 95% CI: 1.01-7.20; p = 0.048); while the difference was insignificant for the advanced grade of obesity (n = 17; 89.5%) vs. controls (n = 233; 82.3%; p > 0.05). There was no significant difference in prevalence of other comorbidities (diabetes, glucose intolerance, hypercholesterolaemia, chronic renal and chronic obstructive pulmonary disease) between studied groups (p > 0.05). Utilisation of lipid-lowering drugs was of similar range between the studied groups (p > 0.05), respectively. LVEF (%) was 50.5 ± 8.2 vs. 50.7 ± 7.7 (p > 0.05) and 50.6 ± 7.8 vs. 49.6 ± 10.9 (p > 0.05; Rho = 0.001; p > 0.05), respectively. CONCLUSION: In studied set of patients, BMI positively correlated with left ventricle dimension and thickness. No significant connection of obesity was found with the prevalence of chronic comorbidities, increased nutritional risk, laboratory diagnostics or systolic function of left ventricle. Existence of obesity paradox in clinical practice was in part reaffirmed with our study.
