This study evaluated the impact of a new epoetin alfa dosing regimen on quality of life (QOL), transfusion requirements, and hemoglobin (Hb) levels in 133 patients with low-risk myelodysplastic syndrome (MDS) and Hb < or =10 g/dl. Epoetin alfa 40,000 IU was given subcutaneously twice weekly; after 4 weeks, the dose could be reduced to 40,000 IU weekly in patients achieving erythroid response. QOL was assessed using the functional assessment of cancer therapy-anemia (FACT-An) questionnaire. FACT-An scores increased on average by 7.5 after 4 weeks and by 8.8 after 8 weeks compared with baseline. FACT-An scores were positively associated with Hb values (r=0.53, P<0.01). The mean FACT-An score increase at week 8 was 10.2 in responders and 5.6 in nonresponders. The overall erythroid response rate at week 8 was 68%: 74% in transfusion-independent patients and 59% in transfusion-dependent patients. Of all responders at week 8, response was maintained in 86% at week 12, 71% at week 16, 65% at week 20, and 54% at week 24. Treatment was generally well tolerated. Our data provide new and encouraging results regarding the benefits of 40,000 IU biweekly induction doses followed by 40,000 IU weekly in improving QOL, correcting anemia, and reducing transfusion requirements in low-risk MDS patients.
Tobacco use is strongly associated with a variety of psychiatric disorders. Smokers are more likely than non-smokers to meet current criteria for mental health conditions, such as mood disorders, anxiety disorders and psychosis. Evidence also suggest that smokers with psychiatric disorders may have more difficulty quitting, offering at least a partial explanation for why smoking rates are higher in this population. The mechanisms linking mental health conditions and cigarette smoking are complex and likely differ across each of the various disorders. The most commonly held view is that patients with mental health conditions smoke in an effort to regulate the symptoms associated with their disorder. However some recent evidence suggests that quitting smoking may actually improve mental health symptoms. This is particularly true if the tobacco cessation intervention is integrated into the context of ongoing mental health treatment. In this paper we reviewed and summarized the most relevant knowledge about the relationship between tobacco use and dependence and psychiatric disorders. We also reviewed the most effective smoking cessation strategies available for patients with psychiatric comorbidity and the impact of smoking behavior on psychiatric medication.
Background: No study has investigated the role of inflammation in explaining the association between early exposures to adverse life events and depressive symptoms in adolescence. Method: Using data from the Avon Longitudinal Study of Parents and Children, we tested if inflammatory markers [serum C-reactive protein (CRP) and interleukin 6 (IL-6)] at age 9 years mediated the association between adverse life events, measured separately for the prenatal (since the beginning of pregnancy) and the childhood (ages 0-9 years) periods, and the development of depressive symptoms at ages 10-17 years. Data (n=4,263) were analysed using mediation analysis in a latent growth curve modelling framework. Results: Depressive symptoms at the beginning of adolescence (age 10) were associated with the number of prenatal events, the number of events around birth and the increase in events over time in childhood (ages 0-9), even after adjustment for confounders. IL-6 partially mediated the association between increasing exposure to events over time in childhood and depressive symptoms at the beginning of adolescence. IL-6 did not mediate any other association between events and symptoms. There was no evidence for mediation by CRP, which was generally unrelated to events. Limitations: The small size of the mediation effect and the robust direct effects of events prenatally and around birth suggest there are multiple routes from early stressors to adolescent depression. Conclusions: In the general adolescent population, increasing exposure to psychosocial stressors over time during childhood is associated with the early onset of depressive symptoms, partly via increasing levels of plasma IL-6.
Obesity and overeating are among the most prevalent health concerns worldwide and individuals are increasingly using performance and image-enhancing drugs (PIEDs) as an easy and fast way to control their weight. Among these, herbal weight-loss products (HWLPs) often attract users due to their health claims, assumed safety, easy availability, affordable price, extensive marketing, and the perceived lack of need for professional oversight. Reports suggest that certain HWLPs may lead to onset or exacerbation of psychiatric disturbances. Here we review the available evidence on psychiatric adverse effects of HWLPs due to their intrinsic toxicity and potential for interaction with psychiatric medications.
Objective: To test the hypothesis that higher plasma levels of inflammatory markers due to exposure to adverse life events may lead to internalising and externalising symptoms in children. Method: Using data from the Avon Longitudinal Study of Parents and Children, a general population birth cohort, we explored if inflammatory markers [serum C-reactive protein (CRP) and interleukin-6 (IL-6)] at age 9 years explain the longitudinal association between adverse life events (at ages 1-9 and 9-11 years) and internalising and externalising symptoms (at ages 9 and 11 years). Data (n=4,583) were analysed using cross-lagged panel modelling to take into account reciprocal associations and reverse causality, and path analyses to test for mediation. Gender, ethnicity, body mass index, maternal education, paternal social class and maternal depression were used as potential confounders. Results: CRP was not associated with adverse life events. There was evidence for partial mediation by IL-6 such that exposure to adverse life events was associated with increased levels of IL-6 later, in turn associated with later internalising symptoms. These associations were robust to adjustment for confounders. IL-6 did not explain part of the opposite association, that of earlier internalising symptoms and later life events, nor did it explain either direction of the association between life events and externalising symptoms. Conclusion: Our findings suggest a pathway that may connect early psychosocial adversity and childhood internalising symptoms via higher plasma levels of inflammatory markers such as IL-6. Highlights
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