BackgroundEfforts to improve treatment of pain using opioids have to adequately take into account their therapeutic shortcomings which involve addictiveness. While there are no signs of an “opioid epidemic” in Germany similar to that in the US, there is little data on the prevalence of prescription opioid misuse and addiction. Therefore, our objective was to screen primary care patients on long-term opioid therapy for signs of misuse of prescription opioids.MethodsWe recruited 15 GPs practices and asked all patients on long-term opioid therapy (> 6 months) to fill out a questionnaire including the “Current Opioid Misuse Measure” (COMM®), a self-report questionnaire. Patients with a malignant disease were excluded.ResultsN = 91 patients participated in the study (response rate: 75.2%). A third (31.5%) showed a positive COMM® - Score which represents a high risk of aberrant drug behaviour. A positive COMM® - Score showed a statistically significant correlation with a lifetime diagnosis of depression and neck pain.ConclusionsWhile Germany does not face an “opioid eoidemic”, addictiveness of opioids should be considered when using them in chronic non-tumor pain. In our study population, almost every third patient was at risk and should therefore be followed up closely. Co-prevalence of depression is a significant issue and should always be screened for in patients with chronic pain, especially thus with aberrant drug behaviour.
Introduction: Endovascular infections with bacteria are often devastating with subsequent high morbidity and mortality. Exo- and or endotoxins of bacteria can activate endothelial cells, leukocytes and platelets. Platelets are first line defence they accumulate at sites of vascular injury or infection. Platelet activation is a necessary step in thrombus formation. Nevertheless, stimulation of platelets will result in de novo protein synthesis despite missing nucleus since platelets armed with translational equipment. Methods: In the present study we determined the effect of staphylococcus aureus α-toxin on platelet activation and de novo protein synthesis analysed with 2-D gels, proteomics and phosphorylation analysis. Results: α-toxin induced platelet activation resulted in modulation of de novo protein synthesis of DJ-1 Protein, ras suppressor protein1, PLEK protein, fumaryl aceto acetase sowie das coronin actin binding protein. This synthesis was time- and concentration-dependent and was markedly increased when platelets adhered to collagen or fibrinogen and required ligation of α IIb β 3 . Accumulation of protein synthesis in platelets was blocked by global translational inhibitors and attenuated by inhibitors that regulate signalling through the mammalian Target of Rapamycin (mTOR). In addition with phosphorylation analysis we were able demonstrate modulation of threonine phosphorylation of fumaryl aceto acetase, phosphor threonin signal of coronin actin binding protein, phosphorylation of peroxiredoxin-6, phosphorylation of tropomyosin-2, phosphothreonin signal of H + transporting two sector ATPase upon α-toxin stimulation. Conclusion: Interactions with staphylococcus aureus α-toxin and platelets might lead to their activation and de novo protein synthesis. These results suggest that platelets have an important role in inflammation besides their aggregating duties in inflammatory disease.
Introduction: Despite improved supportive care, cardiogenic shock still has a significantly high mortality. Among many factors, multiple changes in the neuroendocrine system, are responsible for the high morbidity and mortality. Reduced circulating level of insuline-like growth factor and an elevated level of growth hormone are the reported characteristic findings early in the course of sepsis and. The role of insuline-like growth factor and growth hormone levels in patients with cardiogenic shock has not been described. Methods: The aim of this study was to evaluate the changes of growth hormone/ insuline-like growth factor 1 axis in patients with cardiogenic shock. Results: When admitted, the average GH value of the patient collective was 2.86 μg / l ± 0.78. The values of the majority of the patients (31/41 = 75.6%) were within the normal range. There we no differences among survivors and non-survivors over the 96h observational period. We did not observe differences between either elder and younger patients or female and male CS patients. On admission IGF-1 levels were 76.23 ± 5.67 μg/l (normal range 70– 270 μg/l) at the lower end of the normal range. Over the next 48-72 hours, the value dropped to 66.8 μg/l. However, the drop was not significant (p = 0.14). Non-survivors showed a more rapid decline compared to survivors which stayed within the normal range.Considering the subgroup analysis, it emerges that the average IGF-1 value of male patients remains above 70 μg/l and thus within the normal range, while the IGF-1 level of the female patients during the course which was up to 55.3 μg/l decreases in the course. Clearly female CS patients showed a steeper decline compared to the male patients. Further younger CS patients showed higher levels compared to patients above 70 years. Conclusion: There were no significant changes of growth hormone levels over time and we observed a decrease of insuline-like growth factor 1 in cardiogenic shock patients. In addition, in non-survivors we detected even lower levels of growth hormone and lower levels of insuline-like growth factor 1. We think that both growth hormone and insuline-like growth factor 1 may have l prognostic value to serve as a marker in cardiogenic shock.
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