Multiple effectiveness aspects of tapentadol for moderate-severe cancer-pain treatment: an observational prospective study.

BACKGROUND: Previous studies have shown the efficacy of tapentadol (TP) for chronic cancer pain. We evaluated multiple effectiveness aspects of TP prolonged release on moderate-severe cancer-related pain, neuropathic pain (NeP), patient satisfaction, and quality of life. METHODS: An observational prospective study was conducted on 80 cancer patients. Opioid-naïve patients received a starting dose of prolonged-release TP 50 mg twice daily, and opioid-experienced patients were switched to TP, not to exceed 500 mg/day. Treatment response was evaluated at 3, 6, 30-40, and 60-70 days through response rate, numeric rating-scale scoring, survival analysis (time to event for response), pain-intensity difference, TP escalation-index percentage, and effects on NeP. The drug-sparing effect on concomitant therapies was evaluated. RESULTS: Seventy of 80 patients (88%) were responders to treatment (95% CI 78%-94%). Compared to T0, pain-intensity reductions were statistically significant for all intervals (P<0.01), with better results at T3/T4. NeP was significantly reduced at T4 (P<0.01). The probability of response was low at the initial stages and increased during the study. Pain-intensity differences decreased during the study, though without significance. Two patients (2.5%) left the study for TP-induced side effects. A significant improvement in quality of life was observed after 30-40 days (P<0.01). The majority of patients were "satisfied", "very satisfied", or "extremely satisfied" (T3-T4). CONCLUSION: TP was effective in terms of drug-sparing effect, response rate, TP escalation-index percentage, and NeP management. By comparing data from the survival analysis with the response rate and time to response (numeric rating scale from T0 to T4), we found that although TP induced a quick response, a longer period of therapy and higher doses were needed to improve the positive result.

Fasting lipids and anticardiolipin antibodies as risk factors for vascular disease in systemic lupus erythematosus.

Fasting cholesterol, triglyceride, low density lipoprotein cholesterol, high density lipoprotein cholesterol, apoprotein AI, and apoprotein B were measured in 64 patients with systemic lupus erythematosus to assess the risk factors for vascular disease. The relation between the lipid profile, steroid treatment, the presence of anticardiolipin antibodies, and the prevalence of vascular disease was examined. Raised concentrations of triglyceride and apoprotein B were seen in those patients treated with more than the equivalent of 10 mg prednisolone a day in the six months before testing. An increase in vascular disease was found only in the subgroup of patients with increased triglycerides who also expressed anticardiolipin antibodies. This study confirms the association between treatment with high doses of steroids in lupus and the development of an atherogenic plasma lipid profile. The presence of anticardiolipin antibodies compounds the risk of developing vascular disease.

Carnitine and acetylcarnitine in red blood cells.

Carnitine and acetylcarnitine were found to be present in human erythrocytes. Their presence was not as a factor of leucocyte contamination. Carnitine is present within the erythrocyte at a level comparable to that of the plasma, whilst acetylcarnitine is more concentrated within the cell. Red blood cell carnitine and acetylcarnitine do not freely exchange with plasma but intra-erythrocyte acetylcarnitine has a significant relationship to the plasma levels.

The effect of oral supplementation with L-carnitine on maximum and submaximum exercise capacity.

Two trials were conducted to investigate the effects of L-carnitine supplementation upon maximum and submaximum exercise capacity. Two groups of healthy, untrained subjects were studied in double-blind cross-over trails. Oral supplementation of 2 g per day L-carnitine was used for 2 weeks in the first trial and the same dose but for 4 weeks in the second trial. Maximum and submaximum exercise capacity were assessed during a continuous progressive cycle ergometer exercise test performed at 70 rpm. In trial 1, plasma concentrations of lactate and beta-hydroxybutyrate were measured pre- and post-exercise. In trial 2, pre- and post-exercise plasma lactate were measured. The results of treatment with L-carnitine demonstrated no significant changes in maximum oxygen uptake (VO2max) or in maximum heart rate. In trial 1, there was a small improvement in submaximal performance as evidenced by a decrease in the heart-rate response to a work-load requiring 50% of VO2max. The more extensive trial 2 did not reproduce the significant result obtained in trial 1, that is, there was no significant decrease in heart rate at any given submaximal exercise intensity, under carnitine-supplemented conditions. Plasma metabolic concentrations were unchanged following L-carnitine, in both trials. It is concluded, that in contrast to other reports, carnitine supplementation may be of little benefit to exercise performance since the observed effects were small and inconsistent.

Citrate interference with the determination of acetylcarnitine: a method for its elimination.

Citrate can interfere with the determination of acetylcarnitine when measured by a radioisotopic method. In this report we present a modified procedure designed to avoid this effect. Recovery of added acetylcarnitine was approximately 95%. Acetylcarnitine in normal human plasma was found to range from 0.8 to 19.9 nmol/ml with a mean of 6.3; that of human skeletal muscle ranged from 0.1 to 1.6 nmol/mg protein with a mean of 1.08. The results confirm that exercise gives rise to increased acetylcarnitine content of plasma.