The journal of pain : official journal of the American Pain Society
-
Chronic fatigue syndrome (CFS) is characterized by debilitating fatigue, often accompanied by widespread muscle pain that meets criteria for fibromyalgia syndrome (FMS). Symptoms become markedly worse after exercise. Previous studies implicated dysregulation of the sympathetic nervous system (SNS), and immune system (IS) in CFS and FMS. We recently demonstrated that acid sensing ion channel (probably ASIC3), purinergic type 2X receptors (probably P2X4 and P2X5) and the transient receptor potential vanilloid type 1 (TRPV1) are molecular receptors in mouse sensory neurons detecting metabolites that cause acute muscle pain and possibly muscle fatigue. These molecular receptors are found on human leukocytes along with SNS and IS genes. Real-time, quantitative PCR showed that 19 CFS patients had lower expression of beta-2 adrenergic receptors but otherwise did not differ from 16 control subjects before exercise. After a sustained moderate exercise test, CFS patients showed greater increases than control subjects in gene expression for metabolite detecting receptors ASIC3, P2X4, and P2X5, for SNS receptors alpha-2A, beta-1, beta-2, and COMT and IS genes for IL10 and TLR4 lasting from 0.5 to 48 hours (P < .05). These increases were also seen in the CFS subgroup with comorbid FMS and were highly correlated with symptoms of physical fatigue, mental fatigue, and pain. These new findings suggest dysregulation of metabolite detecting receptors as well as SNS and IS in CFS and CFS-FMS. ⋯ Muscle fatigue and pain are major symptoms of CFS. After moderate exercise, CFS and CFS-FMS patients show enhanced gene expression for receptors detecting muscle metabolites and for SNS and IS, which correlate with these symptoms. These findings suggest possible new causes, points for intervention, and objective biomarkers for these disorders.
-
To examine the use of extended-release (ER) opioids relative to immediate-release (IR) opioids in chronic opioid prescription episodes, pharmacy claim data from a national health plan database were analyzed. Enrollees having at least 1 pharmacy claim for an opioid formulation between June 2003 and May 2006, and at least 1 year of continuous enrollment after their first observed pharmacy claim were included. Opioid prescription episodes were created by combining contiguous days of therapy, allowing for a maximum of 7 days between refills (>or=8 d = new episode). Outcomes are reported in the form of probabilities and odds ratios (ORs). A total of 3,993,011 opioid prescription episodes were derived from 1,967,898 enrollees. Overall, prescription episodes involving IR preparations (97.7%) were more prevalent than episodes using ER preparations (2.3%). The odds of an ER preparation being prescribed chronically (>or=60 d) were approximately 11 times that of an IR preparation (OR = 10.7); however, the majority of chronic prescription episodes used IR formulations (84.8%). When stratified by prescriber type (specialist vs nonspecialists), the probability of a specialist prescribing ER opioids in these chronic prescription episodes was 19.1% versus 13.7% for nonspecialists. Specialists were about 50% more likely to prescribe ER opioids relative to nonspecialists (OR = 1.49). ⋯ This analysis suggests that the availability of pain-treatment guidelines, recommendations, and education alone may not be enough to influence opioid-prescribing practices in the treatment of chronic pain.
-
The purpose of this study was to identify racial and ethnic differences in patient-reported rates of treatment for chronic pain and ratings of pain-treatment effectiveness among veterans treated in Veterans Affairs (VA) facilities. This was a cross-sectional analysis of data from 255,522 veterans who participated in the VA Survey of the Healthcare Experiences of Patients (SHEP) in Fiscal Year 2005. Measures included demographics, the Veterans Rand Health Survey-12, a single item inquiring if the patient received treatment for chronic pain in the VA within the prior 12 months, and a single item asking the patient to rate the effectiveness of chronic pain care. In a logistic model adjusting for demographics, pain interference, and mental health status, male and female veterans who were Hispanic (OR 1.39 [95%CI 1.26-1.53] and OR 1.57 [1.02-2.43], respectively) or non Hispanic black (OR 1.43 [1.33-1.54] and OR 1.35 [1.02-1.78], respectively) were more likely to report receiving treatment for chronic pain in the prior 12 months compared to non Hispanic white veterans. Among veterans who reported receiving treatment for chronic pain, non Hispanic black men were less likely to rate pain-treatment effectiveness as very good or excellent, compared to non Hispanic white men (OR .809 [.720-.910]). ⋯ In our study, Hispanic and non Hispanic black veterans reported receiving chronic pain treatment more frequently than white veterans. Among veterans reporting pain treatment, non Hispanic black men were somewhat less likely to report receiving highly effective treatment than white men. Further research is needed to understand the reasons for these differences and their potential clinical implications.
-
Although stress plays an important role in chronic widespread pain syndromes, such as fibromyalgia, the underlying mechanism has remained elusive. We have recently demonstrated, in a model of chronic widespread pain, that prolonged enhancement of immune mediator hyperalgesia, induced by unpredictable sound stress, requires a contribution of both the sympathoadrenal (epinephrine) and the hypothalamic-pituitary adrenal (corticosterone) neuroendocrine stress axes. Because this stress protocol produced sustained elevation of plasma epinephrine, in the current study we tested the hypothesis that the sympathoadrenal axis also plays a role in maintenance of symptoms in this model of chronic widespread pain. After establishment, adrenal medullectomy abolished the enhancement of epinephrine-induced cutaneous and muscle hyperalgesia. Administration of stress levels of epinephrine to adrenal medullectomized rats reconstituted the pain phenotype. These observations suggest that the sympathoadrenal stress axis plays a major role in the induction as well as maintenance of stress-induced enhancement of mechanical hyperalgesia, mediated by prolonged elevation of circulating epinephrine. ⋯ We present data showing mechanical hyperalgesia persisting for up to 28 days after exposure to sound stress, with evidence that the sympathoadrenal axis mediator epinephrine plays a major role. These findings could have clinical implications with regard to novel potential treatments for chronic widespread pain syndromes, such as fibromyalgia.