Biomedical subjects

Nicole Kotzailias

Publications and source records attributed to Nicole Kotzailias.

5 recordsLinked to original sources

PubMed2006

Antiplatelet activity during coadministration of the selective serotonin reuptake inhibitor paroxetine and aspirin in male smokers: a randomized, placebo-controlled, double-blind trial.

Depression is associated with an increased incidence of vascular events and develops after stroke and myocardial infarction. Beside potential clinical outcome benefits of selective serotonin reuptake inhibitors for vascular diseases, bleeding events were reported. We investigated whether paroxetine and aspirin synergistically inhibit platelet function. Paroxetine (20 mg/d) was administered over 18 days to 20 men in a randomized, placebo-controlled, crossover design. Aspirin (100 mg/d) was coadministered within the last 4 study days. Platelet function was assessed by the platelet function analyzer and by flow cytometry. Paroxetine prolonged epinephrine-dependent predictive index within 14 days (P<.02). Aspirin enhanced the predictive index (P<.004 vs baseline and P>.05 between periods). A trend toward decreased thrombin receptor-activating peptide-induced CD62P expression after paroxetine was further enhanced by aspirin treatment (P>.05 between periods). The combination of paroxetine and aspirin did not further inhibit platelet plug formation under high shear stress in male smokers.

Adult↗

PubMed2004

Early effects of paroxetine on serotonin storage, plasma levels, and urinary excretion: a randomized, double-blind, placebo-controlled trial.

Selective serotonin reuptake inhibitors efficiently decrease intraplatelet concentrations of the platelet activator and potent vasoconstrictor serotonin within 2 weeks of treatment. As elevated plasma serotonin levels potentially lead to vascular adverse events, like vasoconstriction, it is of interest to examine whether selective serotonin reuptake inhibitors may acutely increase plasma serotonin levels. Twenty healthy male smoking volunteers received the selective serotonin reuptake inhibitors paroxetine 20 mg/d for 18 days in a double-blind, placebo-controlled, block-randomized, 2-way crossover study to characterize the acute effect of paroxetine on serotonin plasma levels and urinary excretion. Paroxetine decreased intraplatelet serotonin concentrations by a median of 16% after 24 hours and by -93% after 18 days (P < 0.001). After 24 hours, there was a slight transient rise in plasma serotonin concentration by 36%-which ranged within physiologic concentrations of the control period. Concomitantly, urinary serotonin excretion increased by 89% after 24 hours. In conclusion, initiation of paroxetine treatment does not increase plasma concentrations of the potent vasoconstrictor serotonin to a pathologically relevant extent.

Adult↗

PubMed2004

Platelet function in mitochondriopathy with stroke and stroke-like episodes.

Stroke and stroke-like episodes are frequent complications in mitochondriopathy, particularly in MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes) which is a disorder of the mitochondrial oxidative metabolism in diverse cell types. To clarify a possible pathological aspect of stroke in these patients, we investigated platelet function before and after physical exercise. Ten patients with mitochondriopathy and stroke and ten healthy sex and age matched controls were investigated in an analyst blinded, prospective cross-sectional trial. Exercise decreased intraplatelet adenosine triphosphate (ATP) concentrations by -22% from baseline in patients with mitochondriopathy (p<0.01 between groups) while exercise increased ATP-levels by 28% healthy controls (p=0.01 vs baseline). Thrombin receptor activating peptide (TRAP) stimulated P-selectin expression increased up to 50% (p<0.05) in healthy subjects following exercise compared to 39% (p>0.05) in patients with mitochondriopathy. Exercise trendwise decreased platelet plug formation under shear stress by 24% in patients as measured by the platelet function analyzer PFA-100(R). Tromboelastography showed firm thrombus formation and delayed lysis in patients following exercise. In conclusion, this trial has shown that ATP depletion during and after exercise probably accounts for a defective oxidative metabolism in platelets of patients with mitochondriopathy and stroke. This might induce decreased platelet function in these patients but fails to explain the increased stroke rate. Therefore other mechanisms seem to be etiologically involved in the pathogenesis of stroke in patients with mitochondriopathy.

Adenosine Triphosphate↗

PubMed2003

Influence of tiapride on platelet counts in healthy volunteers and patients with movement disorders.

BACKGROUND: The selective D2 antagonist tiapride is administered in various movement disorders. Furthermore, there are indications that tiapride increases platelet counts. AIM: To characterize tiapride's potential to increase platelet counts in healthy subjects and patients with movement disorders. METHODS: In Part A, 10 healthy volunteers received tiapride (300 mg/day) for 21 days in a longitudinal, prospective, open trial. One hundred healthy subjects served as controls. Part B was a retrospective analysis of 15 patients with movement disorders on tiapride [Huntington's disease (n=6), Morbus Little (n=3), hyperkinetic syndromes of undetermined etiology (n=3), blepharospasm (n=1), cervical dystonia (n=1), perioral dyskinesia (n=1)] and 15 age- and sex-matched controls. RESULTS: Part A: Although serum prolactin levels increased by 526+/-14%, confirming good drug compliance, tiapride elicited only minor changes in platelet counts. Part B: Platelet counts correlated positively with the dose of tiapride (100-800 mg/day; r=.67; P=.007). Platelet counts were significantly higher in patients on tiapride compared to healthy age-matched controls (P<.001). Four patients responded to an increase in the tiapride dosage with an increase in platelet count by 97-173 cells/nl. CONCLUSION: Three weeks of treatment with tiapride (300 mg/day) is insufficient to elevate platelet counts to a clinically relevant extent in young healthy volunteers. However, in elderly patients with movement disorders tiapride treatment is associated with markedly increased platelet counts.

Administration, Oral↗

PubMed2003

Thrombocytosis under ciprofloxacin and tazobactam/piperacillin.

Whether the simultaneous administration of ciprofloxacin or tazobactam/piperacillin increases the risk of thrombocytosis is unknown. Broncho-pulmonary infection in a 50-year-old male with acute, hypertensive, intracerebral bleeding, necessitated therapy with cefpirome (2 g/day, 6 days), ciprofloxacin (800 mg/d, 11 days) and tazobactam/piperacillin (9 g/day, 11 days). Starting with the 8th hospital day, the thrombocyte count steadily increased from 410000/microl to a maximum of 1132000/microl on hospital day 16. Afterwards the thrombocyte count continuously decreased to normal values. Primary thrombocytosis and secondary causes were excluded. Since the thrombocyte count started to increase immediately after initiation and dropped immediately after discontinuation of ciprofloxacin and tazobactam/piperacillin and all other drugs were discontinued already before or were started after the nadir of the thrombocyte count, these two antibiotics were regarded causative. It is concluded that simultaneous administration of ciprofloxacin and tazobactam/piperacillin may cause marked thrombocytosis. Discontinuation of these two antibiotics results in an immediate decline of the thrombocyte count to normal values within three weeks.

Anti-Bacterial Agents↗