This article presents an experiment suggesting that a placebo treatment applied to a rubber hand during the rubber hand illusion can produce placebo analgesia. This finding indicates that embodiment may influence the placebo effect, a previously unexamined factor in the treatment process with potential applications to treatment administration.
Placebo analgesia is a robust experimental and clinical phenomenon. While our understanding of the mechanisms of placebo analgesia has developed rapidly, some central questions remain unanswered. Among the important questions is how placebo anal-gesia interacts with active analgesic effects. It is an assumption underlying double-blind randomized placebo-controlled trials (RCTs) that the true effect of a treatment can be determined by examining the effect of the active treatment arm and subtracting the response in the placebo group (“the assumption of additivity”). However, despite the importance of this assumption for the interpretation of RCTs, it has rarely been formally examined. This article reviews the assumption of additivity in placebo analgesia by examining studies employing factorial designs manipulating both the receipt of an active analgesic and instructions about the treatment being delivered. In reviewing the literature, we identified seven studies that allowed a test of additivity. Of these, four found evidence against additivity, while the remaining three studies found results consistent with additivity. While the limited available data are somewhat mixed, the evidence suggests that at least under some conditions the assumption of additivity does not hold in placebo analgesia. The concordance between mechanisms of the active analgesic and placebo analgesia may influence whether additivity occurs or not. However, more research using factorial designs is needed to disentangle the relationship between placebo analgesia and the active effect of analgesic treatments.
Aim: Gout is the most common form of inflammatory arthritis in men. Despite the availability of effective urate-lowering therapies (ULT), the management of gout is suboptimal due to poor persistence with ULT. This study examined national prescribing patterns of ULT to determine persistence with allopurinol in Australia.Methods: A 10% sample of the Australian Pharmaceutical Benefits Scheme dispensing claims database was used to identify individuals initiated on allopurinol between April 2014 and December 2019. The number of allopurinol scripts dispensed was used to estimate persistence with allopurinol. Persistence was defined as the number of months from initiation until discontinuation (last prescription with no further scripts acquired for a period thereafter). Kaplan-Meier curves were used to examine persistence, while Cox regression analysis was used to examine the influence of gender, concomitant colchicine and age.Results: The largest drop in persistence occurred immediately after initiation, with 34% of patients discontinuing allopurinol 300-mg therapy in the first month. Median persistence with allopurinol 300 mg was 5 months (95% confidence interval 4.76-5.24), with around 63% of individuals not persisting with this therapy for more than 12 months. Concomitant prescription of colchicine on the day of allopurinol initiation only occurred in 7% of allopurinol initiations. No increase in persistence was observed for those co-prescribed colchicine. Conclusion:Persistence with allopurinol was poor. More effective methods targeting prescribers, patients and systems are required to promote persistence with allopurinol. Improving persistence to allopurinol is an important public health goal given the proven potential of this medication to eliminate gout.
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