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Aleksander Danikiewicz

Publications and source records attributed to Aleksander Danikiewicz.

3 recordsLinked to original sources

Effects of simvastatin on pro-inflammatory cytokines in patients with hypercholesterolemia.

BACKGROUND: The role of inflammation in the development of atherosclerosis and its complications has been recently documented. Pro-inflammatory cytokines are among many postulated factors. It is possible that the imbalance between protective cytokines and cytokines affecting endothelial function is one of the underlying mechanisms of myocardial ischaemia. AIM: To examine the effects of simvastatin on IL-2 and TNFalpha levels in patients with hypercholesterolemia. METHODS: The study group consisted of 64 males (age 20-65 years) with hypercholesterolemia. The control group was composed of 10 healthy male volunteers (age 25-40 years) with normal lipid profile. Total cholesterol, LDL-cholesterol, IL-2 and TNFalpha were measured in both groups at baseline, after three months of dietary treatment, and after a further three months of simvastatin therapy. RESULTS: Simvastatin caused a significant decrease in the total and LDL-cholesterol levels compared both with baseline measurements (p=0.0001) and after dietary treatment (p=0.0001). Moreover, simvastatin significantly reduced the IL-2 plasma concentration (p=0.0003). There were no significant differences between IL-2 levels before and following dietary treatment. The TNFalpha serum concentration significantly decreased following the implementation of diet (p=0.0001). Subsequent simvastatin therapy caused further decrease in the TNFalpha serum concentration but this difference did not achieve statistical significance. CONCLUSIONS: A hypolipemic diet significantly decreases TNFalpha serum concentration without affecting the IL-2 level. The subsequent simvastatin therapy significantly reduces IL-2 but not TNFalpha when compared with the post-diet values.

Adult↗

[Hypothalamic-pituitary-thyroid axis in depression].

Depressed patients, although viewed as chemically euthyroid, have alterations in the function of hypothalamic-pituitary-thyroid axis including slight elevation of the serum thyroxine (T4), loss of the nocturnal TSH rise, blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) stimulation and predisposition to autoimmune thyroiditis. Both hypothyroid and depressed patients share a number of clinical features in common. This is the reason that some research workers use the "brain hypothyroidism" hypothesis to explain the pathogenesis of depression. They suggest that depression is a state of local hypothyroidism in brain with normal peripheral thyroid hormone concentrations as a result of brain type II deiodinase inhibition and impaired transport T4 across the blood brain barrier. This theory seems to be compatible with the serotonin deficiency hypothesis of depression. Some studies confirm the existence of classical feedback between serotoninergic and hypothalamus-pituitary-thyroid systems. TRH remains under a constant inhibition by serotonin and reduced intracerebral serotonin concentration seen in depression will lead to increased TRH concentration in brain tissue. This mechanism is probably responsible for blunted TSH response to TRH stimulation.

Depressive Disorder↗