The journal of pain : official journal of the American Pain Society
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Hyperglycaemia and high adiposity are risk factors for pain in diabetes. To clarify these links with pain, the effects of a glucose load on sensory detection, pain sensitivity, conditioned pain modulation (primary aims), and autonomic and endothelial functions (secondary aims) were examined in 64 pain-free participants: 22 with normal adiposity (determined by dual-energy X-ray absorptiometry), 29 with high adiposity, and 13 with combined high adiposity and elevated glycated haemoglobin (HbA1c; including prediabetes and type 2 diabetes). Participants ingested either 37.5-g glucose or 200-mg sucralose (taste-matched) in the first session and crossed over to the other substance in the second session one month later. ⋯ The disruptive effect of hyperglycaemia on conditioned pain modulation increases in line with central obesity, which might facilitate pain in diabetes. PERSPECTIVE: Ingesting 37.5-g glucose (approximately 350-mL soft drink) interfered with pain modulation in pain-free adults with normal adiposity or with combined high adiposity and HbA1c levels. The interference was stronger alongside increasing central obesity, suggesting that controlling blood glucose and body fat mass might help preserve pain modulation.
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Investigating how individual characteristics modify treatment effects can improve understanding, interpretation, and translation of trial findings. The purpose of this secondary analysis was to identify treatment effect modifiers of the MI-NAV trial, a three arm, parallel randomized controlled trial which compared motivational interviewing and stratified vocational advice intervention in addition to usual case management, to usual case management alone. This study included (n=514) participants with musculoskeletal disorders on sick leave for at least 50% of their contracted work hours for at least 7 consecutive weeks with the Norwegian Labour and Welfare Administration. ⋯ For stratified vocational advice intervention versus usual case management, analgesic medication use (MD -26.2, 95% CI -45.7 to -6.7; P=0.009) was identified as a treatment effect modifier (p ≤ 0.05). These findings may assist in more targeted treatment adaptation and translation as well as the planning of future clinical trials. PERSPECTIVE: This secondary analysis of the MI-NAV trial found that analgesic medication use, age and self-perceived health may modify the effect of two vocational interventions on reducing sickness absence in people with musculoskeletal disorders.
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U. S. military veterans experience higher pain prevalence than nonveterans. However, it is unclear how the disparities in pain prevalence have changed over time because previous trend studies are limited to veterans using the Veterans Health Administration. ⋯ PERSPECTIVE: This article uses routinely-collected cross-sectional data that are nationally representative of U. S. adults to present changes in pain prevalence among military veterans compared to nonveterans. The findings underscore the need for improved prevention and pain care programs for veterans, who experienced a widening disproportionate pain burden from 2002 to 2018.
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Chronic pain is driven by factors across the biopsychosocial spectrum. Previously, we demonstrated that magnetic resonance images (MRI)-based brain-predicted age differences (brain-PAD: brain-predicted age minus chronological age) were significantly associated with pain severity in individuals with chronic knee pain. We also previously identified four distinct, replicable, multidimensional psychological profiles significantly associated with clinical pain. ⋯ Repeated measures ANOVA revealed no significant change in profile-related brain-PAD differences over time, but there was a significant decrease in brain-PAD for profile 4 (high optimism/high positive affect), with P = .045. Moreover, profile-related differences in pain severity at baseline were partly explained by brain-PAD differences between profile 3 and 1, or 2; but brain-PAD did not significantly mediate the influence of variations in profiles on changes in pain severity over time. PERSPECTIVE: Accelerated brain aging could underlie the psychological-pain relationship, and psychological characteristics may predispose individuals with chronic knee pain to worse health outcomes via neuropsychological processes.
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Lazertinib (JNJ-73841937, YH25448) is a mutant-selective irreversible epidermal growth factor receptor tyrosine kinase inhibitor targeting both the T790M and activating mutation while sparing wild-type epidermal growth factor receptor. Paresthesia is one of the most common adverse events seen with lazertinib treatment, suggesting that lazertinib could affect the sensory nervous system. However, the mechanism of action for this paresthesia remains unclear. ⋯ Collectively, our data suggest a direct effect of lazertinib on nociceptive sensory neurons via TRPA1 selective mechanisms, which could be a putative mechanism of lazertinib-induced sensory abnormalities in clinical patients. PERSPECTIVE: This article presents a TRPA1-dependent, lazertinib-induced activation of mouse sensory neurons in vitro and lazertinib-induced pain-like behaviors in vivo. The same mechanisms may underlie the clinical condition, suggesting that TRPA1 could be a potential therapeutic target to manage lazertinib-induced paresthesia.