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The purpose of this study was to describe the methodology to assess the stability of all-in-one (AIO) parenteral nutrition admixtures, containing glucose, proteins, and lipids, to the standards of U.S. Pharmacopoeia (USP729). The influence of calcium and commercially available lipid emulsions and amino acid solutions were also examined.Four batches of 5 AIO admixtures containing calcium were compounded with commercially available lipid emulsions and amino acid solutions. Two of them contained calcium. Their stability was tested under conditions simulating clinical use. All the admixtures were assessed for criteria set by the USP729: (1) mean droplet diameter (MDD) and (2) percentage of volume weighted particles with diameter5 μm (PFAT5).All admixtures were within the specifications set by the USP with respect to the MDD at 0, 24, and 48 hours, but only those batches lacking calcium met the benchmarks set by the pharmacopoeia, with respect to PFAT5, on the day of preparation.The presence of calcium destabilized the admixtures, while the use of different commercial ingredients altered the admixtures' characteristics. Only 1 batch of the AIO admixtures studied was found to be compliant with USP729standards.

Background Endothelial dysfunction and oxidative stress are believed to be central mechanisms in atherogenesis. We aimed to determine the effects of tirofiban on oxidative stress and neutrophil–endothelium interaction markers in patients with acute coronary syndromes (ACS). Materials and methods We measured malondialdehyde (MDA), interleukin-6 (IL-6) and soluble endothelial intercellular and vascular adhesion molecules (sICAM-1 and sVCAM-1) on admission, at 48 and 72 h and on 5th day of hospitalization in 34 patients (age 66.5 ± 1.8 years) with ACS. Patients with recurrent angina, changes on the electrocardiogram and/or elevated troponin I received intravenously tirofiban for 48 h and the others received normal saline. Results Baseline concentrations of all markers did not differ significantly and compared with placebo, tirofiban infusion markedly reduced MDA, IL-6, sICAM-1 and sVCAM-1 at 48 h (− 31 ± 6% vs. 84 ± 49%, p = 0.007, − 12 ± 14% vs. 23 ± 10%, p = 0.05, − 20 ± 6% vs. 36 ± 25%, p = 0.04 and − 10 ± 5% vs. 6 ± 5%, p = 0.02, respectively). Relative to baseline, significant reductions were observed for all 4 markers at 72 h and day 5 (p Conclusion Tirofiban potentiates the decline in oxidative stress and may reverse abnormal endothelial activation in patients with ACS. This benefit seems to remain over the following 5 days.

Aim To investigate the effect of a new inotropic drug, levosimendan compared with dobutamine on levels of brain natriuretic peptide (BNP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and malondialdehyde (MDA) in patients with severe decompensated heart failure. Methods and results Twenty-nine consecutive patients (22 males and 7 females), mean age 70.5±9.9 years, with decompensated heart failure on standard medical therapy, were randomised to receive either a 24 h infusion of levosimendan (n=15) or dobutamine (n=14). Blood samples were drawn at baseline, 48 h and 5 days post infusion. Levosimendan produced a significant reduction in BNP compared to baseline, at both 48 h (744.1±100 vs 1136.3±93.7 pg/ml, p=0.04) and 5 days (446±119.3 vs 1136.3±93.7 pg/ml, p=0.03), while IL-6 values decreased after 5 days (4.8±1.3 vs 8.6±1.5 pg/ml, p=0.01). MDA levels were significantly lower 5 days after levosimendan compared to baseline (2.3±0.2 vs 3±0.3 μM, p=0.01). TNF-α levels did not differ between the groups. The comparison of percentage alteration compared to baseline showed that BNP (–44.5±7.6% vs 4.8±18.7%, p=0.025), MDA (–21.8±5.1% vs 14.9±8.5%, p=0.001) and IL-6 (–38.8±12.5% vs 70.2±24%, p=0.001) levels were significantly lower in the levosimendan group 5 days after treatment compared to the dobutamine group. Conclusions Treatment with levosimendan in advanced decompensated heart failure exerts a beneficial hemodynamic, anti-inflammatory and antioxidant effect. These findings may give an insight into the favourable impact on mortality that levosimendan appears to have in published multicenter trials.

Background Depression is a common comorbid condition in patients with chronic heart failure (CHF). This pilot study investigated the plasma levels of oxidative stress markers in depressed CHF patients as well as the effects of antidepressant treatment with sertraline on these markers in the same patient population. Methods and Results Patients with positive depression screening [Beck Depression Inventory (BDI) score >10 and/or Zung Self-Rating Depression Scale >40] underwent a psychiatric interview. Patients newly diagnosed as depressed received pharmacologic treatment with sertraline for 3 months (arm A) and were compared with those who did not comply with the antidepressant treatment (arm B). Markers of oxidative stress [malondialdehyde (MDA) and protein carbonyls (PC)], and nitrosative stress [nitrotyrosine (NT)] were assessed at baseline and 3 months later. Fifty-two out of 254 screened hospitalized CHF patients were diagnosed as depressed. Depressed patients had significantly higher levels of MDA compared with age- and gender-matched nondepressed patients (n = 40; 3.2 ± 2.0 vs 2.8 ± 3.8 μmol/L; P = .02). Twenty-eight patients received sertraline (arm A), and 24 refused to receive antidepressant treatment on the top of optimal heart failure treatment (arm B). Although baseline levels of MDA and PC in arm A and arm B did not differ significantly ( P > .05), arm A patients demonstrated a significant reduction in MDA (F = 4.657; P = .037) and arm B patients demonstrated no change after 3 months. Regarding the examined scores, arm A patients had a decrease in BDI score (28 ± 11 vs 21 ± 13; P = .008), and arm B patients had no change in BDI score at follow-up ( P > .05). Arm A had an increase in 6-minute walking distance (291 ± 110 vs 361 ± 87 m; P = .02), and arm B experienced no change ( P > .05). Conclusions Increased oxidative stress may play a critical role in the pathophysiology of depression in CHF. Treatment with sertraline improves depressive symptoms and reduces plasma markers of oxidative stress in depressed CHF patients.