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Investigations of migraine among childhood cancer survivors have predominantly relied on self-reported information and hospital discharge diagnoses. Alone, both approaches are liable to bias. We used Danish nationwide registers to obtain data on both prescriptions of acute migraine medications (antimigraines) and hospital discharge diagnoses of migraine to assess the relative risk of migraine across a wider spectrum of migraine presentations than previously studied.
Learn More >Migraine and headache frequently co-occur with type 2 diabetes (T2D), suggesting a shared aetiology between the two conditions. We used genome-wide association study (GWAS) data to investigate the genetic overlap and causal relationship between migraine and headache with T2D. Using linkage disequilibrium score regression (LDSC), we found a significant genetic correlation between migraine and T2D ( = 0.06, = 1.37 × 10) and between headache and T2D ( = 0.07, = 3.0 × 10). Using pairwise GWAS (GWAS-PW) analysis, we identified 11 pleiotropic regions between migraine and T2D and 5 pleiotropic regions between headache and T2D. Cross-trait SNP meta-analysis identified 23 novel SNP loci ( < 5 × 10) associated with migraine and T2D, and three novel SNP loci associated with headache and T2D. Cross-trait gene-based overlap analysis identified 33 genes significantly associated ( < 3.85 × 10) with migraine and T2D, and 11 genes associated with headache and T2D, with 7 genes (, , , , , , and ) common between them. There was also a significant overlap of genes nominally associated ( < 0.05) with both migraine and T2D ( = 2.83 × 10) and headache and T2D ( = 4.08 × 10). Mendelian randomisation (MR) analyses did not provide consistent evidence for a causal relationship between migraine and T2D. However, we found headache was causally associated (inverse-variance weighted, OR = 0.90, = 7 × 10) with T2D. Our findings robustly confirm the comorbidity of migraine and headache with T2D, with shared genetically controlled biological mechanisms contributing to their co-occurrence, and evidence for a causal relationship between headache and T2D.
Learn More >This study assessed the impact of cancer-related neuropathic pain (CRNP) on patients and the importance of the patient-healthcare professional (HCP) relationship in diagnosis and management.
Learn More >Active duty (AD) women suffer with chronic pelvic pain (CPP) while providers tackle diagnoses and treatments to keep them functional without contributing to the opioid epidemic. The purpose of this randomized trial was to determine the effectiveness of noninvasive, self-explanatory mindfulness-based stress reduction (MBSR) or self-paced healthy lifestyle (HL) interventions on CPP in AD women. A 6-week, interventional prospective study with AD women aged 21-55 years at Mountain Home (MTHM), Idaho, was conducted. Women were randomly assigned to MBSR ( = 21) or HL ( = 20) interventions. The primary outcome was pain perception. The secondary outcomes were depression and circulating cytokine levels. Women in the MBSR group exhibited reduced pain interference ( < 0.01) and depression ( < 0.05) alongside decreased interleukin (IL)-4 ( < 0.05), IL-6 ( < 0.05), eotaxin ( < 0.05), monocyte chemoattractant protein-1 ( = 0.06), and interleukin-1 receptor antagonist (IL-1ra) ( < 0.01) and increased vascular endothelial growth factor ( < 0.05). Women in the HL group did not have changes in pain; however, they did exhibit reduced depression ( < 0.05) alongside decreased granulocyte-macrophage colony-stimulating factor ( < 0.05) and increased tumor necrosis factor alpha ( < 0.05), stromal cell-derived factor-1 ( < 0.01), and IL-1ra ( < 0.01). AD women receiving MBSR or HL had reduced depression scores and altered circulating cytokine levels; however, only those receiving MBSR had reduced pain perception. Findings support MBSR as an effective and viable behavioral treatment for AD women suffering from CPP and provide premise for larger randomized controlled studies. MOCHI-An RCT of mindfulness as a treatment for CPP in AD Women NCT04104542 (September 26, 2019).
Learn More >Fatigue is a major complaint in primary Sjögren's syndrome (pSS). To acquire a better understanding of fatigue in pSS, we investigated objective measures of performance decline (performance fatigability). Furthermore, we evaluated the relationship of self-reported fatigue with performance fatigability and factors modulating perceptions of fatigability (perceived fatigability).
Learn More >Etrolizumab is a gut-targeted anti-β7 monoclonal antibody targeting α4β7 and αEβ7 integrins. We aimed to compare the safety and efficacy of two doses of etrolizumab with placebo in patients with Crohn's disease.
Learn More >The mechanisms of chronic pain are complex, and genetic factors play an essential role in the development of chronic pain. Neuropathic pain (NP) and inflammatory pain (IP) are two primary components of chronic pain. Previous studies have uncovered some common biological processes in NP and IP. However, the shared genetic mechanisms remained poorly studied. We utilized multi-omics systematic analyses to investigate the shared genetic mechanisms of NP and IP. First, by integrating several genome-wide association studies (GWASs) with multi-omics data, we revealed the significant overlap of the gene co-expression modules in NP and IP. Further, we uncovered the shared biological pathways, including the previously reported mitochondrial electron transport and ATP metabolism, and stressed the role of genetic factors in chronic pain with neurodegenerative diseases. Second, we identified 24 conservative key drivers (KDs) contributing to NP and IP, containing two well-established pain genes, and , and some novel potential pain genes, such as and . The subnetwork of those KDs highlighted the processes involving the immune system. Finally, gene expression analysis of the KDs in mouse models underlined two of the KDs, and , with unidirectional regulatory functions in NP and IP. Our study provides strong evidence to support the current understanding of the shared genetic regulatory networks underlying NP and IP and potentially benefit the future common therapeutic avenues for chronic pain.
Learn More >The aim of this study was to evaluate laboratory parameters for investigating their potential predictive ability to differentiate patients with fibromyalgia (FM) from healthy subjects. We carried out a case-control study with 79 FM patients and 20 controls to analyze complete blood count, serum chemistry profile, glycosylated hemoglobin (HbA1c), and erythrocyte sedimentation rate (ESR). The predictive value of these parameters was determined by receiver operating characteristic (ROC) analysis. We also examined the relationships with clinical parameters (functional capacity, pain, and physical and mental health status). Results showed significant differences in red blood cell count, hematocrit, mean corpuscular hemoglobin concentration, platelet count, creatinine, HbA1c, and ESR between groups. According to ROC analysis, all these parameters may assist in making FM diagnosis. Hematocrit and ESR values were correlated with FM clinical parameters. The determination of these routine laboratory parameters may be an uncomplicated means of facilitating FM diagnosis, together with the clinical data of the patient.
Learn More >Pain catastrophizing is understood as a negative cognitive and emotional response to pain. Researchers, advocates and patients have reported stigmatizing effects of the term in clinical settings and the media. We conducted an international study to investigate patient perspectives on the term pain catastrophizing. Open-ended electronic patient and caregiver proxy surveys were promoted internationally by collaborator stakeholders and through social media. 3,521 surveys were received from 47 countries (77.3% from the U.S.). The sample was mainly female (82.1%), with a mean age of 41.62 (SD 12.03) years; 95% reported ongoing pain and pain duration > 10 years (68.4%). Forty-five percent (n = 1,295) had heard of the term pain catastrophizing; 12% (n= 349) reported being described as a 'pain catastrophizer' by a clinician with associated high levels of feeling blamed, judged, and dismissed. We present qualitative thematic data analytics for responses to open-ended questions, with 32% of responses highlighting the problematic nature of the term. We present the patients' perspective on the term pain catastrophizing, its material effect on clinical experiences, and associations with negative gender stereotypes. Use of patient-centered terminology may be important for favorably shaping the social context of patients' experience of pain and pain care. PERSPECTIVE: : Our large international patient survey results show that 45% of the sample had heard of the term pain catastrophizing, about one-third spontaneously rated the term as problematic, and 12% reported having the term applied to them with most reporting this to be a negative experience. Clinician education regarding the use of patient-centered terminology may help to improve patients' experience of care and reduce stigma.
Learn More >Tropomyosin receptor kinase A (TrkA/NTRK1) is a high-affinity receptor for nerve growth factor (NGF), a potent pain mediator. NGF/TrkA signaling elevates synovial sensory neuronal distributions in the joints and causes osteoarthritis (OA) pain. We investigated the mechanisms of pain transmission as to whether peripheral sensory neurons are linked to the cellular plasticity in the dorsal root ganglia (DRG) and are critical for OA hyperalgesia. Sensory neuron-specific deletion of was achieved by tamoxifen injection in 4-week-old () mice. OA was induced by partial medial meniscectomy (PMM) in 12-week-old mice, and OA-pain-related behavior was analyzed for 12 weeks followed by comprehensive histopathological examinations. OA-associated joint pain was markedly improved without cartilage protection in sensory-neuron-specific conditional knock-out (cKO) mice. Alleviated hyperalgesia was associated with suppression of the NGF/TrkA pathway and reduced angiogenesis in fibroblast-like synovial cells. Elevated pain transmitters in the DRG of OA-induced mice were significantly diminished in sensory-neuron-specific cKO and global cKO mice. Spinal glial activity and brain-derived neurotropic factor (BDNF) were significantly increased in OA-induced mice but were substantially eliminated by sensory-neuron-specific deletion. Our results suggest that augmentation of NGF/TrkA signaling in the joint synovium and the peripheral sensory neurons facilitate pro-nociception and centralized pain sensitization.
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