Etanercept and clinical outcomes, fatigue, and depression in psoriasis: double-blind placebo-controlled randomised phase III trial

Tyring, Stephen K.; Gottlieb, Alice B.; Papp, Kim; Gordon, Ken; Leonardi, Craig L.; Wang, Andrea; Lalla, Deepa; Woolley, Michael; Jahreis, Angelika; Zitnik, Ralph; Cella, David; Krishnan, Ranga

doi:10.1016/s0140-6736(05)67763-x

Cited by 988 publications

(801 citation statements)

References 32 publications

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“…In all, 38 RCTs (identified in 38 reports)20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57 met the eligibility criteria and were included, as shown in Figure 1. These trials involved a total of 18 024 patients with plaque psoriasis.…”

Section: Resultsmentioning

confidence: 99%

“…Eighteen RCTs compared TNFi (four adalimumab,20, 21, 22, 23, 24 nine etanercept,26, 27, 28, 29, 30, 31, 32, 34, 35 five infliximab36, 37, 38, 39, 40) with placebo, with three studies reporting MACEs; four RCTs compared ustekinumab (anti‐IL‐12/23) with placebo46, 47, 48 with no MACEs reported. One RCT compared ixekizumab with placebo without MACEs reported 56, 57.…”

Section: Resultsmentioning

confidence: 99%

“…Patients in 27 RCTs20, 21, 22, 25, 27, 28, 29, 30, 31, 34, 35, 36, 37, 38, 39, 40, 43, 45, 46, 47, 48, 50, 52, 53, 57 did not experience MACEs while exposed to any interventions but 10 MACEs were observed during the randomized controlled phase of nine studies 23, 26, 32, 33, 42, 44, 49, 51. Overall, the pooled analysis of these nine trials found that there was no statistically significant difference in the risk of MACEs when comparing biologic therapies with placebo (pooled OR 1·45, 95% CI 0·34–6·24, P = 0·62), as shown in Figure 2a.…”

Section: Resultsmentioning

confidence: 99%

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Impact of biologic therapies on risk of major adverse cardiovascular events in patients with psoriasis: systematic review and meta-analysis of randomized controlled trials

et al. 2017

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SummaryConcerns have been raised regarding an increased risk of major adverse cardiovascular events (MACEs) (myocardial infarction, cerebrovascular accident or cardiovascular death) in patients treated with anti‐interleukin (IL)‐12/23 agents for moderate‐to‐severe psoriasis. We aimed to examine the risk of MACEs in adult patients with plaque psoriasis that are exposed to biologic therapies via a meta‐analysis of randomized controlled trials (RCTs). Data were obtained from systematic searches in the Cochrane Library, MEDLINE and Embase, U.S. Food and Drug Administration, European Medicines Agency, individual pharmaceutical companies online search platforms and five trials registers (up to 31 March 2016). We selected RCTs reporting adverse events in adults with plaque psoriasis receiving at least one licensed dose of biologic therapy, conventional systematic therapy or placebo. We calculated Peto odds ratios (ORs) with 95% confidence intervals (CIs) and calculated I 2 statistics to assess heterogeneity. Overall, 38 RCTs involving 18 024 patients were included. No MACEs were observed in 29 studies, while nine RCTs reported 10 patients experiencing MACEs. There was no statistically significant difference in risk of MACEs associated with the use of biologic therapies overall (OR 1·45, 95% CI 0·34–6·24); tumour necrosis factor‐α inhibitors (adalimumab, etanercept and infliximab) (OR 0·67, 95% CI 0·10–4·63); anti‐IL‐17A agents (secukinumab and ixekizumab) (OR 1·00, 95% CI 0·09–11·09) or ustekinumab (OR 4·48, 95% CI 0·24–84·77). No heterogeneity was observed in these comparisons. In conclusion, the limited existing evidence suggests that licensed biologic therapies are not associated with MACEs during the short randomized controlled periods in clinical trials.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Impact of biologic therapies on risk of major adverse cardiovascular events in patients with psoriasis: systematic review and meta-analysis of randomized controlled trials

et al. 2017

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“…In patients with cancer and rheumatoid arthritis, the FACIT fatigue scale has shown excellent reliability and strong association with the vitality scales of the SF-36. [26][27][28][29] While most fatigue instruments measure the overall experience of fatigue over a period of time ranging from weeks to months, dialysis patients also experience day-to-day and diurnal variation in fatigue. Fatigue assessments using traditional instruments may fail to capture this variability due to recall bias.…”

Section: Measurement Of Fatiguementioning

confidence: 99%

Fatigue in Patients Receiving Maintenance Dialysis: A Review of Definitions, Measures, and Contributing Factors

Jhamb

Weisbord

Steel

et al. 2008

American Journal of Kidney Diseases

284

300

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Fatigue is a debilitating symptom or side effect experienced by many patients on long-term dialysis. Fatigue has a considerable effect on patients' health-related quality of life and is viewed as being more important than survival by some patients. There are many challenges renal providers face when attempting to reduce fatigue in dialysis patients. The lack of a reliable, valid, and sensitive fatigue scale complicates the accurate identification of this symptom. Symptoms of daytime sleepiness and depression overlap with fatigue, making it difficult to target specific therapies. Moreover, many chronic health conditions common in the long-term dialysis population may lead to the development of fatigue and contribute to the day-to-day and diurnal variation of fatigue in patients. Key to improving the assessment and treatment of fatigue is improving our understanding of potential mediators, as well as potential therapies. Cytokines have emerged as an important mediator of fatigue and have been studied extensively in cancer related fatigue. In addition, although erythropoietin stimulating agents (ESA) have been shown to mitigate fatigue, the recent controversy regarding ESA dosing in chronic kidney disease (CKD) suggests that ESA therapy may not serve as the sole therapy to improve fatigue in this population. In conclusion, fatigue is an important and often underrecognized symptom in the dialysis population. Possible interventions for minimizing fatigue in patients on long-term dialysis should be aimed at improving health care provider awareness, developing improved methods of measurement, better understanding of the pathogenesis, as well as management of known contributing factors.

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“…35-37 Further, antidepressants have been shown to reduce inflammatory markers 38-40 and some anti-inflammatory agents appear to have antidepressant properties. 41-43 …”

Section: Current Hypotheses For Biological Mechanisms Promoting Lldmentioning

confidence: 99%

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

McKinney

Sibille

2013

The American Journal of Geriatric Psychiatry

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The phenomenological diagnosis of depression is successful in increasing diagnostic reliability, but it is a classification scheme without biological bases. One subtype of depression for which evidence suggests a unique biological basis is late-life depression (LLD), with first onset of symptoms after the age of 65. LLD is common and poses a significant burden on affected individuals, caretakers, and society. The pathophysiology of LLD includes disruptions of the neural network underlying mood, which can be conceptualized as the result of dysfunction in multiple underlying biological processes. Here, we briefly review current LLD hypotheses and then describe the characteristics of molecular brain aging and their overlap with disease processes. Further, we propose a new hypothesis for LLD, the Age-by-Disease Interaction hypothesis, which posits that the clinical presentation of LLD is the integrated output of specific biological processes that are pushed in LLD-promoting directions by changes in gene expression naturally occurring during brain aging, hence leading the brain to a physiological state that is more susceptible to LLD, since additional pushes by genetic, environmental and biochemical factors may now be sufficient to generate dysfunctional states that produce depressive symptoms. We put our propositions together into a decanalization model to aid in illustrating how age-related biological changes of the brain can shift the repertoire of available functional states in a pro-depression direction, and how additional factors can readily lead the system into distinct and stable maladaptive phenotypes, including LLD. This model brings together basic research on neuropsychiatric and neurodegenerative diseases more closely with the investigation of normal aging. Specifically, identifying biological processes affected during normal aging may inform the development of new interventions for the prevention and treatment of LLD.

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Etanercept and clinical outcomes, fatigue, and depression in psoriasis: double-blind placebo-controlled randomised phase III trial

Cited by 988 publications

References 32 publications

Impact of biologic therapies on risk of major adverse cardiovascular events in patients with psoriasis: systematic review and meta-analysis of randomized controlled trials

Impact of biologic therapies on risk of major adverse cardiovascular events in patients with psoriasis: systematic review and meta-analysis of randomized controlled trials

Fatigue in Patients Receiving Maintenance Dialysis: A Review of Definitions, Measures, and Contributing Factors

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

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