In lone PAF, GERD should be investigated as a potential pathogenetic mechanism. PPI therapy reduces not only GERD-related but also PAF-related symptoms.

Granulocyte colony-stimulating factor (G-CSF) stimulates the bone marrow to produce granulocytes and stem cells and is widely used to accelerate neutrophil recovery after chemotherapy. Interestingly, specific G-CSF receptors have been demonstrated not only on myeloid cells, but also on platelets. Data on the effects of G-CSF on platelet function are limited and partly conflicting. The objective of this study was to determine the effect of G-CSF on platelet aggregation and in vivo platelet activation. Seventy-eight, healthy volunteers were enrolled into this randomised, placebo-controlled trial. Subjects received 5 μg/kg methionyl human granulocyte colony-stimulating factor (r-metHuG-CSF, filgrastim) or placebo subcutaneously for four days. We determined platelet aggregation with a whole blood impedance aggregometer with various, clinically relevant platelet agonists (adenosine diphosphate [ADP], collagen, arachidonic acid [AA], ristocetin and thrombin receptor activating peptide 6 [TRAP]). Filgrastim injection significantly enhanced ADP (+40%), collagen (+60%) and AA (+75%)-induced platelet aggregation (all p<0.01 as compared to placebo and p<0.001 as compared to baseline). In addition, G-CSF enhanced ristocetin-induced platelet aggregation (+18%) whereas TRAP-induced platelet aggregation decreased slightly (-14%) in response to filgrastim. While baseline aggregation with all agonists was only slightly but insignificantly higher in women than in men, this sex difference was enhanced by G-CSF treatment, and became most pronounced for ADP after five days (p<0.001). Enhanced platelet aggregation translated into a 75% increase in platelet activation as measured by circulating soluble P-selectin. G-CSF enhances platelet aggregation and activation in humans. This may put patients suffering from cardiovascular disease and cancer at risk for thrombotic events.

No abstract

To determine the degree of neurocognitive dysfunction after placement of internal cardioverter defibrillators (ICD) and its relationship to the extent of neuronal injury, we studied 42 patients undergoing ICD (n = 21) or pacemaker (PM) insertion (control patients, n = 21). The Mini Mental State Examination, the Trailmaking A test and the forward and backward Digit Span tests were used and P300 latencies were determined preoperatively and postoperatively. Serum neuron-specific enolase (NSE) was determined before and at the end of, as well as 2, 6, and 24 h after surgery. Preoperatively, PM patients scored worse in the Digit Span backward and the Trailmaking tests and showed prolonged P300 latencies. Postoperatively, the Digit Span backward scores declined and NSE levels increased only in the ICD group (P < or = 0.05). The difference between preoperative and postoperative Digit Span backward scores correlated with the increase in serum NSE levels (r2 = 0.3, P < or = 0.05). Moreover, P300 latencies increased in 13 of 17 ICD patients, but decreased in 7 of 10 PM patients (P < or = 0.05). PM patients even improved in the Trailmaking test (P < or = 0.05). Neuronal injury from even brief periods of global brain ischemia seems to be associated with deteriorating neurocognitive function.

Magnesium gluconate moderately reduced the remifentanil consumption without serious side-effects. The opioid-sparing effect of magnesium may be greater at higher pain intensities and with increased dosages.