Neutrophil/HDL-C, Lymphocyte/HDL-C and Monocyte/HDL-C in subjects with asymptomatic carotid atherosclerosis.

BACKGROUND: Leukocyte count is a prognostic marker for cardiovascular diseases, with key role in atherosclerosis development. Specific number of neutrophils, lymphocytes and monocytes can predict cardiovascular risk, also in asymptomatic subjects. Among the lipoprotein fractions, HDL-C is a protective factor in the cardiovascular disorders. For the above reason, we have examined the peripheral count of leukocytes, neutrophils, lymphocytes and monocytes, and the ratios between neutrophils/HDL-cholesterol, lymphocytes/HDL-cholesterol, and monocytes/HDL-cholesterol, to evaluate the possible utility of the obtained values in progression of asymptomatic carotid atherosclerosis. METHODS: We performed our analysis in a cohort of 100 subjects with asymptomatic carotid atherosclerosis, of which 43 men and 57 women. The data were expressed as medians and IQR. To analyse the differences in leukocyte, neutrophil, lymphocyte, monocytes count and their ratio with HDL-cholesterol the Mann-Whitney test was employed. RESULTS: The peripheral count of leukocyte subtypes and the ratios, they change in relation to the number of cardiovascular risk factors and the degree of insulin resistance. CONCLUSIONS: In this cohort of subjects, the percentage of observed cardiovascular risk factors significantly affect some leukocyte parameters. These results, allow us to underline the importance of the leukocyte indices in the evaluation of subjects with asymptomatic vascular atherosclerosis.

Uric acid and uric acid/creatinine ratio and their correlations with the hemorheological determinants in subjects with subclinical carotid atherosclerosis.

BACKGROUND AND OBJECTIVE: we have examined the concentration of serum uric acid and the serum uric acid/creatinine ratio as well as their correlations with the main determinants of the hemorheological profile in a group of subjects with subclinical carotid atherosclerosis. METHODS: we evaluated the concentration of serum uric acid and the serum uric acid/creatine ratio in 43 men and 57 women [median age 66.00 (25)] with subclinical carotid atherosclerosis, subsequently divided according to the number of traditional cardiovascular risk factors and to the insulin resistance degree. RESULTS: serum uric acid, but not the serum uric acid/creatinine ratio, results strongly influenced by the number of cardiovascular risk factors and by the insulin resistance degree. In the whole group and in the subgroups of subclinical carotid atherosclerosis subjects, serum uric acid and serum uric acid/creatinine ratio show significant correlation, besides with whole blood viscosity, with plasma viscosity and erythrocyte aggregation. The influence of the serum uric acid on the erythrocyte aggregability that is a part of the erythrocyte aggregation is to ascribe to the action carried out by serum uric acid on the erythrocyte zeta potential. CONCLUSIONS: it is reasonable to think that the treatment of the asymptomatic or symptomatic hyperuricemia with the urate-lowering therapy that reduces the serum uric acid concentration may reflect on the hemorheological profile which role on the atherosclerotic cardiovascular disease is well known.

[Analysis of the parameters, traditional or not, for the evaluation of the metabolic acidosis]. / Considerazioni sui parametri di valutazione, tradizionali e non, delle acidosi metaboliche.

Despite huge progress in acidbase knowledge, several confusing, irrational and controversial issues still remain. Acid-base disturbances have been usually evaluated with the traditional Henderson-Hasselbach method and with BE evaluation that seem inadequate since they define the magnitude of metabolic acidosis rather than its cause. Some studies have shown that the traditional approach is often not able to highlight the complicated acid-base disorders in critically ill patients; in these subjects, the possibility to identify tissue acids could offer a greater prognostic value than the evaluation of traditional parameters. An alternative approach is the Stewarts physiochemical method that defines the aetiology of a metabolic acidosis by quantifying the tissue acids. But the clinical utility of this method is limited due to its mathematical complexity. Therefore, some parameters of simplification were proposed in order to allow greater clinical applicability of this system. Specifically, it was observed that in the presence of metabolic acidosis, the chloride/sodium ratio (Cl-/Na+ ratio) or the sodium-chloride difference (DiffNa-Cl) would be useful indicators of the presence of unmeasured anions (UMA) and/or lactate.

Acid-base and electrolyte abnormalities in heart failure: pathophysiology and implications.

Electrolyte and acid-base abnormalities are a frequent and potentially dangerous complication in subjects with congestive heart failure. This may be due either to the pathophysiological alterations present in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), or to the adverse events of therapy with diuretics, cardiac glycosides, and ACE inhibitors. Subjects with heart failure may show hyponatremia, magnesium, and potassium deficiencies; the latter two play a pivotal role in the development of cardiac arrhythmias. The early identification of these alterations and the knowledge of the pathophysiological mechanisms are very useful for the management of these patients.

Physiopathological, Epidemiological, Clinical and Therapeutic Aspects of Exercise-Associated Hyponatremia.

Exercise-associated hyponatremia (EAH) is dilutional hyponatremia, a variant of inappropriate antidiuretic hormone secretion (SIADH), characterized by a plasma concentration of sodium lower than 135 mEq/L. The prevalence of EAH is common in endurance (<6 hours) and ultra-endurance events (>6 hours in duration), in which both athletes and medical providers need to be aware of risk factors, symptom presentation, and management. The development of EAH is a combination of excessive water intake, inadequate suppression of the secretion of the antidiuretic hormone (ADH) (due to non osmotic stimuli), long race duration, and very high or very low ambient temperatures. Additional risk factors include female gender, slower race times, and use of nonsteroidal anti-inflammatory drugs. Signs and symptoms of EAH include nausea, vomiting, confusion, headache and seizures; it may result in severe clinical conditions associated with pulmonary and cerebral edema, respiratory failure and death. A rapid diagnosis and appropriate treatment with a hypertonic saline solution is essential in the severe form to ensure a positive outcome.